Obesity and weight regulation

On the greatly-exaggerated demise of the insulin-hypothesis

February 6, 2012 241 Comments

Last week, I tweeted a New England Journal of Medicine image challenge, part of the journal’s continuing education program for physicians. I suggested that it might be a source of comfort to those who were worried about the insulin hypothesis as a viable hypothesis to explain obesity and excess fat accumulation. Although I linked to the NEJM page and the link worked for me, I gather some who tried to click on it were presented with other image challenges and were wondering, for instance, why I cared if they could diagnose a pneumothorax when they saw one. So here’s the image challenge I had in mind, and the correct response is below. The relevance should be reasonably obvious.

Download NEJM Image Challenge (PDF)

Filed Under: Obesity and weight regulation Tagged With: fat accumulation, insulin hypothesis, insulin lipohypertrophy, New England Journal of Medicine, obesity

Updates for 2012

January 21, 2012 120 Comments

Checking in after a long absence (working too hard, and blogging too little), I have news and updates for 2012.

The first order of business is a letter to the editor of the New York Times in response to Tara Parker-Pope’s “The Fat Trap” article that ran on the cover of the January 1st NYT Magazine. I wrote the letter with my colleague Peter Attia, more on whom shortly, and we posted it online at ipetitions.com. We tried to get it signed by as many MDs and PhDs as possible, to make the case to the editors at the Times and to Tara herself that a significant number of medical professionals and researchers take the alternative hypothesis of obesity seriously and so should they. As it is, we were able to get over 250 such degreed cosigners, which was more than we expected and more than we hoped. The Times is running a 150-word summary of the letter as a letter to the editor in this week’s magazine with a link to the full letter on line, which you should all feel free to sign. I also recommend you click on the signatures link to see who’s signed it and read the comments.

“The Fat Trap” made the point that obesity is effectively incurable. The letter argues that it only appears to be incurable because the wrong treatment is being used, and the wrong treatment is being used because the people studying the disorder don’t understand what causes it in the first place – like trying to treat a bacterial infection with an anti-viral medication and then throwing up your hands and saying it’s hopeless when the treatment doesn’t work. Should they ever get the cause right, then the correct treatment becomes obvious.

Second order of business is my colleague Peter Attia. Peter and I started working together last April after he came to San Francisco to meet me. He had recently read Why We Get Fat and Good Calories, Bad Calories and my sugar article in The New York Times, and he had 27-pages of questions he wanted to ask. I was impressed, if not awed, and we hit it off. I suggested to Peter that he should take over the insurgency and I’d be the figurehead, as I’ve been burnt out and overworked for a decade. The good news is he took me up on it, except that now he has me working twice as hard as ever to help.

Among the projects we have in the works is a non-profit, the Nutrition Science Initiative (NuSI), to raise money for the kind of research we think is necessary to clarify the relationship between dietary nutrients, obesity. diabetes and their related chronic diseases. We have a specific plan of research to pursue (or rather to fund so that established, unbiased researchers can then do the studies) and have already recruited a world class scientific advisory board and executive board. I’ll fill in the details in the next couple of weeks as we get closer to going on-line.

Peter’s blog, The War on Insulin.com, is up and running. Peter takes many of my ideas and expands on them from his own unique perspective. He also blogs about his own personal experience on a conventional healthy diet and then a ketogenic diet. What makes this particularly interesting is that Peter is a fanatic endurance athlete and an obsessive self-experimenter, and he comes at his experience and his blog with a significant amount of medical training and acumen. I highly recommend that he be read. (And if anyone can figure out how he manages to workout 23 hours a week, function in a full-time job, blog regularly on nutrition and physical activity, and be there for his family and not collapse in a puddle of exhaustion, please let me know.)

The next order of business is an exciting and promising project. My friend Larry Istrail is a medical student at Virginia Commonwealth University. He’s recently created the Ancestral Weight Loss Registry, to collect and publish data on individuals who have tried to lose weight with a paleo/carbohydrate-restricted diet. He’s also spent much of the last few years compiling clinical data on many aspects of carb-restricted eating in the related science section, such as the efficacy of such diets for weight loss or the effects of saturated fats and cholesterol intake on heart disease. Tara Parker-Pope’s article in The New York Times claimed that the National Weight Control Registry (about which I could easily fill up a few blog posts with criticisms) has some 10,000 people registered in over 15 years. We’re hoping that the Ancestral Weight Loss Registry will beat that in a few months. Using this kind of self-selected data to do good science is tricky if not perhaps impossible, but it will be interesting to see what happens.

If you’re reading this and you’ve lost significant weight on a carb-restricted/paleo diet (or if you haven’t), please check out the Ancestral Weight Loss Registry and enter your details. I’m also hoping you’ll pass this on to your friends and if you have a blog or a podcast, to your readers and/or listeners.

The last order of nutrition/obesity-related interest is that I have some speaking engagements coming up in the next few months and I thought I’d mention them, which I’ve been lax in doing in the past. I’m giving a couple of readings in the Berkeley/Oakland area, a lecture at the Seattle Town Hall and the University of Texas San Antonio, an after dinner talk at a diabetes conference at Auburn University, a talk at an integrative health conference in Los Angeles and a lecture in Santa Cruz, courtesy of the local office of education. There’s also a couple of talks coming up in Europe — in Amsterdam and Brussels — and a slew of conferences and keynote addresses into the summer and fall, details of which will go up shortly. The dates and locations and links through April (Amsterdam not yet included) are up on my calendar, and I promise I’ll do a much better job in the future of keeping the calendar updated far in advance.

Along these lines (okay, this is the last order of nutrition/obesity-related interest), the email subscription to my blog now works as it should, and will NOT subscribe readers to “Two and the Zoo” like it used to. Feel free to sign up if you’re interested.

Finally, my best friend Marion Smith recently did a post on her website about our shared history with one of the more distasteful but apt terms in journalism and writing. Marion credits me for the terminology, although I’m going to give credit here to Calvin Trillin, who came up with it. It was from reading Trillin in my salad days — back when I had time to read — that I learned of the term and the technique and embraced it. Either way, Marion is a wonderful writer and nutrition and weight is not the subject. Both reasons to read her blog.

And with that, a belated Happy New Years.

Filed Under: Diets, Events, General, News, Obesity and weight regulation, Weightloss Diets

Catching up on lost time – the Ancestral Health Symposium, food reward, palatability, insulin signaling and carbohydrates… Part II(d)

November 23, 2011 46 Comments

When last I left off, the subject of discussion was the critical question about the food reward/palatability hypothesis of obesity: Can palatability and reward value of foods be disassociated from the metabolic and hormonal effects of the individual nutrients being consumed and, in particular, the sugar and refined grains that “hyper-rewarding” foods seem to invariably contain?

Let’s start with the experiment in humans that Dr. Stephan Guyenet of wholehealthsource.org finds such compelling support of the food reward hypothesis. This was work done by Ted Van Itallie and Sami Hashim back in the 1960s. (For an idea of the simplistic notions held by Dr. Hashim about obesity and its cause and prevention, I highly recommend this video here. I discuss Dr. Van Itallie’s critical role in shaping the current thinking about obesity — i.e., the mess we’re in today — in chapter 23 of Good Calories, Bad Calories.)

In his “Case for the Food Reward Hypothesis of Obesity, Part II” post, Dr. Guyenet argues that this experiment is important because it demonstrates what he considers one of several critical requirements for the validity of the food reward hypothesis: “Decreasing the reward/palatability of the diet should cause fat loss in animals and humans that carry excess fat.” Here’s what he says:

One of the most striking weight loss studies I’ve seen was conducted in 1965 and involved feeding a bland liquid diet through a dispensing straw (12). Lean and obese volunteers were instructed to eat as much of the liquid food as they wanted, but they were permitted no other food. While lean volunteers ate a normal amount of calories and maintained weight, obese volunteers dramatically reduced their spontaneous calorie intake and lost fat rapidly, with one man losing 200 lbs in 255 days without hunger. This is exactly what one would expect if unpalatable/unrewarding food lowered the biologically “defended” level of fat mass. Interestingly, the diet was high in sugar but was otherwise very low in palatability/reward value.

This was Dr. Guyenet’s second discussion of the tube-feeding paper. As he explained in an earlier post on this experiment, the total number of subjects was four: two lean and two obese. The two lean were kept on the feeding machine for 16 and 9 days. They didn’t bother to decrease caloric intake, and so their experiment ended then. The two obese subjects, however, curtailed intake dramatically, to 275 calories per day for the male volunteer and 144 for the female). The man stayed with the feeding machine for another 70 days and was then sent home with the formula and the instruction to drink only 400 calories a day. He kept this up for another half year until he had lost the 200 pounds. Says Dr. Guyenet (in “Food Reward: a Dominant Factor in Obesity, Part II”, his earlier post):

This machine-feeding regimen was nearly as close as one can get to a diet with no rewarding properties whatsoever. Although it contained carbohydrate and fat, it did not contain any flavor or texture to associate them with, and thus the reward value of the diet was minimized. As one would expect if food reward influences the body fat setpoint, lean volunteers maintained starting weight and a normal calorie intake, while their obese counterparts rapidly lost a massive amount of fat and reduced calorie intake dramatically without hunger. This suggests that obesity is not entirely due to a “broken” metabolism (although that may still contribute), but also at least in part to a heightened sensitivity to food reward in susceptible people. [The italics are mine.]

So immediately we have a problem, and it strikes me as near-fatal for the food reward hypothesis of obesity. In Dr. Guyenet’s first post on the experiment (the one immediately above), he says that the regimen “was nearly as close as one can get to a diet with no rewarding properties whatsoever…. It did not contain any flavor or texture to associate them with, and thus the reward value of the diet was minimized.” In his second post (the first of the two I quote, just to make life confusing), he notes that the diet was “high in sugar” although he tries to hold onto the food reward hypothesis by stating that it “was otherwise very low in palatability/reward value.”

This is why I asked Dr. Guyenet at the AHS whether the formula diet had sugar in it. If it did, then how could it be bland? And how could it have a low food reward value, which is, more or less, the whole point? It might have a lower food value than what the two obese subjects were eating prior to the experiment, but low?

As Hashim and Van Italie noted in a footnote in their 1965 paper, and as Dr. Guyenet notes in his blog, the formula used was Nutrament. This was a liquid diet formula that went on sale in 1960 (according to Wikipedia), and if the composition then was anything like the composition now, a significant portion of the carbohydrate calories came from sugar.

So was it non-rewarding? Hashim and Van Italie refer to it as “bland” and Guyenet assumes it was as well, hence his description of it as “otherwise very low in palatabily/reward value.” But it had to be sweet if it had significant sugar in it; and indeed in the modern incarnation of Nutrament, which may or may not be the same as the original, there are 47 grams in every 12-ounce serving. This happens to be more sugar than you’d find in a 12-ounce can of Coke.

Frankly, the stuff sounds awful, but low in reward value? Well, only if a Coke is, too, and certainly not if Dr. Guyenet includes “liquid calories, particularly sweetened beverages” among the low-hanging fruit of the food reward hypothesis, which he does.

In fact, the point of a diet formula like Nutrament is not just that it contains enough protein and other nutrients that people can thrive on, say, 400 or 800 calories-a-day of the stuff. But it also has to taste good, so that consumers will continue to buy it and drink it day in and day out, even after they’ve moved into the weight maintenance phase of their lives — i.e., for the rest of their lives. It’s an example from the 1960s of what Dr. Guyenet describes as “the goal of processed food manufacturers… to create a product that maximally reinforces purchase and consumption behaviors—food reward!”

We can try to get around this problem by suggesting that bland and sweet is just not high in food reward value, as Dr. Guyenet tries to do, but we’re going to resort to this kind of, well, blatant contradiction only because we want to salvage this experiment as support for the hypothesis. So this formula must have a low-food reward value because an obese subject consumed less of it and lost weight and because we believe that foods with high reward value cause people to gain weight. Now we’re back to circular-definition land, a place I would prefer to never visit.

Now, how about the idea that a “cafeteria” or “junk food” diet makes humans and animals fat, a concept that was pioneered by Anthony Sclafani. The assumption is that such a diet is fattening because there’s something about eating a variety of foods, mostly junk foods, that is so rewarding or at least so less bland than a plain chow diet that both humans and animals get fat eating it. Here’s how Dr. Guyenet describes it:

In this model, animals are allowed free access to standard chow and water while concurrently offered highly palatable, energy dense, unhealthy human foods ad libitum.

In other words, they’re given an unlimited amount of human junk food in addition to their whole food-based “standard chow.” In this particular paper, the junk foods included Froot Loops, Cocoa Puffs, peanut butter cookies, Reese’s Pieces, Hostess Blueberry MiniMuffins, Cheez-its, nacho cheese Doritos, hot dogs, cheese, wedding cake, pork rinds, pepperoni slices and other industrial delicacies. Rats exposed to this food almost completely ignored their healthier, more nutritious and less palatable chow, instead gorging on junk food and rapidly attaining an obese state.

Aside from Dr. Guyenet’s description of standard rat chow as “whole-food based,” my major problem with this (which is the same problem Ramirez et al had 20-odd years ago with the existing research then) is that this is an experiment that changes an unholy host of variables, and the results are evoked to make a point about one: food reward value.

One advantage I have in this nutrition business as an arguably ignorant journalist is that I actually get to interview the researchers who do the work. (Technically anyone could do this, but the researchers are certainly more likely to give their time to a journalist, ignorant or not, than to what one of my acquaintances in academia refers to as “just a person.”) I interviewed Sclafani back on January 30, 2003 for GC,BC, and the interview revealed the obvious problem with this interpretation. As Sclafani told me, they started their cafeteria diet (which he was calling the “supermarket” diet at the time) with a variety of different foods (not quite as wide a variety as Dr. Guyenet is discussing above, but wide nonetheless): chocolate chip cookies, salami, cheese, bananas, marshmallows, milk chocolate, peanut butter and sweetened condensed milk, and then they later simplified it to four foods because the rats didn’t eat all the foods they gave them.

Which foods did they ignore? Sclafani said they never did a systematic study, nor had anyone else, as far as he knew (as of January 2003), but cheese, salami and peanut butter—the foods highest in fat and lowest in refined grains and sugar—seemed to be the foods they avoided in favor of the sweeter, starchy options. So the obvious question: are refined grains and/or sugar necessary to impart not just reward value, but reward value that leads to people and animals getting fat?

In fact, Sclafani told me that they had based their selection of foods on a hunch about what rats preferentially like, and so that’s why they included cheese in the list. It seemed like an obvious choice. After all, don’t you stick cheese in mouse traps when you want to rid your house of mice? And yet, cheese was not among the foods the Sclafani’s rats preferentially ate when given all these other refined carbs and sugary foods to eat instead. Maybe because the cheese was unrewarding. Or maybe because it was relatively if not completely refined-carb and sugar free, as were the salami and peanut butter.

This inability to differentiate food reward and/or palatability from the presence of refined carbs and sugars haunts virtually every example of the studies cited to document food reward and/or palatability.

Another example, not one used by Dr. Guyenet, is Kelly Brownell’s Yale Food Addiction Scale . This scale attempts to identify people who suffer from addiction to certain foods. The scale is based on a survey that gives a series of statements about eating habits. Subjects must say how true each statement is, on a scale from “never” to “four or more times or daily.” This goes along with a list of foods of which food addicted subjects might have “difficulty controlling their intake.” Here are the first four statements to give you an idea of what Brownell is getting at:

I find that when I start eating certain foods, I end up eating much more than planned.
I find myself continuing to consume certain foods even though I am no longer hungry.
I eat to the point where I feel physically ill.
Not eating certain types of food or cutting down on certain type of food is something I worry about.

So let’s assume, for the sake of argument at least, that the “certain foods” that illicit addictive behavior is very similar to the list of hyper-rewarding foods, the ones most likely to cause obesity. Here’s Brownell’s list of the foods that are most likely to be addictive:

-       Sweets like ice cream, chocolate, doughnuts, cookies, cake, candy, ice cream [yes, ice cream is listed twice.]

-       Starches like white bread, rolls, pasta, and rice

-       Salty snacks like chips, pretzels, and crackers

-       Fatty foods like steak, bacon, hamburgers, cheeseburgers, pizza, and French fries

-       Sugary drinks like soda pop

With the exception of steak and bacon, all of these foods are high in carbohydrates — refined or otherwise (the French Fries) — and/or sugars, even the foods defined as “fatty” with the aforesaid exceptions. If these foods are addictive and if they cause obesity, is it because they’re addictive or is it because of the metabolic and hormonal effects of consuming them — their effects on insulin signalling? There’s no way to tell without an exceedingly well-controlled and well-conceived experiment, but you can guess where my vote lies.

