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


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 .

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?


Speak Your Mind



  1. Dave Nelson says:

    Well said Gary. As you point out there is more work to be done. The greatest thing here is the requirement for more dialogue and research (good research that is). Bravo and keep the discussion-rich material coming!

  2. I have two problems with your arguments. The first is the idea that food reward fails because it doesn’t explain all modern obesity. As the discussion I started on paleohacks* suggests, any hypothesis that does must be one big-assed hypothesis! In reality, there are many contributors to modern obesity and I certainly agree with Stephan Guyenet that hyperpalatable industrial food is a major contributor!

    Secondly, I don’t see how you can hold food reward up to a standard that your carbohydrate-insulin hypothesis fails. There are many populations for whom carbs do not lead to IR and/or obesity. Wiggling out of it at by pointing fingers to fructose and refined carbs as the trigger is likewise unsatisfactory. My brother eats tons of those things and has never had a weight problem. Why not?

    That said, while I’ve long been a fan of Stephan’s, I’m not particularly invested in his theory for one main reason: while I suspect it will work in the short-term (probably for the reason LCing does … it removes nutrient-poor, toxin-filled, energy dense SAD foods) I don’t see how folks will be any more compliant on a long-term food reward-based diet than they are on a low carb diet.

    I think the answer is elsewhere: restoring insulin sensitivity through moderating carbs (carb intake should be proportional to activity), increasing essential micronutrients that support digestion and metabolism, and increasing specific types of exercise (resistance training and HIIT) to enhance fat metabolism, not to burn calories.


    • BlueEyesSF says:

      “. My brother eats tons of those things and has never had a weight problem. Why not?”

      Is weight the only kind of problem? And he may not have it – yet. Take this challenge – have your brother take a finger stick of his blood sugar, “eat plenty” of pizza and then do a second finger stick. Tell us the results. Better yet, tell us the results when he’s 45 years old after eating this way for 20 years. Also please tell us his genome, in case your family or he in particular has unusual genetics. Thanks! Without that data, your brother can’t really be used in this argument, can he?

      Just as I criticize Guyenet’s advocates for trotting out 150 remote islanders – the Kitavans – whose unusual genetics may not be known, I also criticize Taubes for constantly relying on the Pima, another isolated and remote population with distinct genetics.

      The Neapolitans and Chileans are a better study, as they are a larger, more normal and diverse population.

      But if we have to talk about the Kitavans, why do they “disprove” low-carb – elderly Kitavans appear to sick too, and btw, even the strictest Atkins dieters eat sweet potatoes, carrots, peas and winter squash in Phase 4 of the diet.

      The main culprits for the large populations studied are clearly sugar, fructose, and white flour. We can watch this process in action in Asia today – for example, take the skyrocketing rate of child obesity in Indonesia! In the Philippines! This isn’t an arcane debate – it’s happening right before our eyes, if only the Guyenet folks would stop cherry-picking evidence.

      Oh, and offer a detailed mechanism on how a pinch of salt on your steak leads you gain 100 pounds. 🙂

      • It’s not just the Kitavans. Aside from Asian populations, what about the 30% of Americans who are neither overweight nor obese … are they all low-carbing or avoiding sugar, fructose, and white flour?

        • Howard says:

          I have wondered about that myself. In fact, I believe that’s one of the most important questions that can be asked about nutrition, and I also believe that despite claims to the contrary, the correct answer is not known. I do know for sure that I’m *not* in that 30%, because in order to keep from blowing up like a tick, I *must* restrict sugar, starches, and grains from my diet.

          • Warren Dew says:

            I am in the 30%, and I have been all my life. For the first 45 years, when I was often high carb, it was because I was young. At 45, I started gaining 5 lb/year until 48, when I switched to a low carb diet, dropped the weight, and remain weight stable.

            So in answer to Beth’s anecdotal evidence, my anecdotal evidence indicates that everyone who is not overweight is either low carbing or is on a path to becoming overweight when they get older.

        • Mike says:

          Again, looking at people who are not obese does not necessarily say much about those who are. The smoking analogy (which I believe Gary has used) is an excellent one. If only 10% of people who smoke get lung cancer, that does not mean the 90% of people who smoke that don’t get lung cancer disprove the smoking-lung cancer connection, especially if 99% of people who get lung cancer are smokers or people with heavy exposure to tobacco smoke.

