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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:

  1. I find that when I start eating certain foods, I end up eating much more than planned.
  2. I find myself continuing to consume certain foods even though I am no longer hungry.
  3. I eat to the point where I feel physically ill.
  4. 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 25th 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

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 21st 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