What about the steak and bacon, then? Well, if you ate nothing but those—steak and bacon every day, plus, say, the hamburgers or cheeseburgers without the refined grains attached, i.e., the buns—you’d be eating a weight loss diet (a ketogenic diet) and would almost assuredly lose weight doing it. So whether or not you consider steak and bacon addictive, it’s unlikely that they could be defined as foods high in reward value because they would tend to refute the hypothesis that high food reward value causes obesity. And now we’d be back to this problem of having to differentiate between hyper-rewarding foods or at least addictive foods that come with refined/easily digestible carbohydrates and sugars and cause fat accumulation and hyper-rewarding foods that don’t, and well, don’t.

Of the examples I could find in Dr. Guyenet’s discussions of the food reward/palatability hypothesis that held the promise of differentiating food reward value from underlying metabolic effects of the foods themselves (and the presence of refined or easily-digestible carbs and sugars), none of them actually came through with meaningful evidence.

The studies most likely to offer such a differentiation were those mentioned by Dr. Guyenet in his post, “The Case for the Food Reward Hypothesis of Obesity, Part II.” These were the studies evoked as evidence for the hypothesis because they demonstrate that “Individual sensitivity to food reward should predict future fat gain.” About this evidence he says:

I’m aware of three studies that have investigated this question. In the first, researchers found that the reinforcing value of food relative to a non-food stimulus predicted fat gain over the next year in 7-10 year old children (19). In the second, the responsiveness of reward-related brain regions to imagining palatable vs. unpalatable foods (as assessed using fMRI) predicted body mass index (BMI) gains in adolescent girls, and this effect was modified by gene polymorphisms in dopamine receptor genes (20). The third study also used fMRI to demonstrate that greater activation in reward-related brain regions during exposure to appetizing food cues predicted greater BMI gains over time in adolescent girls (21).

But of those three studies, none of them define what the high reward foods were, which foods were considered palatable and which were unpalatable. For all we know, the palatable foods were the ones rich with refined grains and sugars and the reason reward-related regions of our brain light up when we eat them (or at least when obese people do) is because our brains are responding to what these foods do to our bodies.

Reference 19 doesn’t specify at all which foods are actually high in reward value, nor do references 20 and 21, which are both by the same authors. They do, however, include a “cheeseburger” as an example of a processed food, demonstrating a certain bias against cheeseburgers that may be misplaced.

And reference 21 says that while BMI may have been related to the extent of activation in reward-related brain regions, as Dr. Guyenet points out, this was true regardless of whether the food being imagined was rewarding or palatable or not. Or the authors put it, “BMI [body mass index] was positively correlated with behavioral response to both appetizing and unappetizing food images, implying that food cues in general trigger greater attention in overweight vs. lean individuals.”

One obvious interpretation is that overweight individuals are hungrier than lean individuals, and so they have a greater response to any food in their reward centers. And, in fact, one point Dr. Guyenet’s mentor, Michael Schwartz, made of interest in his 2006 review in Nature “Central nervous system control of food intake and body weight” was that “food deprivation strongly augments the reward value… reduced food availability seems to exert a global, stimulatory effect on reward perception.” And so maybe the greater the BMI, the more likely the subjects were hungry or food deprived—a phenomenon I discuss at length in GC,BC— a state that could be due to increased insulin secretion and chronic hyperinsulinemia. And maybe refined grains and sugars augment reward value because they cause us to secrete more insulin and store calories away as fat and glycogen and make us hungry.

In GC,BC I quote Mark Friedman commenting on this potential carbs-insulin-hunger connection regarding just the cephalic phase of insulin secretion, the one that comes just by thinking about a particular food:

This cephalic release of insulin also serves to clear the circulation of “essentially anything an animal or a person can use for fuel. Not just blood sugar, but fatty acids, as well. All those nutrients just go away.” Hence, the thought of eating makes us hungry, because the insulin secreted in response depletes the bloodstream of the fuel that the peripheral tissues and organs need to survive.

And if this happens more in individuals who are insulin resistant, as most obese individuals are, we’re now back at a hypothesis that maybe the insulin signaling in the body is running the brain’s response, not vice versa. Yes, it’s the brain that’s stimulating the insulin secretion when we think about food, but what makes us hungry and makes the food then seem so rewarding is the effect of the insulin secreted in the body.

Filed Under: Bad Science, Calories-in-Calories-out, Diets, food reward/palatability hypothesis, General, Glycemic Index, Obesity and weight regulation, Weightloss Diets

Catching up on lost time – the Ancestral Health Symposium, food reward, palatability, insulin signaling and carbohydrates… Part II(c)

November 18, 2011 148 Comments

We’ve been discussing the food reward/palatability hypothesis of obesity and whether this idea adds anything meaningful to our understanding of obesity. Is the evidence for it sufficiently compelling that we should cease to pay attention to the fact that insulin, as Yalow and Berson noted in 1965, is “the principal regulator of fat metabolism?”

One point I’ve been making in my posts and in my books is that it’s possible to find evidence in favor of virtually any idea – including the Flying Spaghetti Monster as the ruling force in the universe. More important to the validation of an idea or a hypothesis is the strength of the evidence that seems to refute it. Can the hypothesis survive more or less intact our best attempts to refute it?

This is one of the points I was trying to get across at the Ancestral Health Symposium: that the foods we eat today during our current obesity epidemic might have a high reward value, and that diets consumed by lean populations in faraway locales might not, isn’t particularly interesting. Yes, it supports the hypothesis, but how do we explain epidemics of obesity in populations that eat diets that don’t appear to have a high reward value? Do we need an entirely different hypothesis for them? That would be unfortunate.

“Here’s the fundamental concept that I think explains a lot of obesity in industrialized nations,” writes Dr. Stephen Guyenet of wholehealthsource.org .

We live in a more or less Darwinian economic framework (capitalism). Food manufacturers are in constant competition, and any food that sells poorly will rapidly disappear from stores. How do you get people to buy your product? You produce something that causes them to come back and buy it again. In other words, the goal of processed food manufacturers is to create a product that maximally reinforces purchase and consumption behaviors – food reward! If the product is not extremely rewarding, it won’t sell because it’s competing against other products that are extremely rewarding. Only the most rewarding products survive.

This certainly sounds reasonable, but don’t we also want a hypothesis of obesity that explains obesity rates in populations that lack such highly evolved food industries – obesity in non-industrialized nations? This would be a hypothesis that explains obesity-ridden populations in which the local industry isn’t quite so diligent in increasing food reward, if there are food manufacturers to speak of at all?

This is the question I asked in chapter one of Why We Get Fat. It’s why I listed a host of populations in which levels of obesity were reported, in some cases, approaching or exceeding those in the U.S. today, and yet with none of this Darwinian competition between food manufacturers, none of this extremely rewarding food (or at least not extremely-rewarding as we would define it today).

These populations included the Pima in 1902, the Sioux on the Crow Creek Reservation in 1928, the citizens of Naples in the years of extreme poverty following the Second World War and African-Americans in Charleston South Carolina in 1959. They included Zulu in Durban South Africa in 1960, and the citizens of Nauru in the South Pacific in 1961 — “By European standards,” a local physician wrote, “everyone past puberty is grossly overweight.” They included Trinidadians in the early 1960s and Chilean factory workers. They included urban Bantu pensioners “the most indigent of elderly Bantu,” in Johannesburg, South Africa in 1965, and so on.

What these populations had in common was varying degrees of poverty — from very poor to unimaginably poor — and the absence of a Darwinian food industry as Dr. Guyenet and others would describe it. They did have sugar and refined grains, but don’t we want a hypothesis of food reward that can make a claim more meaningful than “rewarding (or hyper-rewarding) foods are foods with sugar and/or refined grains in them?” (And if this ultimately is our definition, as I’ll discuss shortly, then we should be able to establish whether the reason they’re rewarding is or is not due to the peripheral effects of these foods, rather than their ability to influence brain chemistry, set point, etc.)

We also want a concept (or at least I do) that explains how we can have populations in which obesity and malnutrition and under-nutrition co-exist — for example, obese mothers with starving children, a common observation now in the literature.

Take Jamaica, for instance, where the British-trained diabetologist Rolf Richards, as I have quoted in Why We Get Fat and in my lectures, discussed the situation in 1973:

It is difficult to explain the high frequency of obesity seen in a relatively impecunious [very poor] society such as exists in the West Indies, when compared to the standard of living enjoyed in the more developed countries. Malnutrition and subnutrition are common disorders in the first two years of life in these areas, and account for almost 25 per cent of all admissions to pediatric wards in Jamaica. Subnutrition continues in early childhood to the early teens. Obesity begins to manifest itself in the female population from the 25th year of life and reaches enormous proportions from 30 onwards.

Now if we blame the mother’s obesity on the hyper-rewarding nature of the food she’s eating, we have to ask why these foods are rewarding only to the women and not to their children. The children aren’t fat, after all (not yet, anyway). In fact they’re starving. They’re under-nourished. We also have to explain why these foods only become rewarding from “the 25^th year of life” onward? And, perhaps most important, we have to explain why these women don’t fight the hyper-rewarding nature of these foods and remain lean.

After all, the food reward/palatability hypothesis of obesity, as we discussed in the first post on the subject, dictates that these foods cause neurochemical changes in the brain, which then raises the adiposity set point, thus making us eat more and get fat. Put simply, raising the set point in the brain makes us hungry or at least hungrier. Okay, so if this is right, then we can assume that the reward value of the food eaten in Jamaica made these women hungrier; they ate more, they got fatter. But why couldn’t they control their impulses and remain lean? Why couldn’t they experience the semi-starvation—or at least the perception of not having enough to eat—rather than their children who are indeed semi-starved?

Rather than giving in to the urge, consuming the superfluous calories themselves, and getting fat, why didn’t these mothers fight the urge and give those excess calories to their starving kids? If one of them has to go hungry or at least feel hungry, evolution, it seems, would always favor the mother doing it rather than the child.

We can try to rescue the food reward/palatability hypothesis of obesity in a case like this by simply making the claim that if these people are fat, then obviously something about their food must have been hyper-rewarding. (Something other than the refined carbs and sugars, as we’ll discuss in the next post.) But now our definition is becoming circular: The women get fat because of the hyper-rewarding nature of the food they’re eating, and we know that the food is hyper-rewarding because they’re fat. We just have to find or identify the particular foods in their diet that are the hyper-rewarding ones, and, as I said, it would be nice if they weren’t just sugar and refined carbs.

In his blogs, Dr. Guyenet suggests that home cooked food has a lower food reward value than processed, restaurant-produced fast food. This is one reason why, he suggests, populations like the Ache of Paraguay, the !Kung San, Polynesians and Melanesians (not counting those on Nauru and other islands that were obese) were lean: They “cooked their food in earth ovens and used no flavorings or salt .“

That we don’t cook our foods by these simple, spice-free, salt-free methods is offered as another explanation for the current obesity epidemic — “the shift from simpler home-cooked food to professionally engineered/processed food designed to maximize palatability and reward.” And this is also an explanation often offered for why carbohydrate restriction and paleo diets (not necessarily two different things) are weight loss diets. It’s not that they’re simply absent refined grains and sugars, as they are, but that the meats, fish, fowl, vegetables, and maybe tubers consumed are home cooked and/or so relatively bland that somehow they are low in food reward value.

But we can be confident that these extremely poor populations with high levels of obesity were also getting by on simple home-cooked food. Without having had the opportunity to visit Trinidad in the early 1960s or the South Dakota Crow Creek Reservation in 1928, I’m going to assume with confidence that a large proportion of the population, if not all, were not frequenting fast food joints and buying hyper-rewarding candy bars and soft drinks. So why were they fat? Certainly the presence or absence of flavorless home cooking is not enough to explain it. Nor can we explain it by claiming that only the affluent were obese, as Dr. Guyenet suggests, because these populations were anything but affluent.

So why were they fat? A familiar question.

Well, maybe it’s the low-hanging fruit of food reward—the refined grains and sugars? Populations that got fat ate significant quantities—particularly, the sugar—and populations that didn’t, well, didn’t. And when obesity suddenly blossomed in populations, it was because sugar and refined grains were new additions to their diets. And so diets that work for weight loss and weight maintenance are those that restrict refined grains and sugars (and maybe easily digestible starchy vegetables, as well, or maybe not) and diets that don’t, well, don’t.

This is what I argued in my books, although I’m arguing that the problem is caused by the metabolic hormonal effects of these foods in the periphery, their effect primarily on insulin signaling and, ultimately, fat accumulation. And the reason we find these foods rewarding and palatable is because of these metabolic hormonal effects.

As I’ve suggested in prior posts, the kinds of observations that are meaningful in situations like this—two competing hypotheses/paradigms—are only those that can differentiate between the two competitors. Evidence or observations that can be explained equally well by either hypothesis might have rhetorical value—good in an argument, in the spur of the moment—but they don’t add much to the scientific question at hand: Which hypothesis/paradigm is the right one?

This is why the observation that the Ache, the !Kung San, the Polynesians and Kitavans and Masai are lean or were lean, for instance, doesn’t tell us anything of significance about which hypothesis is right: Their lack of excess adiposity might be a result of their bland, unrewarding diets or it might be because their diets lack or lacked any significant amount of refined grains and/or sugars.

And even if the foods or diets that are consumed by obese populations and individuals today in the U.S. and elsewhere do seem indisputably rewarding and palatable, we’re still left having to demonstrate that this palatability, this high food reward value, is not due to the nutritional composition of the diet and the peripheral effects of the nutrients—the metabolic and hormonal effects in the body.

This was a point made back in 1989 by Israel Ramirez, Michael Tordoff and Mark Friedman of the Monell Chemical Senses Center in Philadelphia in an article entitled “Dietary Hyperphagia and Obesity: What causes them?”(Friedman is one of the scientists whose thoughts on obesity and over-eating significantly shaped my own. I owe him a debt of gratitude. For those who want to read what I think may be the single most thoughtful article written on obesity and hunger in the post-WW2 era, I’d recommend Friedman’s article with Edward Stricker, The Physiological Psychology of Hunger: A Physiological Perspective.)

The Monell researchers were discussing only the concept of palatability, not the food reward value of a particular food. (The idea that food reward and palatability could be differentiated — that they weren’t precisely the same thing — hadn’t gotten much if any play up until then.) So the question was whether or not palatability (whether a food tastes good) could be legitimately disassociated from nutrient composition and peripheral effects of the food. As Ramirez et al said repeatedly in this article, researchers almost invariably assumed that a food could be defined as palatable if the animals (or humans) ate more of that food than some other food, but this was an inference and nothing more.

It was well known at the time (although it may have been forgotten since then), as I discussed in Good Calories, Bad Calories, that animals can be made to like one food more than another, and so eat more of the one than the other, by interventions that influenced their underlying physiologic/metabolic/hormonal states. Here’s how I illustrated this in GC,BC:

Throughout the first half of the twentieth century, a series of experimental observations, many of them from [Curt] Richter’s laboratory [at Johns Hopkins University], raised questions about what is meant by the concepts of hunger, thirst and palatability, and how they might reflect metabolic and physiological needs. For example, rats in which the adrenal glands are removed cannot retain salt and will die within two weeks on their usual diet from the consequences of salt depletion. If given a supply of salt in their cages, however, or given the choice of drinking salt water or pure water, they will chose to either eat or drink the salt and, by doing so, keep themselves alive indefinitely. These rats will develop a “taste” for salt that did not exist prior to the removal of their adrenal glands. Rats that have had their parathyroid glands removed will die within days of tetany, a disorder of calcium deficiency. If given the opportunity, however, they will drink a solution of calcium lactate rather than water—not the case with healthy rats—and will stay alive because of that choice. They will appear to like the calcium lactate more than water. And rats rendered diabetic voluntarily choose diets devoid of carbohydrates, consuming only protein and fat. “As a result,” Richter said, “they lost their symptoms of diabetes, i.e., their blood sugar fell to its normal level, they gained weight, ate less food and drank only normal amounts of water.

In short, change underlying physiologic/hormonal conditions and it will affect what an animal chooses to eat and so seems to like or find rewarding. The animal’s behavior and perceptions will change in response to a change in homeostasis – in the hormonal milieu of the cells in the body.

It’s quite possible that all those foods we seem to like, or even the ones we find rewarding but don’t particularly like, as Dr. Guyenet argues, and that subsequently cause obesity (not necessarily the same thing) are those foods that somehow satisfy an underlying metabolic and physiological demand. This in turn might induce our brains to register them as more palatable or rewarding, but the initial cause would be the effect in the periphery. The nutrient composition of the food, in this case, would be the key—what it’s doing in the body, not necessarily the brain.

Here’s how Ramirez, Tordoff and Friedman phrased this issue back in 1989:

In order to demonstrate that diet palatability per se causes hyperphagia [overeating or a voracious appetite], it must be shown that obesity-inducing foods are more palatable than control foods, this greater palatability is not merely a reflection of the postingestive [after entering the digestive tract] consequences of the foods, and altering palatability without altering nutritional composition can cause obesity. This has not been done.… Although various experiments have been cited as supporting the palatability hypothesis, they are not decisive because, in every case, palatability was confounded with changes in nutritional composition.

That an experiment is “not decisive” unless this is done is the critical point. If an experiment that ostensibly changes food reward makes an animal eat more of a particular food and/or get fatter, and it does so by changing nutritional composition—say, the foods that are defined as more rewarding have more sugar in them, or are more refined, or have a greater water or fat content—then the researchers have to demonstrate that it’s not the change in nutritional composition and post-ingestive effects of that change that is causing the overeating and obesity. An observation that one diet produces obesity compared to another because it’s ostensibly more rewarding or palatable has to do the same. Otherwise either hypothesis could be true, and we haven’t learned anything.

Take the idea, as Dr. Guyenet suggests, that people will eat more at a sitting if foods are palatable than if they’re not, which seems kind of obvious. The better a food tastes, the more likely we are to eat more of it. But then Dr. Guyenet adds that this is true even of foods with “little or no nutritional quality.” This is how he phrases it in a recent post:

Many human studies have shown that people eat more food at a sitting if the food is higher palatability than if it is lower palatability (11). This is true even if palatability is manipulated using substances that have little or no impact on the nutritional quality of the food, including saccharin (sweet), monosodium glutamate (savory) and herbs/spices.

The reference is a review article that actually makes the point that the evidence is ambiguous on the eating more issue when the foods have little or no nutritional quality. “Several studies showed no effect of sweet taste on either hunger ratings or food intake,” the authors write, “when the sweetener was provided in the form of gelatine, corn flakes or fromage blanc or as aspartame- or saccharin-sweetened drinks.” In fact, the authors then go on to suggest this is true of all “sweet taste” whether from caloric sweeteners or non-caloric, which doesn’t seem to do my hypothesis any favors either.

But what I’m arguing is that the key isn’t whether people eat more, but whether the foods stimulate fat accumulation. And if they do make us fatter, how?

The food reward hypothesis suggests that it happens because of the effect of the sweet taste in the brain, not in the body. If the former, then sugar and saccharine might be expected to be equally fattening, so long as we consider sugar and saccharine-sweetened beverages to have equal reward value or to be considered equally palatable by humans.

If the reward value is not the critical factor, then it’s a reasonable assumption that sugar-sweetened beverages will be more fattening than saccharine or aspartame-sweetened beverages. And we could do a clinical trial and see which turns out to be true, although we can also guess what we think such a trial (randomized, well-controlled) would find. Not surprisingly, I’d vote for the sugar-sweetened beverages being more fattening.

This doesn’t mean, by the way, that artificially-sweetened beverages could be absolved of having any fattening properties because we might still secrete insulin in response to these beverages. They may fool us into thinking that they have carbohydrate or sugar calories in them. And this insulin secretion could be cephalic — a kind of Pavlovian response — which would mean that the brain is telling the pancreas to secrete insulin (via the vagus nerve). But it would now be doing so not because the food is rewarding necessarily, but because the body has come to associate sweet taste with the presence of carbohydrates and feedback loops in the brain are working to get the body ready by secreting insulin.

In my next post, I’ll discuss more of the evidence offered in support of the food reward/palatability hypothesis and ask the question that Ramirez et al did: are palatability and food reward confounded with changes in nutritional composition, and if so, what might that confounding be?

Filed Under: Bad Science, Calories-in-Calories-out, Diets, food reward/palatability hypothesis, General, Obesity and weight regulation, Weightloss Diets

Catching up on lost time – the Ancestral Health Symposium, food reward, palatability, insulin signaling and carbohydrates… Part II(b)

November 14, 2011 156 Comments

When last we left off, the subject was the food reward/palatability hypothesis of obesity and why I find it so unconvincing and problematic.

This post is going to address that issue by first discussing three new papers published on the subject of sugar. Then I’m going to ask a lot of questions, hoping at least some of the answers will be obvious. All three papers are from Peter Havel and his collaborators at U.C. Davis and Vanderbilt; all three looked at the metabolic effect of the fructose-component of sugar, while one of them one also looked at the effect of sugar itself in the form of high fructose corn syrup (HFCS).

Paper number one describes an experiment in which rhesus monkeys were fed their usual monkey chow diet supplemented by a daily 300-calorie ration of fructose-sweetened water. After a year, every last one of the 29 monkeys had developed “insulin resistance and many features of metabolic syndrome, including central obesity, dyslipidemia and inflammation.” Four of the monkeys progressed to type 2 diabetes.

Worth noting is that the monkeys apparently drank all the fructose-sweetened drinks they were given, but they adjusted for the 300 additional calories by cutting back significantly on the chow. All in all, they averaged only 26 calories per day more with the fructose than they did without it. This suggests that the negative sequelae observed over the course of the year were indeed caused by the fructose itself and not an increased intake of total calories (unless we’re willing to accept that increasing calories by just a couple a dozen a day is sufficient to do some very bad things to monkeys and do them relatively quickly.)

The second and third papers, both published in October, were randomized controlled trials in humans — rather than primates or rodents — which is always a nice attraction in nutrition research since there’s no guarantee any animal model really reflects the physiological situation in, well, us.

The second paper reported that overweight and obese older adults (40 to 72 years-old) getting a quarter of their calories from fructose-sweetened beverages used less fat for fuel and actually expended less energy than did the same subjects when they were getting the equivalent calories from glucose drinks. So the calories were the same; the metabolic effects were different. For the fructose, the effects were what we’d expect (okay, what I’d expect) if the fructose beverages were causing or exacerbating insulin resistance, an observation that Havel et al had published earlier. The more insulin resistant these people became, the less fat they used for fuel—hence, we can assume, the more fat they stored—and the lower their basal metabolic rate. (The rhesus monkeys, too, had decreased their energy expenditure in response to drinking fructose.)

The third study was a trial in younger subjects (18 to 40-year-olds), some lean, some not. These subjects were given three beverages to drink every day, constituting again about a quarter of their day’s ration of calories. The beverages were sweetened either with fructose, glucose or high fructose corn syrup. For the HFCS group, this 25 percent of calories was compatible with what the U.S. Dietary Guidelines considers a safe upper limit for sugar consumption. Still, after only 12 days—less than two weeks—subjects in both the HFCS and fructose groups, but not the glucose group, saw a significant increase in heart disease risk. Triglycerides went up; LDL cholesterol went up, and ApoB concentrations, a measure of the number of LDL particles, increased.

What can we take away from these studies? Well, these three papers certainly support the contention that the sugars consumed in western diets have very specific deleterious metabolic effects, and that maybe these sugars are the, or at least a proximate cause of insulin resistance and metabolic syndrome, and so, we can assume, obesity and type 2 diabetes and perhaps all the other chronic diseases that associate with these two conditions (cancer anyone?). This was the thesis of my April New York Times Magazine cover article “Is Sugar Toxic.” Here’s how Havel et al phrased this notion in the monkey paper:

The incidence and prevalence of insulin resistance and metabolic syndrome in the United States has increased dramatically over the past several years, and we and others have proposed that this increase may in part be attributable to increased consumption of fructose derived from dietary sugars, principally sucrose and high-fructose corn syrup (HFCS).

And, yes, the three papers certainly add fuel to this possible fire.

So on one hand, we can explain the metabolic abnormalities observed in these three studies—the insulin resistance, metabolic syndrome, raised triglycerides and increases in ApoB and LDL cholesterol—as all caused by the metabolism of the fructose in the liver in concert perhaps with the insulin-stimulating effects of glucose. This is not a particularly controversial position. The sugar industry is not a fan, but research has consistently demonstrated these effects and has since the 1960s, and the biochemistry behind them is well understood.

So now we have three clear propositions and we’ll follow them up with the obvious question:

Proposition #1: The metabolism of fructose in large quantities by the liver results in a system-wide hormonal disruption — insulin resistance, in particular.

Proposition #2: Insulin resistance is intimately associated with obesity and is the underlying defect in type 2 diabetes.

Proposition #3: Insulin is the fundamental hormonal regulator of fat accumulation in fat cells.

Obvious question: Considering these three propositions, isn’t it likely that insulin resistance and the chronically elevated levels of insulin that go with it are causal factors in the obesity seen in the monkeys and, well, in humans who consume significant sugar, too?

This line of reasoning is one of the principle reasons that I’ve argued in my books and this blog that the carb/insulin hypothesis should be considered the null hypothesis of obesity, the one we believe until remarkable, unambiguous evidence comes along to refute it.

We have a disorder, obesity, that associates with a host of chronic diseases of western diets, all of which are associated as well with metabolic syndrome – i.e., insulin resistance — and type 2 diabetes. So if insulin plays a major role in regulating fat accumulation in individual fat cells, which is not a point of controversy, and if dysregulation of insulin signaling is a major component if not the causal factor in the diseases that associate with obesity, also not particularly controversial, it seems like a very good assumption that obesity, too, is caused by a the same dysregulation in insulin signaling.

Now the salient questions are these: How remarkable and unambiguous does the evidence have to be before we toss all this out in favor of the idea that we get fat because rewarding foods stimulate neurochemical changes in brain centers that raise our adiposity set point and ultimately make us eat more than we expend? And what do we gain by doing it?

I will argue that tossing out the role of insulin on fat accumulation to embrace the idea that rewarding foods stimulate brain centers seems inherently foolish, because the evidence is by no means unambiguous and in the process we disassociate weight gain from all these other insulin-mediated and very closely related disorders.

Let’s first try to address this cost-benefit ratio — what we gain from the food reward/palatability hypothesis compared to what we lose — by narrowing our scope to the three sugar papers from Havel’s group. We want to answer these two questions: 1). what does the food reward/palatability hypothesis of obesity add to our understanding of the fructose-related effects documented in these papers? 2). Is it a valuable addition?

As I said, few of us, if any, would doubt that sugar-sweetened beverages (SSBs, as they’re now fashionably known) or fructose-sweetened beverages have a high-food reward value. The monkeys seemed content to drink all their 300 calories-a-day of fructose, and to do so at the expense of other more nourishing food (the chow). Put simply, they apparently found the fructose more rewarding. Havel told me when I interviewed him for the NYT Magazine article that they had difficulty finding any of the younger (human) subjects for their experiments who didn’t already drink at least two daily sugar-sweetened beverages, and quite a few were drinking six.

So it’s certainly a reasonable assumption that SSBs are hyper-rewarding, among the low-hanging fruit in the food reward/palatability world, as , as Dr. Guyenet of Whole Health Source has categorized them in his posts on this subject. Easy targets in other words—indisputably rewarding.

Now these highly rewarding beverages are given in a randomized-controlled trial to human subjects, as Havel and colleagues did, and the amount given is fixed. They’re given daily to monkeys as part of their dietary regimen, as Havel and colleagues did, again a fixed amount. In both species, they cause the metabolic/hormonal effects we would expect on the basis of a few decades of biochemical and endocrinological research on insulin and on the metabolism of fructose in the liver.

So now we’re going to take a leap of faith and assume that the hyper-rewarding nature of these beverages explains why the monkeys got fatter drinking them, and maybe the humans, too, if any of them did indeed gain fat in such a short period on the beverages, but what about the metabolic and hormonal effects observed? Does the fact that SSBs have a high food reward/palatability value tell us anything meaningful about why these sugar- or fructose-sweetened beverages cause peripheral effects in addition to increased adiposity—insulin resistance, metabolic syndrome, type 2 diabetes, raised triglycerides and ApoB number, etc.?

Here’s another way to phrase that same question: If consuming these different sugar waters have very well-specified effects in the body (peripheral effects, as they’re known in the lingo), and these effects are sufficient to explain all the observations – increases in adiposity, insulin resistance, dyslipidemia, type 2 diabetes, etc. — why evoke a couple of arguably vague concepts like food reward and palatability to explain one of them alone, the increase in adiposity?

Let’s agree for the moment, that it’s worth it. We’re going to accept this hypothesis because it’s just right and the carbohydrate/insulin hypothesis is not. It’s the hyper-rewarding nature of sugar- and fructose-sweetened beverages causes fat accumulation, as seen in the monkeys in paper number one, and in free-living humans drinking SSBs. If we decide this reward value thing is at least a major contributor, we’re still stuck with having to explain the metabolic and hormonal disorders. We can’t just ignore those, so we have to complicate the hypothesis to do so — add epicycles, as historians or philosophers of science would put it. We have to explain how these SSBs also cause insulin resistance and metabolic syndrome, why they raise triglycerides and LDL cholesterol and ApoB etc..

Researchers who study obesity and insulin resistance have been confronted with this same problem since the early 1960s, once they decided that obesity had to be caused by taking in more calories than we expend. The way they’ve traditionally done it is to say that we get fatter because we take in more calories than we expend, and then we get insulin resistant because we are getting fatter. Two different mechanisms.

This rationale can help proponents of the food reward/palatability hypothesis out of the same hole. In this case, blame the excess fat accumulation on the hyper-rewarding nature of sugar and the neurochemical effects it induces in the brain; this raises set point and so we eat more than we did and get fatter. Then we can blame the insulin resistance and all that goes with it on the process of getting fatter.

Not too bad, but then we have to explain why the same metabolic effects happen in individuals who remain lean, who do not accumulate the offending fat, and we can’t, or at least not without adding yet another mechanism (another epicycle) for the lean people. Because lean people can also be insulin resistant and dyslipidemic and get type 2 diabetes and all the associated chronic diseases. So one way or the other (or so it seems to me), we need our knowledge of the peripheral effects of sugar consumption – the metabolic and hormonal effects in the liver, the pancreas and other organs – to understand at least some of the observations, if not all of them.

In its current form, the palatability/food reward hypothesis explains only fat accumulation. It explains why the monkeys gained weight, and I guess why we do too when we drink a lot of sugared beverages, but it offers no explanation for the the metabolic consequences that accompany the weight gain, both in the studies discussed and in real life.

Here’s yet another question to always keep in mind when thinking about the food reward/palatability hypothesis of obesity: Do we gain anything from it other than the obvious: that if these foods weren’t highly rewarding or palatable, we probably wouldn’t eat them, or at least not enough of them to make us fat and cause the deleterious metabolic effects?

And even if we do gain something meaningful from acknowledging that the food reward/palatability value of foods causes us to consume more of them, this benefit to our understanding would still come with a very important caveat: Maybe the reason these foods have a high reward value or are so palatable is because of the metabolic and hormonal effects of eating them. Maybe a food that can cause insulin resistance or hyperinsulinemia can also cause us, through its various peripheral effects, to crave it more, to find it more rewarding.

Anything’s possible, and this is one hypothesis, a very important one, we should always keep in mind. And it’s one I’ll return to shortly, or at least shortly by my standards—i.e., over a few more posts and several thousand words more words.

(And when I’m done with these food reward hypothesis posts, I’ll get to the evidence against the insulin hypothesis. Lord knows when that will be, but I’ll get there.)

Filed Under: Calories-in-Calories-out, food reward/palatability hypothesis, General, Obesity and weight regulation

Catching up on lost time – the Ancestral Health Symposium, food reward, palatability, insulin signaling and carbohydrates… Part II(a)

November 9, 2011 212 Comments

When last I posted, oh so long ago, I promised next to discuss the food reward/palatability hypothesis of obesity and why I find it so uncompelling and more than a little bit disheartening. Why, in effect, I think it is the kind of bad science that begs to be challenged, as I did, when it is presented in a public forum, as Dr. Stephan Guyenet of Whole Health Source did at the Ancestral Health Symposium back in August. This is the first of five posts to address this and I promise (really) that it will be days between posts, not months.

Here’s how Dr. Guyenet describes his hypothesis in his sixth of an increasing number of blog posts on food reward:

…The evidence as a whole shows that chronic consumption of foods with an excessive reward value causes abnormalities in parts of the brain that regulate body fatness, metabolism and reward/motivation. This can lead to weight gain and metabolic problems, and favor addictive and compulsive relationships to food and other things. The combination of readily accessible, cheap, high-reward food, and stressful lifestyles that drive us to eat it, is probably a major contributor to overweight, obesity, diabetes and perhaps other health problems in affluent nations.

What makes this hypothesis novel is that the ability of a particular food to make us fat — what makes a food fattening, in effect — is mediated, according to Dr. Guyenet, through its ability to stimulate neurochemical effects in the brain.

So why do I find this intriguing idea objectionable, so objectionable, in fact, that I was willing to stand up at the AHS and make a bit of spectacle of myself? Well, for starters, the food reward/palatability hypothesis can’t explain the kinds of observations about obesity and weight regulation that I’ve been arguing in my books must be explained by any viable hypothesis of why we get fat. This is the primary issue, obviously, as a hypothesis that can’t explain the necessary observations is a failed hypothesis. And we’ll get to this issue in the posts to come.

The lesser reason for my objections, and the subject of this post, is that this hypothesis seems to be yet another thinly-veiled variation on the energy balance paradigm of obesity — calories-in, calories-out — and I’ve been arguing that this particular paradigm is fatally misguided in a variety of different ways. I believe that obesity researchers will never make meaningful progress until they rid themselves of this belief system, and that so long as they hold onto it they’ll be effectively blaming the obese for the problem of their obesity. Hence, finding yet a new way to embrace it, or popularizing an old way, as Dr. Guyenet has, seems to be a step in precisely the wrong direction.

Ultimately, this comes down to what I consider the two competing obesity paradigms or belief systems.

Competing paradigms: 1. body rules

One is a body-rules paradigm and I’ve been arguing that it’s the only one that can do a reasonable job of explaining all the meaningful observations. Changes in the hormonal and enzymatic regulation of fat metabolism—in the regulation of fat storage and oxidation—drive changes in adiposity; and changes in adiposity drive compensatory changes in intake and expenditure.

Here, the body is running things. Indeed the organ in control may be the fat tissue itself in concert with the liver. The University of Vienna endocrinologist/geneticist Julius Bauer described this fat-rules concept back in 1929 by saying that the fat tissue of someone who’s obese (what he called “abnormal lipophilic tissue) “maintains its stock, and may increase it independent of the requirements of the organism. A sort of anarchy exists; the adipose tissue lives for itself and does not fit into the precisely regulated management of the whole organism.”

In this scenario, the brain plays no more role in regulating the growth of the fat tissue than it would regulating the growth of any tissue — a tumor, for instance, which is a metaphor that Bauer uses, or the growth of fat tissue in breasts and hips and butt when a young girl goes through puberty, or the fat put on by a mother-to-be when she is pregnant, another Bauer metaphor, or just the growth of lean and fat tissue in children as they develop and mature.

In all these cases, the body is doing its own thing, more or less independent of the brain’s input, even though the brain, in the case of growing children, is the source of the growth hormone that is driving the growth. More energy has to be taken in than expended while growth is occurring (at least by the tissue itself, if not the whole body), but that “positive energy balance” — calories in greater than calories out — is a compensatory effect of the growth; it’s not a cause. The brain does what it always does, which is reacting and modulating homeostasis in response to environmental signals. But it’s a secondary organ in this sense.

In this paradigm, specific foods are fattening because they induce metabolic and hormonal responses in the body — in the periphery, as its known in the lingo — that in turn induce fat cells to accumulate fat. The brain has little say in the matter. As I describe it in my books (and as it was described to me by the few researchers today who hold this view), we don’t get fat because we overeat; we overeat because we’re getting fat.

If we come to crave specific foods or find them more rewarding than others and these foods are fattening — not necessarily the same thing — then we likely do so because of their physiologic effects, the changes in the hormonal milieu of the body caused by the consumption of these foods. Foods that make us fat come to be foods we crave, because these foods are also the foods that make us hungry. So how much we might like a food or how rewarding we might find it or how much we might crave it are primarily consequences of the peripheral metabolic/hormonal effects.

In this paradigm, meals stimulate hormonal responses—insulin, in particular, either in the short term (glucose) or the long term (fructose)— and this in turn directly influences both the storage of fat and the oxidation of fatty acids elsewhere in the body. The balance of forces working on the fat tissue, a dynamic equilibrium, ultimately determines how much fat we accumulate. As fat accumulation increases, so does secretion of leptin and other adipokines that work in a variety of feedback loops in the brain and the body (as does insulin itself) to ideally prevent excessive fat accumulation.

This body-rules hypothesis, of course, isn’t the conventional wisdom. If it were, I would be doing something else with my career.

Competing paradigms: 2. brain rules

The conventional wisdom is that we get fat because we take in more calories than we expend. Simple enough. We get fat because we overeat, not the other way around. Changes in energy balance—calories-in minus calories-out—drive changes in adiposity, in how much fat we carry around in our fat cells.

Ultimately, as I discuss in Why We Get Fat, this is a brain-rules paradigm. After all, both the components of overeating — eating too much, aka gluttony, or moving too little, aka sloth — are both behaviors and in this paradigm behaviors are psychological phenomena not physiological.

Researchers who live in this paradigm are invariably trying to discover what’s wrong with our brains or the signaling to our brains that cause this particularly cherished organ (what Woody Allen memorably described as his “second favorite organ”) to screw up. Why can’t the brains of people who become obese or overweight get the energy balance thing right? Or why do these brains effectively desire more fat on the body than is healthy? Why do they set the “set point” of adiposity too high? The problem with people who get obese is in their brains, not their bodies (even though the excess fat is in the body).

In this paradigm, the fat tissue is more or less passively following the brain’s lead. Meals will stimulate a variety of gut hormones and fat-derived hormones like leptin, grhelin, etc., and these in turn signal the brain whether to continue eating or not, whether to act on hunger or satiation, and perhaps how much energy to drive the body to expend. But ultimately the deciding factor on whether a person gets fatter or leaner is the balance of energy expended or consumed—calories-in minus calories-out—and this is regulated by the brain. The fat tissue’s say in the matter is mostly relegated to its secretion of leptin and other adipokines, as these fat-derived hormones are known, that might in turn work in the brain to curb hunger or maybe work in the body to increase expenditure. Energy balance, though, drives adiposity and energy balance (energy homeostasis, as its often called) is ultimately a brain thing not a body thing.

The twist that the food reward/palatability hypothesis of obesity gives to this energy balance paradigm is to make the meaningful effect of a fattening food that of changing the neurochemical balance in the brain. This in turn changes set point and adiposity increases (or decreases) in response. This scenario can appear to be one that rejects, as I do, the simplistic calories-in-calories-out idea, but I’m going to argue that this appearance is an illusion. And that, as I said, is one reason why the hypothesis irks me so.

Here’s one way to look at these two competing paradigms, now with the food reward/palatability hypothesis of obesity standing in for the conventional wisdom:

Here’s the fat-rules paradigm: We’re not getting fat because we are overeating; we are overeating because we’re getting fat—because a hormonal disorder, caused by the consumption of certain foods (refined grains, easily-digestible starches and sugars) drives us to accumulate fat in our fat tissue.

And here’s the food reward/palatability hypothesis, a brain-rules hypothesis: We’re not getting fat because we are overeating; we are overeating because our brains are driving us to get fat—because a neurochemical disorder, caused by the consumption of certain foods (refined grains and sugars, as well as fats and salty foods and industrially processed foods of other types as well), in turn drives us to accumulate fat in our fat tissue.

So you can see how confusing this can be, how similar these two hypotheses can appear. But the question ultimately is how does the brain go about increasing fat accumulation in the food reward/palatability hypothesis. What do these neurochemical changes do to the brain and then what does the brain do that ultimately leads to more fat in the fat cells, which are, after all, mostly half-a-body or so away? What’s ultimately driving the fat?

Here’s where the food reward/palatability hypothesis seems to collapse back down to just another failed twist on calories-in-calories-out. It’s yet another attempt to explain why fat people get fat, and why it’s caused by eating too much (or exercising too little), without explicitly blaming obese or overweight individuals for not being able to control their behaviors (as we lean people do). Chapter 7 in Why We Get Fat goes into this problem in detail.

(A caveat here: I’m willing to be convinced that this hypothesis is not an energy balance hypothesis, and so not a brain-rules-and-the-fat-passively-follows notion, but so far I haven’t seen an argument that’s convincing. I confess, though, that I find the hypothesis surprisingly difficult to understand, which suggests that either I’m losing my intellectual facilities in my dotage — always possible — or that I’m so blinded by my love of my own hypothesis that I refuse to understand it—at least equally likely — or maybe, just maybe, that Dr. Guyenet and other proponents of the hypothesis don’t really understand it either.)

The food reward/palatability hypothesis: looking for a mechanism

As Dr. Guyenet says, as I quoted above, the chain of causality in this hypothesis goes like this: “abnormalities in parts of the brain that regulate body fatness, metabolism and reward/motivation… can lead to weight gain and metabolic problems…” But he doesn’t say how. How do abnormalities in parts of the brain lead to weight gain? The answer seems to be that the brain raises our adiposity set point, but then how does that actually make us fatter? Now we have a change in the brain — set point has gone up — but we still have to explain the change in the body — adiposity increases. How does that happen?

And the answer is that the brain affects this change in fat mass, as proponents of the hypothesis seem to see it (or seem to see it most often), by either increasing food consumption or decreasing expenditure. So the brain is regulating the fat mass not by regulating fat accumulation directly, but by making us eat more and maybe expend less — calories-in-calories-out. And fat people get fat not because their fat tissue is living for itself, as Bauer put it, and increasing its stock of fat, independent of the nutritional state of the organism, but because fat people either respond to rewarding foods differently than lean people do or because they can’t resist this drive to eat more food once their set point goes up. Lean people either can resist the urge, or the rewarding foods don’t have the same neurochemical effects in their brains. Either way, the brains of lean people are more resistant to fattening foods (those with high food reward/palatability value) than the brains of fat people, and the body, in either case, is kind of irrelevant.

Now, the brain could regulate fat mass directly by increasing, for instance, insulin secretion via increased stimulation of the vagus nerve, but Dr. Guyenet would like to dismiss the role of insulin in excess fat accumulation. (This is another post I’ve promised in my last post and one that might come along, well, maybe in a month or two, after we’re done with these food reward posts). As a result, this particular mechanism is not apparently part of the hypothesis.

When I asked Dr. Guyenet, shortly after my last post, why he believed so strongly that the food reward hypothesis was not an energy balance idea, he suggested that I could significantly improve my understanding of this issue by reading his current mentor Michael Schwartz’s 2006 review article in Nature – “Central nervous system control of food intake and body weight.”

A lengthy but not necessarily irrelevant digression

Curiously enough, I had a run-in with Professor Schwartz himself over precisely this issue back in March 2005 when I was reporting Good Calories, Bad Calories. Schwartz built his reputation in obesity research in part by demonstrating that insulin in the brain suppresses food intake – or at least that it does when it is injected directly into the cerebral spinal fluid of baboons. He then argued that this is the hormone’s primary role; Dr. Guyenet is now making very similar arguments. In their opinion, what happens in the brain trumps what happens in the body. Schwartz has actually suggested that one reason for the obesity epidemic may be that we’re not secreting enough insulin because we’re not eating enough carbohydrates. Dr. Guyenet does not go that far.

I argued in an e-mail exchange with Schwartz that because insulin is secreted in the periphery, and that because it can be shown in both humans and animals that increasing insulin in the periphery increases fat accumulation, this would seem to be the primary effect. The appetite-suppression effect in the brain, therefore, would be a secondary effect—a negative feedback loop of the kind that you would expect to see in a homeostatic system.

Schwartz took exception to being questioned by a journalist and he argued that the role of journalists in this field was that of ”helping to debunk profit-motivated, unscientific views that are so prevalent in our culture.” I took exception to being told what my journalistic role should be and replied that my role was to help debunk unscientific views prevalent in our culture, regardless of their institutional provenance or apparent motivation. It took us several e-mails back and forth to achieve a peaceful co-existence again.

Back on track: the mechanism of food reward/palatability

The Schwartz article that Dr. Guyenet suggest I study, though, makes it relatively clear that the food reward/palatability hypothesis of obesity is indeed firmly entrenched in the energy balance paradigm. (I pointed this out to Dr. Guyenet in an e-mail, and he said he would get back to me on it. Apparently other concerns interceded on his side, though, and so I write this without benefit of his clarification.) “Through a process known as energy homeostasis,” Schwarz and his co-author write, “food intake is adjusted over time so as to promote stability in the amount of body fuel stored as fat.” And energy homeostasis, they explain, is regulated via a negative feedback model:

Introduced more than 50 years ago, the `adiposity negative-feedback’ model of energy homeostasis is founded on the premise that circulating signals inform the brain of changes in body fat mass and that in response to this input, the brain mounts adaptive adjustments of energy balance to stabilize fat stores.

So the brain adjusts energy balance (intake and expenditure) to stabilize fat stores; the brain rules, we eat more or expend less, and the fat tissue inflates or deflates accordingly. And this is why Dr. Guyenet and others can write thousands of words about food reward and palatability without ever actually discussing the hormonal/enzymatic regulation of the fat tissue itself, which is, after all, the ultimate organ of interest, and without discussing the hormonal/metabolic regulation of fatty acid oxidation in the lean tissue, when it’s the fatty acids that are ultimately being stored.

The alternative would be to suggest that the brain adjusts fat stores directly via hormonal and central nervous system mechanisms, and this leads to compensatory changes in energy balance. But then, as I said, we would have to discuss the direct peripheral effect of insulin on fat storage and fatty acid oxidation, and that’s not allowed.

“Obesity, by definition, results from ingesting calories in excess of ongoing requirements,” Schwartz and his co-author write, and I’m arguing that any researcher who makes this statement for any reason other than to make the point that it’s meaningless and misleading is living and working in an energy balance paradigm — calories-in, calories-out.

And because I think the energy balance paradigm of obesity is more or less the root of all scientific evil in this business — not just because it’s taken obesity researchers down a century-long blind alley, but because of its implications that fat people just can’t control their urges the way lean people do — I find Dr. Guyenet’s promotion of this hypothesis and its acceptance, limited as it may be, in the paleo and low-carb blogospheres to be very disheartening. I could be wrong (of course) about the scientific bankruptcy of this hypothesis, but I’m going to argue (of course) that I’m not.

In my next post—just a few days from now, I promise (barring extenuating circumstances like the Hayward fault underlying our neighborhood deciding to go off with a magnitude significantly higher than the 3 to 4s we’ve been getting for the past two weeks) — we’ll continue this discussion by looking at the other major limitations of this hypothesis, beginning with some recent observations that it can’t seem to explain.

Filed Under: Calories-in-Calories-out, food reward/palatability hypothesis, General, Obesity and weight regulation

Catching up on lost time – the Ancestral Health Symposium, food reward, palatability, insulin signaling and carbohydrates, kettles, pots and other odds and ends (with some philosophy of science as a special added attraction). Part I.

September 2, 2011 164 Comments

I’m going to start this long-overdue series of posts with a bit of a shaggy dog story, a lengthy preamble (“amble” perhaps being the operative word) before I get to the meatier issues.

One of my supporters in mainstream medical research is Allan Sniderman, a professor of cardiology and medicine at McGill University in Montreal. Since the mid-1980s, Sniderman has been arguing that Apo-B (the protein component of low and very low density lipoproteins) is a far better predictor of heart disease, which it surely is, than the cholesterol that happens to be contained in these lipoproteins. He’s also a co-discoverer of the hormone ASP — acylation stimulating protein — which plays a role, however controversial, in fat storage. Sniderman read Good Calories, Bad Calories shortly after it was published in September 2007 and then invited me up to lecture at McGill. He later described his feelings about GC,BC this way:

I had spent some years studying adipose tissue metabolism but it is fair to say I learned more from [Taubes’s] book than I had from my experiments. He restored a sense of how our ideas about obesity and vascular disease had developed and how a number of them had gone off the track. I did not agree with everything he wrote but I did learn a huge amount and much of what I learned is now core to my thinking about the relations of obesity and metabolic disease.

In May 2008, I decided to take a more proactive approach to motivating obesity researchers to test the critical arguments in GC,BC. Step one was to induce them to read the book, or at least get the arguments on their radar screen. One way to do that, I figured, was to give seminars at institutions that had the requisite capabilities, expertise and experience to do the experiments. I had been lecturing at medical schools and in nutrition departments and even the National Institutes of Health – twice by that time, and once since – but other than the NIH, which had a new metabolic ward facility, none of these institutions had the resources necessary to do the experiments. (And the NIH people told me that they would be happy to do the experiments, if I raised the money from outside sources, something I am working on at the moment.)

One institution that did was the Pennington Biomedical Research Institute in Baton Rouge Louisiana. The PBRC is probably the most influential academic obesity research center in the U.S. if not the world. It has a large metabolic ward facility that can house volunteers for the requisite weeks to months, and it has the equipment to measure body composition, energy expenditure, substrate oxidation, and anything else I could imagine being useful. Its director is Claude Bouchard, who like Sniderman, spent his research career in Quebec – in Bouchard’s case, at Laval University. I guessed that Sniderman probably knew him well, which he did, and so I asked him to put a word in for me, which he did. Just a few days later I received an e-mail from Bouchard. “I had a nice conversation recently with Allan Sniderman,” Bouchard wrote, “who suggested that we should have you at the Pennington Biomedical Research Center for a seminar and perhaps a series of meetings with our scientists interested in obesity, diabetes and metabolism.”

I gave the seminar in January 2009 (after having it postponed once by Hurricane Gustav) and it led to two moments that captured perfectly the challenge of what I’ve been trying to accomplish for the last four years. I’ll discuss the first in this post, and the second will come at the end of this series, when I get around to discussing experimental tests of the competing hypotheses.

The PBRC auditorium was packed — standing-room-only — and I presented a slightly more technical version of the lecture I’ve given frequently – “Why We Get Fat: Adiposity 101 and the Alternative Hypothesis of Obesity.” (For those, who haven’t seen it, you can find a recent version here, from last April at the Ohio State University Medical Center.)

I argued in the lecture that obesity research had made little to no progress in the years since the Second World War (and for anyone who thinks progress has been made see “obesity epidemic” as a counter-argument) and the reason is because the researchers had been laboring under the wrong paradigm. And by paradigm, I didn’t (and don’t) mean how the word is often bastardized nowadays to imply virtually any shift in thinking or technology, no matter how minor. I meant what the philosopher of science Thomas Kuhn defined as “scientific achievements that… provide model problems and solutions for a community of researchers.” By a paradigm shift, Kuhn meant, for example, the shift from Ptolemaic astronomy, in which the sun circles the Earth, to Copernican astronomy, in which the opposite happens, not the replacement, say, of traditional standard-definition televisions with HD.

At the PBRC, as in my books, I argued that obesity researchers had come to universally conceive of obesity as a disorder of energy balance – we get fat because we consume more calories than we expend — when they should have been thinking of it as a disorder of excess fat accumulation as the pre-WW2 Europeans had come to do. Not an issue of overeating or calories in being greater than calories out, but one of how the calories were partitioned in the body – stored as fat or muscle, oxidized for fuel, etc.

If the post-WW2 generation of researchers had simply defined obesity as a disorder of excess fat accumulation rather than one of energy balance, I argued, they would have naturally asked the question, what hormones and enzymes and other factors regulate fat accumulation. And that’s what they would have and should have been studying for the past sixty years. But, with precious few exceptions, that’s precisely what they have not been doing.

Instead, they’ve focused on what factors control eating behavior and physical activity, and they’ve considered the actual regulation of the fat tissue and fatty acid metabolism irrelevant. (As I describe in GC,BC, a handful of influential researchers in the 1970s worked diligently to achieve this state of affairs, removing any discussion of adipose tissue regulation from discussions of obesity itself, largely because they didn’t like the implications.) At the end of my lecture, I proposed the experiment that I thought the PBRC researchers could do, and I explained why this experiment would serve the critical purpose of differentiating between the two paradigms, and why it was precisely the type of experiment they should be doing. (And this is what we’ll discuss at the end of this series of posts, along with iconic moment number two.)

Now for the punch line to my shaggy dog story – i.e. iconic moment number one. In the Q&A session following my hour-long presentation, a member of the PBRC faculty, a distinguished-looking gentleman who I’d guess was in his mid to late sixties, raised his hand and said, “Mr. Taubes, is it fair to say that one subtext of your talk is that you think we are all idiots?”

Is it fair to say that I think they are all idiots? A surprisingly good question.

Certainly one subtext of my talk (and my work) is that a journalist is getting it right and sixty-odd years of nutritionists and obesity researchers got it wrong (with maybe a half dozen exceptions who were marginalized for their beliefs.) So, yes, it was fair to say that I think a large body of otherwise very smart people, Ph.D.s and M.D.s all, were operating with suboptimal intelligence. Certainly in a pursuit — science — in which the one goal is to get the right answer, getting the wrong answer on such a huge and tragic scale borders on inexcusable.

That isn’t, of course, how I responded at the moment. I smiled, and I said, no, what I believed was that researchers of his generation – those who would have started their careers in the 1970s – had inherited a paradigm of obesity from the generation that preceded them. And this paradigm seemed so obvious (we get fat because we take in more calories than we expend) that they never thought to question it. Indeed, I didn’t think to question it myself until 2003 or 2004 when my research took me to the pre-WW2 European ideas about obesity (for which I owe the late Alfred Pennington – no relationship to the Pennington of the PBRC – for showing me the way) and to researchers in the U.S. who were studying fat accumulation in animals for reasons other than necessarily understanding human obesity.

But this was still just a kind way of saying that researchers of this fellow’s generation, and all those who have followed had simply missed the point. They hadn’t done their job. They should have questioned the obvious, even if it was obvious. And had they done so, all the bad science that followed might never have happened, and maybe we wouldn’t be having an obesity epidemic and a diabetes epidemic along with it.

So why didn’t they do it themselves?

Well, one obvious reason is maybe it’s wrong. They thought about it, looked into it, rejected it. That’s what Stephan Guyenet recently argued on his Whole Health Source blog, and we’ll address that directly later on this series of posts — part III, as it looks at the moment. (It was Stephan’s post, not surprisingly, that finally motivated me to find the time to blog again and put aside, momentarily, my other obligations — raising a family, participating in my marriage, earning a living, and trying to influence the 99 percent or so of the medical and public health establishments that aren’t reading any of these blogs. For that, I’m occasionally grateful.)

Assuming for the moment that it’s not wrong – that I’m not wrong or at least not completely wrong – the other obvious explanation is that they didn’t do it because they were living inside the energy balance paradigm and couldn’t see beyond it. Everything they did, all their conversations, every research question they asked and even the funding they received to answer those questions, their ability to move up in the hierarchy of their field, to succeed, in a word – to become an assistant professor and then a professor, to edit journals, and serve on prestigious committees, to thrive, support a family, pay their lab techs, etc. – all existed within the same belief system. And so they had little to no reason to see outside it and little motivation to overturn it. Seeing a reason to challenge the existing paradigm was not only exceedingly difficult from within the paradigm, but following through on this challenge could seriously jeopardize an individual’s ability to succeed — even to be taken seriously from day to day.

This is why, as Kuhn explained in The Structure of Scientific Revolutions, his seminal thesis on paradigm shifts, the people who invariably do manage to shift scientific paradigms are “either very young or very new to the field whose paradigm they change… for obviously these are the men [or women, of course] who, being little committed by prior practice to the traditional rules of normal science, are particularly likely to see that those rules no longer define a playable game and to conceive another set that can replace them.”

So when a shift does happen, it’s almost invariably the case that an outsider or a newcomer, at least, is going to be the one who pulls it off. This is one thing that makes this endeavor of figuring out who’s right or what’s right such a tricky one. Insiders are highly unlikely to shift a paradigm and history tells us they won’t do it. And if outsiders or newcomers take on the task, they not only suffer from the charge that they lack credentials and so credibility, but their work de facto implies that they know something that the insiders don’t – hence, the idiocy implication.

This is why a common and understandable response to any challenge to the existing paradigm – to the conventional wisdom, in effect – from an outsider is this: “who the hell are you (or am I) to be questioning us? You’re not a member of the priesthood. Not an upper wizard of the stratosphere. You haven’t trained in the field. You haven’t proven yourself. You haven’t done, in effect, what we have done; you haven’t learned what we have learned. You didn’t have the necessary apprenticeship in the relevant arts. Bug off!” (Although, this is by no means a universal response, as this paper – “Obesity and Energy Balance – Is the Tail Wagging the Dog?” — published in July in the European Journal of Clinical Nutrition demonstrates, taking my ideas and those of Robert Lustig’s and exploring the implications.)

This knee-jerk rejection is indeed a valid response, because most outsiders who challenge the conventional wisdom are dead wrong. Some huge majority are quacks – assuredly greater than 99 percent and we can probably add a few more 9s to this percentage and still be on the safe side.

When I wrote for Discover magazine in the 1980s, one of my beats was high energy particle physics, which was also the subject of my first book. Every time I wrote a story on the new theory or elementary particle de jour, I would receive letters written in crayon (implying, as it was explained to me at the time, that the letters had been written by prison inmates who weren’t allowed to use sharp objects like pencils and pens for the purpose). These letters would typically explain why Einstein or Dirac or the latest generation of theoretical physicists had been wrong, and they would propose a new theory of quantum mechanics or relativity or just a theory of everything – known in the jargon as a T.O.E. — that the authors invariably had absolute confidence was correct. And, for all I know, one or more of these incarcerated amateur physicists might have been dead on. Maybe they had created a working theory of everything, but into the waste paper basket these letters went. The odds against them being right were astronomical and time is short. And the odds wouldn’t have been significantly better had the letters been written by fellow journalists or even science journalists using IBM Selectric typewriters or even the few desktop computers that had begun slipping into the offices of the era.

A good rule of thumb is that outsiders challenging establishment science are invariably wrong. And we don’t want our experts and authorities wasting their time vetting every last crackpot theory that arrives over the transom. Crayon or not. We have better uses for their time.

And here’s the challenge to both the scientist working in the field and the lay observer following along: how do we tell the difference between the one in a million times, say, that an outsider comes along and gets it right, and the other 999,999 quack-driven attempts? The numbers alone tell us that the best idea is always to bet against the outsider, that we’re always best served by ignoring him or her and getting back to science as usual (what Kuhn called “normal science”). The odds are enormously in our favor if we do so. But, still, when a paradigm is shifted, it’s going to be an outsider who does it, so keeping an open mind is a reasonably good idea, particularly when the evidence suggests such a shift is in order (see aforementioned obesity epidemic).

This leads to a second major problem with making these assessments – who’s right or what’s right. As Kuhn explained, shifting a paradigm includes not just providing a solution to the outstanding problems in the field, but a rethinking of the questions that are asked, the observations that are considered and how those observations are interpreted, and even the technologies that are used to answer the questions. In fact, often the problems that the new paradigm solves, the questions it answers, are not the problems and the questions that practitioners living in the old paradigm would have recognized as useful.

“Paradigms provide scientists not only with a map but also with some of the direction essential for map-making,” wrote Kuhn. “In learning a paradigm the scientist acquires theory, methods, and standards together, usually in an inextricable mixture. Therefore, when paradigms change, there are usually significant shifts in the criteria determining the legitimacy both of problems and of proposed solutions.”

As a result, Kuhn said, researchers on different sides of conflicting paradigms can barely discuss their differences in any meaningful way: “They will inevitably talk through each other when debating the relative merits of their respective paradigms. In the partially circular arguments that regularly result, each paradigm will be shown to satisfy more or less the criteria that it dictates for itself and to fall short of a few of those dictated by its opponent.”

So this can be considered a warning. I’m about to launch into a discussion of two hypotheses of obesity that exist in competing paradigms – the food reward/palatability hypothesis that Stephan Guyenet has revived, which lives firmly within the energy balance paradigm (calories-in>calories-out) and the carbohydrate/insulin hypothesis, which I’ve been pushing and which lives in the fat accumulation disorder/fuel partitioning paradigm.

In explaining my problems with food reward and palatability as a viable hypothesis of obesity, I’m going to repeat many of the arguments I made in my books for why the energy balance paradigm itself seems to be such a failure. (Not all of them because life is short, but many.) And these, of course, will also provide the rationale for why something like the carbohydrate/insulin hypothesis is necessary. It doesn’t imply that the carbohydrate/insulin hypothesis is right, but that something very much like it almost assuredly is. I’ll also explain why I find many of the observations and some of the experiments used to support the hypothesis meaningless and inconsequential. I hope, as I did with my books, to create what Kuhn called a “playable game.”

But here’s another catch: This map-making exercise can be perceived as a justification for cherry-picking of the data, which, in a way, it is. But I’m arguing that such selective interpretation of the data is a fundamental requirement to make progress in any field of science, and particularly one as off the rails as that of obesity and nutrition. It is inherent to the process that Kuhn described as “map-making,” to taking a non-playable game – a dysfunctional paradigm – and making it playable.

This was a point the physicist Richard Feynman made indirectly back in 1965 in The Character of Physical Law, the book version of a series of lectures he gave the year before at Cornell University. (The lectures themselves are available on line and are worth viewing for many reasons, one of which is the experience of listening to one of the great thinkers of the 20^th century express himself in a thick New Yawk/Queens accent.) Feynman was talking about how physicists find a new law of nature, and this is what he said:

In general we look for a new law by the following process. First we guess it. Then we compute the consequences of the guess to see what would be implied if this law that we guessed is right. Then we compare the result of the computation to nature, with experiment or experience, compare it directly with observation, to see if it works. If it disagrees with experiment it is wrong. In that simple statement is the key to science. It does not make any difference how beautiful your guess is. It does not make any difference how smart you are, who made the guess, or what his name is — if it disagrees with experiment it is wrong. That is all there is to it.

But then he added the caveat:

It is true that one has to check a little to make sure that it is wrong, because whoever did the experiment may have reported incorrectly, or there may have been some feature in the experiment that was not noticed, some dirt or something; or the man who computed the consequences, even though it may have been the one who made the guesses, could have made some mistake in the analysis. These are obvious remarks, so when I say if it disagrees with experiment it is wrong, I mean after the experiment has been checked, the calculations have been checked, and the thing has been rubbed back and forth a few times to make sure that the consequences are logical consequences from the guess, and that in fact it disagrees with a very carefully checked experiment.

And this is the point. Experimental results and observations have to be rubbed back and forth a few times to see if the interpretations that first come to mind are really justified, and whether the experiment, for that fact, is a “very carefully checked” experiment. And what we want to know is whether the result really disagrees or agrees with the predictions. Or is something else going on? Not just dirt in the equipment, but maybe another interpretation entirely – an alternative hypothesis? What was missed in the interpretation? Artifacts in the experimental apparatus? Confounding factors that might explain the observational evidence?

Asking these questions, indeed, leads to all kinds of cherry picking of the data, what a Scottish physician once described to me as “Bing Crosby Epidemiology” – i.e., accentuate the positive, eliminate the negative. And the paradigm in which we live, not surprisingly, will determine how we define positive and negative and so what we accentuate and what we eliminate. Depending on our paradigm or our preferred hypotheses, we’ll put more or less effort into the rubbing back and forth process based on whether the experimental results agree with our notions or don’t.

As I’ve said before in various venues, at one time in the writing of Good Calories, Bad Calories I had a 400,000 word unfinished draft. I couldn’t complete it because it was obviously far too long already – twice as long as it should be — and yet I had important chapters yet to write. I solved the problem by giving it to my editor to read with the suggestion that maybe we could make it two books. He read it in its entirety (one of many acts of editorship that earned my undying devotion) and said, no, one book. We proceeded to cut the document by more than half, so I could then write the chapters that still had to be written and end up with a book that was under 200,000 words (bibliography and endnotes, not included).

Much of what was removed was the rubbing back and forth. I would present an observation – high levels of insulin, for instance, in obese subjects first observed in the early 1960s – and then I would explain how it was interpreted to support the conventional wisdom (we get fat because we overeat and being fat then causes insulin resistance and so increases insulin levels) and why that wasn’t necessarily the correct interpretation and how the same observation supported alternative hypotheses as well. And I would go back and forth with arguments and counterarguments.

My editor pointed out that this wasn’t necessary; that my job was to present my interpretation of the evidence and if someone wanted to challenge it later, so be it. I could provide the arguments and counterarguments, the rubbing back and forth, then.

What I always found amusing once the book was published (okay, amusing in an irritating way) were the critics who would first complain that GC,BC was too long – I go “on and on about experiments old and new,” as Gina Kolata put it in the New York Times – and then upbraid me for leaving something out that they considered important. And so when Kolata pointed out that “definitive” experiments by Leibel and Hirsch should have been in my book because they refuted my arguments – thus accusing me, in effect, of the supposedly heinous crime of cherry picking — I was left to point out in a letter to the editor that the experiment (no “s” at the end, as Kolata had it) was poorly done, didn’t address the salient issues, that Kolata got many of her facts wrong, and that her use of the word “definitive” left much to be desired and that “ambiguous” was a far more accurate description.

So Kolata read the Leibel/Hirsch experiment in a way that supported her beliefs and didn’t bother to rub them back and forth. (She had just published a book a few months earlier that adhered closely to the conventional wisdom.) And I did, because of the implication that the experiment refuted my arguments. I had to see if it did indeed do what Kolata claimed and concluded (not surprisingly, considering my bias) that it didn’t. Or at least that it couldn’t be used, as she had used it, to refute my arguments.

This selective interpretation of the evidence is human nature, as Francis Bacon pointed out almost 400 years ago. But it’s a necessary part of science. For a paradigm to shift, a significant proportion of experimental results will have to be reinterpreted – meaning the interpretation in the new paradigm and the significance is going to be different than it had been under the old. Some significant portion of experiment results will be deemed irrelevant, on the basis that they don’t shed meaningful light on the subject. And, of course, how meaningful is defined is dependent on the paradigm.

So we’re back to the tricky business of assessing who or what is right in such a situation – in determining where to place our bets?

The ultimate determination should indeed be based on data, but not just any data or any experiment that seems relevant. A controversy would not exist if it were not possible for most experimental results and most observations to be consistent with both hypotheses, both paradigms. The key to making progress is to identify observations in nature or generate them by experiment that are consistent with the predictions of only one of the competing paradigms or hypotheses, not both — or not all, if there are more than two. (Thus invariably prompting proponents of the unsuccessful paradigms/hypotheses to evoke what philosophers and historians of science would call “epicycles” to rationalize away the negative evidence.) The problem with the Hirsch/Leibel experiments, as I pointed out in my letter to the Times, is that the results were consistent with both hypotheses, and so the solution was not to conclude on the basis of a popularity contest which was right, but to advocate for better experiments.

What we ultimately want, as Feynman suggested, is an experiment or an observation that can unambiguously — i.e., rubbing back and forth gets us as close to nowhere as we can get — differentiate between hypotheses or paradigms. The competing hypotheses/paradigms predict different results and only one of the predictions holds up. Meaningful experimental results or meaningful observations are those that refute one hypothesis but not the other. Anything less doesn’t help us and doesn’t answer the question of what or who is right. So a constant reminder in this business is to ask ourselves whether the observations or experimental results we’re discussing serve this purpose: can they differentiate between the two hypotheses? If they can’t, let’s move on and find (or fund) ones that can.

In the next post, I’ll begin by defining the questions I think have to be answered by any viable hypothesis of obesity, and how this is relevant to the salient issue of food reward and palatability vs. insulin signaling and carbohydrates. And these questions will speak directly to observations and experiments that I believe can be used to establish the validity of one (mine, of course) and not the other. It may take me awhile to finish the series, as the aforesaid obligations are bound to crash back in, so please bear with me and stay tuned.

Filed Under: Calories-in-Calories-out, Diets, Obesity and weight regulation

The Dose of Intervention and the Land of Dr. Oz

March 7, 2011 552 Comments

Today marks my appearance on the Dr. Oz Show, which was, let’s just say, an interesting experience and leave it at that. It was the show, though, that (finally) prompted me to address an issue I’ve wanted to address for quite some time.

The Dr. Oz Show is one part health advice and discussion and quite a few parts entertainment, as Oz’s producers kept telling me in the days before we taped the episode. To make for what they consider good television they played me up as the second coming of Atkins – a persona that my wife likes to refer to as “meat boy” — while Oz got to play the role of the harvest king, extolling the healing virtues of fruits, vegetables and whole grains. This made it more difficult than I would have liked to get across the important messages from my books, but television is television and I certainly knew what they had in store for me.

My message and the message of Why We Get Fat was not that we should all be eating nothing but animal products – and certainly not the unappetizing meat and eggs that Oz’s crew prepared as props — but that carbohydrate-rich foods are inherently fattening, some more so than others, and that those of us predisposed to put on fat do so because of the carbs in the diet. That’s why I called the book Why We Get Fat rather than some variation on The Miracle 24-Hour (or 14-Day or Three Week or Three month) Diet Cure, which is more the norm for lay books in the nutrition genre.

The idea despite all the controversy is pretty simple. I’m arguing, as others have before me, that the same thing that makes our fat cells fat is what makes us fat — a fat person, after all, is a person with a lot of overstuffed fat cells — and what makes our fat cells fat is fundamentally the hormone insulin. Raise insulin levels and we accumulate more fat in our fat cells. Lower insulin and fat is released from the fat cells and the cells of our lean tissue can burn it for fuel.

There’s nothing particularly controversial about the science involved. If you doubt insulin regulates fat accumulation in fat cells, you can literally look it up in any good biochemistry or endocrinology (the study of hormones and related disorders) textbook – the latest editions, say, of Lehningers Principles of Biochemistry or Williams Textbook of Endocrinology, which are the authoritative texts in their respective fields. Look up the word adipocyte (the technical term for fat cell) and this is what you’ll find:

First Williams (and I’ll translate the technical terminology immediately after):

The activity of LPL within individual tissues is a key factor in partitioning triglycerides among different body tissues. Insulin influences this partitioning through its stimulation of LPL activity in adipose tissue. Insulin also promotes triglyceride storage in adipocytes through other mechanisms, including inhibition of lipolysis, stimulation of adipocyte differentiation and escalation of glucose uptake.

To understand what this means you have to know that LPL is the enzyme (in less technical language, the thing) that works to pull fat from the circulation into whatever cell it happens to be sitting on. If that cell is a muscle cell, the fat is used for fuel. If it’s a fat cell, the fat is stored. Triglycerides are the form that fat is stored in fat cells and transported through the blood stream in lipoproteins. Adipose tissue is fat tissue and adipocyte is the fat cell.

So what Williams says is that fat is stored in different tissues (partitioned) depending on how this enzyme LPL is distributed on the cells of those tissues, and its insulin that to a large extent determines this. Then it adds that insulin promotes fat storage through other mechanisms as well — it creates new fat cells (stimulation of adipocyte differentiation), and it inhibits the escape of fat from the fat cell and its use for fuel (lipolysis), and it also increases the uptake of blood sugar (glucose) into the fat cell, which might not be relevant but the authors of the textbook don’t apparently know this, and neither did I when I wrote Good Calories, Bad Calories.

Now here’s Lehningers Principles of Biochemistry:

High blood glucose elicits the release of insulin, which speeds the uptake of glucose by tissues and favors the storage of fuels as glycogen and triaglycerols, while inhibiting fatty acid mobilization in adipose tissue.

Lehningers uses the other spelling of triglyceride – triaglycerol – to denote the fat in the blood and in our fat cells, and we get high blood glucose by consuming carbohydrate rich foods, which end up as glucose (a carbohydrate) in our blood stream. We also tend to have high blood glucose when we have a condition called insulin resistance, which is the underlying defect in obesity, diabetes and heart disease. When Lehningers says insulin inhibits fatty acid mobilization that’s pretty much the equivalent of what Williams is saying about insulin inhibiting lipolysis.

The point of both is simple. Insulin puts fat in fat cells. That’s what it does. And our insulin levels, for the most part, are determined by the carb-content of our diet — the quantity and quality of the carbohydrates consumed. (Or if Jenny Brand Miller and her colleagues are right, also by our fat content — the lower the fat in the diet, the higher the insulin and vice verse.) The way to get fat out of fat cells and burn it, which is what we want to do with it, is to lower insulin. This has been known since the early 1960s.

One point I make in Why We Get Fat is that we all respond to this carbohydrate/insulin effect differently. Some of us can eat carbohydrate-rich meals and burn them off effortlessly. We’re the ones (like Oz) who partition the carbs we consume into energy. (This is the fuel gauge metaphor that I use in WWGF and that Oz’s producers reproduced wonderfully on the show.) And some of us partition the carbs we consume into fat for storage, and that partitioning depends on a lot of different enzymatic and hormonal factors — mostly relating to insulin and LPL as Williams Textbook of Endocrinology said).

There are a few obvious dietary means to reduce the amount of insulin we secrete and ultimately the level of insulin in our circulation day in and day out. One is to eat fewer carbohydrates; one is to improve the quality of the carbs we do eat, which means eating carbs that are less refined (their glycemic index is low or at least lower) and carbs that come with a lot of fiber attached (green leafy vegetables), and then eating less sugars, by which I mean both sucrose and high fructose corn syrup.

And this brings us to the point of controversy on the show – where Oz and I disagree. (Okay, one of the many points on which we disagree, but the one that needs clarification sooner rather than later). This is also the point that public health authorities, physicians and nutritionists almost religiously refuse to accept or even understand, because one implication of what I’m saying is that the good Dr. Atkins was right all along, and they just can’t get it through their head, as Oz can’t, that a diet of the kind Atkins recommended might be not only healthy but the medically appropriate treatment for the condition – in this case, obesity.

There are a couple of helpful ways to think about the role of carbohydrates in obesity and chronic disease, and one of them (the other I’ll discuss at the end of this post) is that some of us are more tolerant to the refined and easily digestible carbs and sugars in our diet than others. The more we can tolerate them the less we have to avoid them. Hence, the dose of carb-restriction that’s necessary to be lean and (probably) healthy is a small one. Again here’s how I put this issue of individual variation in WWGF:

…Multiple hormones and enzymes affect our fat accumulation, and insulin happens to be the one hormone that we can consciously control through our dietary choices. Minimizing the carbohydrates we consume and eliminating the sugars will lower our insulin levels as low as is safe, but it won’t necessarily undo the effects of other hormones—the restraining effect of estrogen that’s lost as women pass through menopause, for instance, or of testosterone as men age—and it might not ultimately reverse all the damage done by a lifetime of eating carbohydrate- and sugar-rich foods.

This means that there’s no one-size-fits-all prescription for the quantity of carbohydrates we can eat and still lose fat or remain lean. For some, staying lean or getting back to being lean might be a matter of merely avoiding sugars and eating the other carbohydrates in the diet, even the fattening ones, in moderation: pasta dinners once a week, say, instead of every other day. For others, moderation in carbohydrate consumption might not be sufficient, and far stricter adherence is necessary. And for some, weight will be lost only on a diet of virtually zero carbohydrates, and even this may not be sufficient to eliminate all our accumulated fat, or even most of it.

Oz and physicians like him think that there’s so much to be gained by eating whole grains and fruits (we agree on the green vegetables, although I do so less because of any compelling scientific evidence than because my mother insisted they were good for me) that they think this should be recommended to anyone and everyone and a diet that restricts them can’t possibly be healthful.

Oz implies on the show that everyone can benefit sufficiently by improving the quality of the carbs they eat and getting rid of the sugars, that any more significant restriction isn’t necessary. And he thinks any significant amount of carb restriction will cause problems because a) people won’t stay on such a restricted diet; b) they’ll replace these foods in their diet with high fat, high saturated fat meats and eggs and so increase their risk of heart disease (a point I discuss at length in both my books and is obviously critical), and c) they’ll develop diseases like cancer that Oz believes can be prevented by eating fruits and vegetables and maybe even whole grains.

As I point out on the show (or at least I did when the segment was taped, but it may or may not make it to the air as our taping session ran long), there’s precious little clinical trial evidence to support this last contention, but Oz and authorities like him believe in the healing power of fruits and vegetables, and they’re not all that bothered by the lack of clinical trials to support it.

This is the same take on the problem used by physicians and nutritionists who recommend low glycemic index diets instead of carbohydrate-restricted diets. They think this is enough to improve the quality of the carbs we consume, and the implicit assumption is that if we cut back on the quantity of carbs to any great extent we’ll either eat too much fat (or too much meat, period) or we won’t stick to the diet and any benefits will be lost.

What I’m arguing is that for many of us who run to fat, cutting down on the refined carbs and starchy carbs (potatoes, for instance) and on the added sugars will help, but it probably won’t help enough. The dose of carb-restriction won’t be sufficient to deal with the problem. We may stay fat. We may even get fatter. A blanket recommendation to eat fruits and vegetables and whole grains, as Oz prescribes and now Weight Watchers and the U.S. Dietary Guidelines, ignores this aspect of human variability completely. It assumes that people who are predisposed to fatten can tolerate the same foods and benefit from the same very mild dose of carb-restriction that the naturally lean can.

I don’t think that’s true. It’s that simple. I think that if we’re so predisposed to fatten that we’re already obese, we’re probably among those who have to restrict carbs far more severely – have a much greater dose of the intervention – to get even relatively lean, which means relatively healthy. So for some of us and maybe most of us, even fruit, the nutritionist’s darling of the early 21^st century, can be fattening , and if it’s fattening, it means it’s probably causing far more problems than whatever antioxidants or phtyochemicals it contains may be preventing. (As even Wikipedia says, as of March 6th 2011 anyway, “While there is abundant scientific and government support for recommending diets rich in fruits and vegetables,there is only limited evidence that health benefits are due to specific phytochemicals.”)

The way I see it, Oz, who’s naturally skinny, can eat fruits and vegetables and whole grains to his hearts content and remain lean. For him, they can be the bulk of his diet and he can tolerate them and burn them off. They give him energy. They don’t make him fat. But most of his audience is not naturally lean, and they probably can’t. I’d argue that many of them have probably been living on diets very similar to the diet Oz is prescribing and it hasn’t helped them or certainly not to any significant degree. I get e-mails all the time now from people who tell me they were getting fatter and fatter on just those “heart healthy” diets.

Assuredly some proportion of the population and so Oz’s audience will lose a little weight eating as Oz recommends and getting rid of the refined grains and sugars in their diet, and they’ll be a little healthier for the effort. Getting rid of the sugars alone might make a significant difference on both counts. But it’s an insufficient dose of the intervention for a serious medical issue that typically requires far more. For those who are obese and want to be anything close to lean and stay that way, they’re likely to be better off getting rid of all the grains and much or most of the fruit, and then eating more of whatever foods they happen to eat or like that provide protein and fat – pulses, for instance, and tofu (a more complicated issue than I have time for here) for the vegetarians and vegans and animal products (meat, fish, fowl and eggs) for the rest.

This also speaks to a question I’ve been asked numerous times in e-mails from readers. Simply put, what about nuts and what about fruit? And here’s my answer: Nuts are not only Oz’s snack of choice, but the snack of choice of many low-carbers. And nuts and fruit are fine if your body can tolerate them. If you’re still heavier than you’d like, maybe it can’t. It’s a trade-off. If I eat fruit, other than maybe a handful of blueberries a day, I start to gain weight, so I don’t eat it. If I was fatter than I wanted to be — which I’m not — I’d consider giving up both the blueberries and the almonds I eat and see what happens. If it didn’t make any difference, I’d go back to them. If it did, I could decide how much I missed them and whether the trade-off of weight vs. fruits and nuts was worth it. You can look at any number of the nutrition websites to see which nuts have the lowest carb content and which fruits have the lowest sugar content and glycemic index and use that as a guide. But there’s no website or diet book that will tell you what your body can tolerate.

Finally, here’s the other way to look at carbohydrate-restricted diets, and it speaks to Oz’s belief that saturated fats are the cause of heart disease. As I explain in WWGF and did so on the Oz show, it’s almost assuredly the case that the same foods that make us fat are the same foods that cause heart disease and diabetes and cancer, etc. — the diseases that associate with obesity. These are the foods that were absent from human diets during the 2.5 million years of evolution leading up to the agricultural era, and so we’re still poorly adapted to dealing with these foods — easily digestible starches, refined carbs and sugars. When we remove these foods from our diets, we get healthier. Insulin levels come down and with them a host of metabolic disturbances normalize.

It was an email from my friend Bob Kaplan a few days before I taped the Oz show that reminded me of how best to phrase this argument. So I’m going to end with Bob’s e-mail because he said it as well or better than I ever could.

I was just thinking about the “beneficial effects” of a low-carb diet and how it’s essentially a misnomer.

When we eat low-carbohydrate diets, our “good” HDL tends to go up, our LDL becomes larger and fluffier (less atherogenic), our blood pressure goes down, and our triglycerides plummet. Does this mean a low-carbohydrate diet is beneficial to health?

Yes and no. While it appears “beneficial,” for me, it’s more of an indicator of our serum lipids “correcting” to levels that we are supposed to find in a healthy individual. In other words, if we look at a population of people who are chronically over-consuming sugar and refined carbohydrates, their serum lipids are going to be abnormal. When they go on a low-carbohydrate diet, they’re correcting the abnormality and the associated lipids will become more “favorable” (while I would argue that they’re just trending toward a normal, healthy human being) depending on which MD or researcher you ask.

So it is with weight “loss,” water “loss,” lipid and metabolic “benefits” of a low-carbohydrate diet. There is nothing magical about restricting carbohydrates, rather it’s closer to the kind of diet that we’ve been eating and are presumably genetically adapted to eat, and any loss of weight and water, any beneficial effects on serum lipids are just a correction rather than an improvement in health.

Benefits v. Correction:

A restricted-carbohydrate diet doesn’t make you lose weight; it corrects your weight.

A restricted-carbohydrate diet doesn’t make you lose water weight; it corrects your water weight.

A restricted-carbohydrate diet doesn’t improve serum lipids; it corrects serum lipids.

A restricted-carbohydrate diet doesn’t improve health; it corrects unhealthiness.

Filed Under: Diets, Dr. Oz, Glycemic Index, News, Obesity and weight regulation, Weightloss Diets

Calories, fat or carbohydrates? Why diets work (when they do).

December 13, 2010 821 Comments

Last September, the Williams College psychologist Susan Engel had an opinion piece in the New York Times on the value of standardized testing as a means of assessing the quality of a child’s education. Engel argued that there was scant evidence that these tests were of any value at all, and that they should be replaced by the many “promising techniques” that psychologists had already identified as valuable in assessing the learning of our children.

So what does this have to do with nutrition and weight control? Well, among the promising techniques, wrote Engel, was this one:

Researchers have also found that the way a student critiques a simple science experiment shows whether he understands the idea of controlling variables, a key component in all science work. To assess children’s scientific skills, an experiment could be described to them, in writing, and then they would explain how they would improve upon it.

So the value of controlling variables in a scientific experiment is something that a reasonably well-educated child supposedly understands. And what I want to know is why don’ t nutritionists understand it and those researchers out there doing diet trials and studying obesity and weight regulation. Because their failure to do so — and I would argue that it may be a willful failure — has led to what may be another of the great misconceptions in modern nutrition research. In particular, that carbohydrated-restricted diets are “valuable tools” in the arsenal against overweight and obesity, but they’re just one of the dietary tools.

This belief stems from the last decade of diet trials comparing carbohydrate-restricted diets (usually Atkins) to low-calorie, low-fat diets. Instead of thinking of low-carbohydrate diets like Atkins as deadly, which was formerly the case, nutritionists and dietitians (or at least most of them) now think of these diets as useful, just as other diets, low in calories or fats, are also useful. The idea now is that some people do well on carbohydrate-restricted diets and some people do well on low-fat diets, and maybe this is a result of whether they happen to be insulin sensitive or insulin resistant or maybe its just a product of their particular food tastes and preferences.

And this belief, of course, is based on the notion that we get fat for reasons other than the nutrient composition of the diet – probably because of some combination of our genes, our tendency to eat to much and our sedentary behavior – and so the diet that works best is the one that allows us to most comfortably restrict our intake of total calories.

This was the conclusion, for instance, of a 2008 article by Chris Gardner and his colleagues at Stanford, reporting on a subgroup analysis of their famous A to Z study. (The trial is famous, at least, in the low-carb world, because the Atkins diet resulted in twice the weight loss of any of the three other diets tested, and it also did a better job of improving heart disease risk factors). In this follow-up study, Gardner and his colleagues reported that in each diet group — from the Atkins diet on the high end of the dietary fat to carbohydrate ratio to the Ornish diet on the low end — the subjects who actually adhered to the diet lost the most weight. Hence, their conclusion: maybe adherence to a diet is more important than the actual nutrient composition of the diet. Here’s the concluding paragraph:

The main findings of this weight loss study, presented in a previous report, indicated that while all three diet groups lost modest amounts of weight, the Atkins group at 12 months lost approximately twice the weight of the other groups. The findings presented here indicate that weight loss in the lowest tertile [third] of adherence was negligible in all three diet groups, and more pronounced in the highest tertile of adherence for each diet group. It appears that substantial differences in proportions of dietary macronutrients play only a modest role in weight loss success, and that success is possible on any of these diets provided there is adequate adherence. Getting individuals to adhere to whatever diet they choose to follow deserves more emphasis. It remains to be determined to what extent there is a need for dietary weight loss programs that are easier to adhere to vs identifying and addressing individual barriers to adherence, or both.

So the nutrient composition of the diet is less important than whether or not the subject can live with the diet and is willing to do so for as long as it takes — ideally, a life time.

This concept of low-carb diets being good for some people and low-fat for others is invariably reinforced by the fact that most of us know someone who has lost weight and kept it off on Weight Watchers or after reading Skinny Bitch or some other popular low-calorie diet book. As a result, we assume that dieting isn’t a one-sized fits all endeavor and that everyone is different – perhaps metabolically and hormonally, as well – and that what works for me won’t necessarily work for you, and vice verse.

So what does this have to do with controlling variables or even understanding the concept of controlling variables?

What researchers like Gardner and his colleagues do in these diet trials (and it’s the same thing most of us do when we think about those people who succeed on conventional diets or after reading diet books like Skinny Bitch) is make the assumption that a diet that is described as a “low-fat diet” is low in fat only and that’s why it works. And they also make the assumption that a diet that restricts total calories works (if it does) because it restricts total calories. Another way of saying this is that we all tend to assume — researchers and lay people alike — that when someone embarks on a low-fat diet, the only meaningful variable that changes in their diet is the fat-to-carbohydrate ratio. The ratio gets smaller. Fat consumption goes down and carbohydrate consumption goes up. And, by the same token, when someone tries to simply eat less, the only meaningful variable that’s changing is the total number of calories they’re consuming.

The most extreme or perhaps egregious example of this thinking was the recent publication by Gary Foster and his colleagues, comparing low-fat diets, as they described them, to low-carbohydrate diets. The title was “Weight and Metabolic Outcomes After 2 years on a Low-Carbohydrate Versus a Low-Fat Diet.” And here was the conclusion as stated in the abstract:

Successful weight loss can be achieved with either a low-fat or low-carbohydrate diet when coupled with behavioral treatment. A low-carbohydrate diet is associated with favorable changes in cardiovascular disease risk factors at 2 years.

So the way the media and the nutrition community treated this was as further evidence that nutrient composition of the diet makes little difference in weight loss — maybe low-carb works for some of us, but low-fat works for others — although, in this case, maybe low-carb had some modest advantage when it came to heart disease risk factors.

But if you read this article carefully, you’d have noticed that there was another significance difference between the “low-fat” and low-carbohydrate diets. The low fat diet was a low-calorie diet also — “A low-fat diet consisted of limited energy intake (1200 to 1800kcal/d; less than or equal to 30 % calories from fat),” the authors explained. The low-carbohydrate diet was not calorie-restricted. And if Foster and his colleagues were being either intellectually honest or good scientists, they’d have defined the two diets to make this clear. Not “low-fat” vs. “low-carbohydrate”, but “low-fat, calorie-restricted” vs, “low-carbohydrate, calorie-unrestricted.”In other words they’d have acknowledged that there was at least one other variable that was different between the two experiments and had to be taken into account when interpreting the results — the amount of calories the subjects were instructed to consume. As we’ll see, there were also other variables that were changing, but this one — how much food can be consumed if desired — is a whopper.

It’s a whopper because it begs this question: is it the total calories consumed that is the variable determining weight loss? And, by the same token, is it the calories consumed (or expended) that determines how much weight we gain?

In this case, both diets resulted in roughly equal weight loss but those subjects randomized to the “low-fat” diet were instructed and counseled to semi-starve themselves (eat a maximum of 1500 calories for women, 1800 for men), while those counseled to eat low-carb were counseled and instructed not to worry about how much they ate and, one hopes, as this was an Atkins diet being prescribed, eat until they were full. So if weight loss is the same in both groups, doesn’t this suggest, at least, that weight loss can be independent of whether dieters semi-starve themselves or eat to satiety? And, if so, of course, wouldn’t you rather get to eat to satiety?

Had Foster and his colleagues understood what school children are supposed to understand, according to Engels, “the idea of controlling variables, a key component in all science work,” they may have decided to control for calories and instructed both groups that they could eat as much as they want, rather than just the low-carbohydrate group. Or, had they had the money to spend, they might have cooked meals for both groups of subjects, say, 2700 calories a day – either low-fat or low-carb – and encouraged both groups to eat all the food prepared. Such an experiment would have gone a long way to “controlling” for calories consumed or for whether the subjects were allowed to eat to satiety or not. In doing so, it might have revealed something meaningful about whether the nutrient composition of the diet plays a role in weight loss or weight gain independent of calories, which is one of the critical questions here. I’d hazard a guess that it surely does, but I could be wrong. It would be an interesting experiment to do and I’ll write considerably more on that in a later post.

As for the other mistake Foster, Gardner and their colleagues make when they assume that a low-fat, calorie-restricted diet (defining it correctly) is restricted only in fat, it’s the same mistake we make when we assume that someone who lost weight following Weight Watchers or after reading Skinny Bitch did it merely because something about these regimens got them to eat fewer calories and maybe fewer fat calories in particular. And this is the other mistake that suggests a lack of understanding of the idea of controlling variables.

Virtually any diet that significantly restricts the number of calories consumed, even a diet that is described as low-fat (because the subjects are instructed to reduce the proportion of fat calories they consume), will cut the total amount of carbohydrate calories consumed as well. This is just simple arithmetic. If we cut all the calories we consume by half, for instance, then we’re cutting the carbohydrates by half, too. And because these typically constitute the largest proportion of calories in our diet to begin with, these will see the greatest absolute reduction. If we preferentially try to cut fat calories, we’ll find it exceedingly difficult to cut more than 400 or 500 calories a day by reducing fat — depending on how much fat we were eating to begin with — and so we’ll have to eat fewer carbohydrates as well.

Put simply, low-fat diets that also cut significant calories will cut carbohydrates significantly as well, and often by more than they cut fat.

Here’s the math: Imagine we want to cut our daily calories from 2,500 to 1,500, hoping to lose two pounds of fat a week. And imagine that the nutrient content of our pre-diet meals is what the authorities consider ideal — 20 percent protein, 30 percent fat and 50 percent carbohydrates. That’s 500 calories of protein, 750 calories of fat and 1,250 of carbohydrates.

If we keep the same balance of nutrients but eat only 1,500 calories a day, we’ll be eating 300 calories of protein, 450 calories of fat and 750 calories of carbohydrates. We’ll be cutting protein calories by 200, fat calories by 300 and carbohydrate calories by 500.

Now let’s make this a “low-fat” diet and try to reduce our fat consumption from 30 percent of calories to, say, 25 percent of calories, which is significantly less than most of us will tolerate. We’ll now be eating 300 calories of protein, 375 calories of fat and 825 of carbohydrates. We’ll be cutting our fat calories by 375 a day, but we’re still cutting carbohydrates by 425. So even though the percentage of carbohydrates consumed on this “low-fat” diet goes up — from 50 to 55 percent — the absolute amount of carbohydrates consumed goes down, and goes down more so than does the calories from fat. And if we increase the amount of protein we eat, we’ll have to eat still fewer carbohydrates to compensate.

If we start off eating enough fat, as I said — say, 40 percent of our calories — we can actually cut fat calories more so than carbs, but carbs are still cut significantly. Imagine our 2500 calorie per day diet is 40 percent fat, 40 percent carbs and 20 percent protein. That’s 1000 calories of fat and carbs each, and 500 calories of protein. If we now cut that to a 1500 calorie diet that’s 30 percent fat and 50 percent carbohydrates, we’ll be eating 450 calories of fat, 750 calories of carbohydrates and 300 calories of protein. So fat calories will have dropped by 550 calories, but we’ll still have reduced carbohydrate calories by 250. Not an enormous amount but an amount that might still have an effect on the regulation of our fat tissue and so fat loss.

Here’s an example of how this plays out in a real dietary trial. Consider an Israeli trial published in the New England Journal of Medicine in 2008 by Iris Shai and her colleagues. This trial compared a low-fat, calorie-restricted diet to a Mediteranean, calorie-restricted diet to a low-carbohydrate Atkins diet, unrestricted in calories. And, you’ll notice here, too, having explained that the first two diets are calorie-restricted and the latter diet isn’t, Shai and company get lazy and shorten their labeling of the diets so that they leave out the critical variable of whether the dieters are instructed or not to semi-starve themselves.

In this study, Shai and her colleagues made an attempt to assess what their subjects were eating before the trial started, and then after 6, 12, and 24 months. Keeping in mind that the dietary records from these studies have to be taken with a grain of salt, here’s the relevant data:

Let’s concentrate on the low-fat, calorie-restricted diet and the low-carb, Atkins diet. The changes in dietary intake and nutrients for the “low-fat diet” are shown in the first column. As you can see after 24 months, the subjects eating the low-fat diet were supposedly restricting calories consumed on average by 572 calories. The reduction in carbohydrates consumed, though, was 330 calories (82.8 grams per day times 4 calories per gram), compared to only a 170-calorie (18.9 grams per day times 9 calories per gram) reduction from baseline in fat. So the “low-fat diet” reduced carbohydrates nearly twice as much as it reduced fat.

The low-carbohydrate diet, on the other hand (the third column), reduced carbohydrate calories by 520 calories per day (129.8 grams per day times 4 calories per gram) and fat calories by a mere 15 calories (1.7 grams/day times 9 calories per gram). So certainly the low-carb diet was correctly described as a low-carb diet, and the question we have to ask is maybe the weight loss seen in the low-fat diet was also due to the restriction in carbohydrates. It is quite possible that even low-fat, calorie-restricted diets work because they restrict carbohydrates and maybe the reason they don’t work as well as the low-carb diets is they don’t restrict them as much. Or maybe they don’t work as well, on average, because they also restrict fat calories when dietary fat has little or no effect on body fat accumulation. We don’t know if this is true or not, but it could be true, and until these researchers realize that another variable is changing significantly on these low-fat, calorie-restricted diets – the amount of carbohydrates consumed — they’ll never bother to test it or take it into account in their interpretation of these clinical trials, and we’ll never know.

Now, here’s yet another variable that’s changing on these diets, and this one the researchers ignore entirely and make no attempts to quantify — the quality of carbohydrates consumed. Any subject in these diet trials and anyone who tries a serious weight loss program on their own (the twinkie diet, perhaps, not included) will make a few consistent changes to what they eat. And they’ll do this regardless of the instructions that they’re given or the diet to which they’re randomized in the trial.

Specifically, they’ll get rid of or cut way back on the high-glycemic index carbohydrates and the foods or drinks with the high sugar or HFCS content. They’ll do so because these foods are the easiest to eliminate and the most obviously inappropriate for anyone trying to get in shape. (And because for a almost 200 years these foods have been considered uniquely fattening.) They’ll stop drinking beer, for instance, or at least drink less beer or drink light beer instead. They might think of this as cutting calories, but the calories they’ll be cutting will be carbohydrates and, more importantly, they’re liquid, refined carbohydrates that are exceedingly easy to digest and so, perhaps, exceedingly fattening.

They’ll stop drinking caloric sodas – Coca Cola, Pepsi, Dr. Pepper – and replace them either with water or diet sodas. In doing so, they’ll be removing not just liquid carbohydrates but specifically sugars — sucrose or HFCS. The same is true of fruit juices. An easy change in any diet is to replace fruit juices with water. Dieters will get rid of candy bars, desserts, donuts and cinnamon buns. Again, they may perceive this as calorie-cutting – and maybe even a way to cut fat, which it is – but they’ll also be cutting carbohydrates, and specifically sugars with their high fructose content. And if sugars with their high fructose content are uniquely fattening as significant evidence suggests, then this reduction in sugar content may be precisely why the diets work. Starches like potatoes and rice, refined carbohydrates like bread and pasta, may also be replaced in these diets — even “low-fat” diets — by green vegetables and salads or at least whole grains, because for the past 30 years, we’ve been all told to eat more fiber and to eat foods that are less energy dense and less processed.

Even the very-low-fat diet made famous by Dean Ornish restricts all refined carbohydrates, including sugars, white rice and white flour. This alone could explain any benefits that result. Ornish’s rationale, as he described it in 1996 is a familiar one: “Simple carbohydrates are absorbed quickly and cause a rapid rise in serum glucose, thereby provoking an insulin response. Insulin also accelerates conversion of calories into triglycerides, [and] stimulates… cholesterol synthesis.”

Simply put, anyone who tries to diet by any of the more accepted methods (i.e., Weight Watchers), and anyone who decides to “eat healthy” as its currently defined, will remove the carbohydrates from the diet that may be — if the carbohydrate/insulin hypothesis is correct — the most fattening. And if they’re trying to cut calories, they’ll be removing some number of total carbohydrates as well. And if these people lose fat on these diets, this is a very likely reason why.

The same is likely to be true for those who swear they lost their excess pounds and kept them off by taking up regular exercise. Rare is the individual who begins running or swimming or doing aerobics regularly with the goal of losing weight and then doesn’t make any concomitant changes in what he or she eats. Rather beer and soda consumption will be reduced; sweet consumption will be reduced, and easily digested starches and high-glycemic index carbs are likely to be replaced by green vegetables and carbohydrates with a lower glycemic index.

So here’s the lesson, the moral of this story: before we assume that low-carbohydrate diets are just one tool in the dietary arsenal against overweight and obesity, and before we assume that everyone is different and that some of us lose weight and keep it off because we eat less fat (and more carbohydrates) and some because we cut carbs (and so eat maybe more fat), we should make an effort to understand the concept of controlling variables and look to see which variables are really changing and by how much. Because it’s quite possible that the only meaningful way to lose fat is to change the regulation of the fat tissue, and the science of fat metabolism strongly implies that the best way to do that, if not the only meaningful way, is by reducing the amount of carbohydrates consumed and/or improving the quality of those carbs we do consume.

Now, one note about comments that I should have made in my last (and first) blog. I appreciate everyone who comments, but time constraints (earning a living, participating in my family life, etc.) makes it necessary that I keep my responses to a minimum. So I am going to thank everyone in advance for their comments. I will be reading all of them (up to the point, at least, that they degenerate into arguments between two or three particularly vociferous and contentious individuals), but I will be responding only to those that raise particularly interesting questions or issues, or point out any bone-head mistakes I may have made that need to be fixed.

Filed Under: Bad Science, Diets, Obesity and weight regulation, Weightloss Diets

The Inanity of Overeating

December 4, 2010 777 Comments

My new book is coming out at the end of the month. It’s called Why We Get Fat and the subtitle is What To Do About it. The book concentrates more on the first because once you understand why we get fat, the what to do about it part is pretty obvious. And the problem is that the conventional wisdom on why we get fat is almost incomprehensibly naïve and wrong-headed.

My goals in writing the book, as I explain in an author’s letter, are to push the issue (I keep wanting to use the cliché, “throw down the gauntlet,” but as I get older I notice I keep wanting to use more and more clichés, and it’s a bad sign for a writer) on this nonsensical notion that we get fat because of overeating and sedentary behavior, and to distill down and extend some of the arguments from my previous book, Good Calories, Bad Calories, into a book that can easily be airplane reading on any flight covering more than one time zone.

In this blog, if it goes as planned, I hope to ask questions as much as provide answers. Over the past decade, as I’ve read more than a century’s worth of literature on obesity and nutrition and chronic disease, I’ve been consistently amazed at the ability of researchers, learned commentators (and the far greater ranks of unlearned commentators), physicians and public health authorities to accept some of the rote ideas about these excruciatingly important subjects without seemingly giving it any conscious thought whatsoever, or without wanting to ask the kinds of questions that a reasonably smart junior high school student should ask if given the opportunity. To this date, I don’t understand this failure of intellect, although I’ll almost assuredly be returning to it regularly in future blogs.

So what do I mean about overeating being a nonsensical explanations for why we get fat? I was just reading Jonah Lehrer’s latest column in the Wall Street Journal–“The Real Culprit in Overeating.”

Now Lehrer is one of the most talented science writers working today. I’m tempted to say one of the brightest young science writers, but that would be to do him a disservice. He’s as good as any of us at any age. But in this column he falls short, as he’s working outside his area of expertise. (A common problem with most science and health writers is that we often write about a different subject every week or month, so if we’re being fed nonsense by the local experts in any particular field we will typically pass that nonsense along to the readers because we don’t know enough not do otherwise.) The underlying assumption of Lehrer’s column is that we get obese because we overeat, and evidence of the fact that Americans eat too much is that a third of us are obese. Okay, so let’s take a look at this concept from a less than conventional perspective and see what questions we might naturally ask.

First, obese people tend to be weight stable for long periods of their life, just like lean people. So when they’re weight stable, the obese and overweight are obviously in energy balance. They’re not overeating during these periods of stable weight. They’re eating to match their expenditure, doing exactly what the lean do (and get copious credit for). So one obvious question is why the overweight and obese are only in energy balance when they’re carrying 10, 20, 30 or maybe 100 pounds of excess fat, and lean people are in energy balance without the excess? What’s the culprit for that? Because the problem isn’t that the obese overeat when they’re obese, it’s that they overeat when they’re lean and they continue to overeat until they become obese.

Second, let’s say you’re carrying around 40 pounds of excess fat and you put on that 40 pounds over the course of 20 years, as many of us do. When you’re in your late 20s, say, you’re still lean, and then, lo and behold, you celebrate your fiftieth birthday and you’re obese and your doctor is lecturing you on eating less and getting to the gym regularly (and probably writing you a prescription for Lipitor, as well). Now, if you gain 40 pounds of fat over 20 years, that’s an average of two pounds of excess fat accumulation every year. Since a pound of fat is roughly equal to 3500 calories, this means you accumulate roughly 7000 calories worth of fat every year. Divide that 7000 by 365 and you get the number of calories of fat you stored each day and never burned – roughly 19 calories. Let’s round up to 20 calories, so we have a nice round number. (In the new book I discuss this issue in a chapter called “The Significance of Twenty Calories a Day.”)

So now the question: if all you have to do to become obese is store 20 extra calories each day on average in your fat tissue — 20 calories that you don’t mobilize and burn — what does overeating have to do with it? And why aren’t we all fat? Twenty calories, after all, is a bite or two of food, a swallow or two of soda or fruit juice or milk or beer. It is an absolutely trivial amount of overeating that the body then chooses, for reasons we’ll have to discuss at some point, not to expend, but to store as fat instead. Does anyone – even Jonah Lehrer or the neuroscientists he consults – think that the brain, perhaps in cohort with the gut, is making decisions about how much we should eat, on how long we stay hungry and when we get full, so that we don’t overshoot by 20 calories a day. That’s matching intake to expenditure with an accuracy of better than 1 percent. (We consume, on average, about 2700 calories a day, so matching energy in to energy out and not overshooting by 20 calories requires better than one percent accuracy.) And, of course, if we only overshoot by ten calories a day on average, we’re still going to put on 20 pounds of excess fat in 20 years. So really when we talk about being in energy balance – or practicing energy balance, as the experts now like to say – we actually have to be perfect in our matching of intake to expenditure or we’re going to get inexorably fatter (or leaner, if we err on the side of going hungry), or at least we have to average perfection over decades.

One way to get around this is to assume that we overeat by this trivial amount for a few years on end and then we realize we’ve put on five or ten pounds – maybe our clothes no longer fit well or we’ve had to let out the belt a notch or two – and then we decide to undereat every day for however long it takes to make up for it. So now we walk away from the table hungry until all is back to leanness. But then how do animals do it? They don’t have mirrors or clothes to tell them they’re getting fat, and the world is full of animals that have plenty of food available all year round, plenty of opportunity to overeat if they want to and do so long enough to get chubby. And yet the only animals that get chronically obese are those that get their food directly from humans – in the laboratory, in the home or the zoo, or at the dinner table, since humans happen to be animals, too.

Considering the fact that not getting fatter year in and year out means literally matching energy in to energy expended without error for years on end, do we really think that this job is done by the brain, by either conscious behavior, or some system that listens to signals from the body and then puts a halt on eating behavior when it decides enough food has come in that the amount so far expended or likely to be expended in the near future is about to be exceeded? Here’s the idea: your gut is sending signals to this monitoring system in the brain and that monitoring system is tallying up calories consumed until it finally senses that it’s near the limit of intake. Uh oh, it’s thinking, that last bite of that hamburger is not going to be expended, abort abort! Put down the fork! Walk away from the table!

If you were designing an organism that didn’t accumulate excess fat in the fat tissue (in other words, any organism that isn’t human or isn’t getting fed by humans, directly or indirectly) would you leave it up to a different organ entirely, an organ off-site so to speak (the brain), to assure that calories consumed matched calories expended, so that no excess energy managed to somehow sneak into the fat tissue, without the fat tissue having any say in the matter? Or would you give the regulation to the fat tissue itself and let it do the job?

The reason people believe we get fat because of overeating and sedentary behavior is because they believe the laws of thermodynamics somehow dictate this to be true. In particular the first law, which tells us that energy is conserved, so if a system takes in more energy than it expends, the energy contained in the system has to increase. If that system happens to be our fat tissue, than the fat tissue accumulates fat. That’s the logic. So if we eat more than we expend, we get fatter and the logic turns this around to say that we get fat because we eat more than we expend. And so, overeating and sedentary behavior are the causes. This is the logic that leads virtually every government health agency and independent health organization (the AHA, the AMA, you name it) to have some variation of this World Health Organization statement on its website or in its promotional material: “The fundamental cause of obesity and overweight is an energy imbalance between calories consumed on one hand, and calories expended on the other hand.”

But now imagine that instead of talking about why we get fat, we’re talking about a different system entirely. This kind of gedanken (thought) experiment is always a good way to examine the viability of your assumptions about any particular problem. Say instead of talking about why fat tissue accumulates too much energy, we want to know why a particular restaurant gets so crowded. Now the energy we’re talking about is contained in entire people rather than just the fat in their fat tissue. Ten people contain so much energy; eleven people contain more, etc.. So what we want to know is why this restaurant is crowded and so over-stuffed with energy (i.e., people) and maybe why some other restaurant down the block has remained relatively empty — lean.

If you asked me this question — why did this restaurant get crowded? — and I said, well, the restaurant got crowded (it got overstuffed with energy) because more people entered the restaurant than left it, you’d probably think I was being a wise guy or an idiot. (If I worked for the World Health Organization, I’d tell you that “the fundamental cause of the crowded restaurant is an energy imbalance between people entering on one hand, and people exiting on the other hand.”) Of course, more people entered than left, you’d say. That’s obvious. But why? And, in fact, saying that a restaurant gets crowded because more people are entering than leaving it is redundant –saying the same thing in two different ways – and so meaningless.

Now, borrowing the logic of the conventional wisdom of obesity, I want to clarify this point. So I say, listen, those restaurants that have more people enter them then leave them will become more crowded. There’s no getting around the laws of thermodynamics. You’d still say, yes, but so what? Or at least I hope you would, because I still haven’t given you any causal information. I’m just repeating the obvious.

This is what happens when the laws of physics (thermodynamics) are used to defend the belief that overeating makes us fat. Thermodynamics tells us that if we get fatter and heavier, more energy enters our body than leaves it. Overeating means we’re consuming more energy than we’re expending. It’s saying the same thing in a different way. (In 1954, the soon-to-be-famous — and often misguided, although not in this case — nutritionist Jean Mayer said that to explain obesity by overeating was about as meaningful as explaining alcoholism by overdrinking, and merely reaffirmed, quite unnecessarily, the fact that the person saying it believed in the laws of thermodynamics.) Neither happens to answer the question why. Why do we take in more energy than we expend? Why do we get fatter?

Answering the “why” question speaks to actual causes. In the restaurant analogy, okay, maybe this restaurant has particularly great food, or it’s happy hour; the drinks are cheap. Maybe it’s pouring outside so a lot of people ran into the restaurant to stay dry. Maybe every other restaurant in the neighborhood, including our lean restaurant down the block, was recently closed by the local health bureau and this is the only one that didn’t have cockroaches in the kitchen and so remained open. Maybe it’s in the theater district and the shows just got out and now every restaurant in the neighborhood is packed with the post-theater crowd. Maybe the word has spread that Brad Pitt and Angelina Jolie frequent this restaurant regularly, or Oprah, and this attracted a crowd hoping for a glimpse of celebrity.

All these would be valid answers to the question we asked. Some speak to the conditions inside the restaurant (the quality of the food, the price of the drinks, celebrity customers); some speak to conditions immediately outside (a rain storm, no competition, the theater schedule). They all provide the causal information we’re seeking. They answer the “why” question. That more people are entering than leaving doesn’t. It’s what logicians call “vacuously” true. It’s true, but meaningless. It tells us nothing. And the same is true of overeating as an explanation for why we get fat. If we got fat, we had to overeat. That’s always true; it’s obvious, and it tells us nothing about why we got fat, or why one person got fat and another didn’t.

Some obesity experts are intuitively aware of this problem, which is why they’ll say, as the National Institutes of Health does on its website, that “Obesity occurs when a person consumes more calories from food than he or she burns.” By using the word occurs, they’re not actually saying that overeating is the cause, only a necessary condition. (It’s like saying “a crowded restaurant occurs when more people enter than leave.”) They’re just saying that when one thing happened – obesity –the other thing also happened – consuming more calories from food than we expend. And now it’s up to us to say, okay, so what? Aren’t you going to tell us why obesity occurs? Rather than tell us what else happens when it does occur.

As for the great majority of experts who say (and apparently believe) that we get fat because we overeat or we get fat as a result of overeating, they’re the ones making the junior-high-school-science-class mistake: they’re taking a law of nature that says absolutely nothing about why we get fat and assuming it says all that needs to be said. This was a common error in the first half of the 20th century. It’s become ubiquitous since.

If the experts had ever been open to a little skeptical thinking from others or had they been appropriately skeptical themselves, this might never have happened. What’s been needed (and still is) was for someone (a reasonably smart 14-year-old would suffice) to ask the obvious questions and then insist on intelligent answers. Here’s how such a dialog might go:

The experts: Obesity is caused by over-eating, by consuming more calories than are expended. There’s no getting around the first law of thermodynamics.

Us: But all that law says is that if somebody gets fat, they have to consume more calories then they expend. So why do they do that?

The experts: Because they do.

Us: That’s not a good enough answer.

The experts: Well, maybe they can’t help themselves.

Us: Why can’t they help themselves?

The experts: Because they can’t.

Us: That’s not a good enough answer either.

The experts: Because the food industry makes them do it. There’s so much good food around and it’s so tasty, they can’t help but eat it.

Us: But obviously some of us can, because we don’t all get fat. Why is it only some people can’t help themselves?

The experts: Because they can’t.

Us: Try again.

The experts: Well, it’s complicated.

Us: What do you mean complicated? We thought it was easy. Just this eating-too-much, exercising-too-little, calories-in-calories-out, thermodynamics thing.

The experts: Okay, how about this? [Now quoting from an NIH report published in 2000.] “Obesity is a complex, multifactorial chronic disease that develops from an interaction of genotype and the environment. Our understanding of how and why obesity develops is incomplete, but involves the integration of social, behavioral, cultural, physiological, metabolic and genetic factors.”

Us: So what do all those have to do with eating too much and the laws of thermodynamics?

Experts: They contribute to making fat people overeat.

Us: How do they do that?

The experts: We don’t know. It’s complicated.

Us: Then maybe there’s another way to look at it. Maybe when we get fat it’s because those physiological, metabolic and genetic factors you mentioned are dysregulating our fat tissue, driving it to accumulate too much fat, and that’s why we eat so much and appear — to you anyway — to be kind of lazy. We’re compensating for the loss of calories into our fat.

The experts: Yeah, well, maybe. Your guess is as good as ours.

Filed Under: Bad Science, Calories-in-Calories-out, Obesity and weight regulation

On the greatly-exaggerated demise of the insulin-hypothesis

Updates for 2012

Catching up on lost time – the Ancestral Health Symposium, food reward, palatability, insulin signaling and carbohydrates… Part II(d)

Catching up on lost time – the Ancestral Health Symposium, food reward, palatability, insulin signaling and carbohydrates… Part II(c)

Catching up on lost time – the Ancestral Health Symposium, food reward, palatability, insulin signaling and carbohydrates… Part II(b)

Catching up on lost time – the Ancestral Health Symposium, food reward, palatability, insulin signaling and carbohydrates… Part II(a)

Catching up on lost time – the Ancestral Health Symposium, food reward, palatability, insulin signaling and carbohydrates, kettles, pots and other odds and ends (with some philosophy of science as a special added attraction). Part I.

The Dose of Intervention and the Land of Dr. Oz

Calories, fat or carbohydrates? Why diets work (when they do).

The Inanity of Overeating

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