          • Well, your mileage may vary, but I think there’s a considerable difference between carbohydrate and nicotine. For me, the presence of amylase in saliva suggests that humans evolved to eat starch. If all of a sudden 2/3rds of the population are unable to tolerate dietary starch, doesn’t that imply there’s something else at work?

          • FrankG says:

            Sure Beth we evolved to eat starch — we are opportunistic omnivores — BUT as so many others do, you are incorrectly characterizing this hypothesis as saying to avoid ALL carbs… that is not the case at all — but hey take anything to an extreme and you can make it seem ridiculous. We are certainly NOT adapted to eat the amounts of sugars and refined starches that are ubiquitous in the “Western” diet… that much is sure 😉

          • Jim says:

            Frank, this “safe starches are OK” line is fairly new in the low carb world. Yes, many diets have maintenance phases that allow up to maybe 20% of calories from carbs, but that’s different than saying there are safe starches that can be eaten in large quantities without much problem, and that it’s pretty much just fructose and refined grains that are problematic.

            If you look at Gary’s advice in WWGF, there is little room for eating even a moderate number of calories in the form of “safe starches”.

            That’s fine if the advice shifts when new information comes a long — to be applauded, in fact. But let’s not pretend the Low Carb crowd has always been just hunkey-dorey with subtstantial amounts of sweet potatoes.

            So Beth isn’t mischaracterizing the classic version of low carb. Maybe she isn’t up on the “new” version of low carb, but give her some time to catch up 🙂

          • FrankG says:

            Jim, I said nothing about “safe starches” being OK or otherwise… please don’t put words in my mouth 😉 What I wrote was quite clear, “We are certainly NOT adapted to eat the amounts of sugars and refined starches that are ubiquitous in the “Western” diet”.

            For someone like myself who is already metabolically damaged there are NO safe starches although I can tolerate carbs in the form of green leafy vegetables and occasional wild berries. For my son who is 21 I see no issue with him eating sweet potatoes (but not in substantial amounts — again putting words in my mouth?) and other similar, real, whole, foods… for now. So long as he minimises his exposure to only reasonable amounts of sugars and refined starches I expect him to be fine. That means he can even goe for occasional beer and pizza with his friends! :-0 It is not carbs per se that are at fault here, just the quantities and quality of them in the Western diet.

            In much the same way that some try to characterise Dr Lustig as calling any amount of Fructose a poison…. he is quite clear that it is only toxic above a given threshold — much like alcohol.

            Even the discussion here of cigarettes and lung cancer does not necessarily implicate tobacco as being all bad — it has been used for millenia by Native Americans for spiritual reasons… so let’s try and keep things in perspective and intellectually honest OK?

            This “argument ad absurdum” that GT is calling “all carbs evil” is ridiculous to anyone who has actually read GC,BC etc… it is not a new departure in the “low carb crowd” — as I have had to remind others many times on the various diabetes forums where I am a member, “low carb does not equal NO carb …it never has.”

        • Margaretrc says:

          Genetics does play a role in this. There are some who are “genetically gifted” who seem to be able to tolerate boatloads of sugar/refined carbs without getting obese. Diabetic and/or heart disease, maybe, but not obese. And some of those 30% of Americans who are not obese are also not eating boat loads of carbohydrates. They are eating a reduced calorie (and therefore reduced carbohydrate) diet or otherwise restricting their carbs, consciously or unconsciously by “eating everything in moderation.” I’d bet you dollars to doughnuts none of them is eating as much as he/she wants of high carbohydrate foods. I believe what GT is saying is that people who eat a disproportionate amount of carbs don’t all necessarily get fat, but if someone is fat, it’s because of the carbs they eat, not the fat or protein. Because of the body’s hormonal response to those carbs. Try to get fat eating fat. It doesn’t work, even though fat is very rewarding–or at least palatable. Try to get fat eating protein and fat. It doesn’t work. Add sugar and starchy carbs into the mix and voila. People get fat, especially if they replace a significant portion of the fat in their diet with those sugar and starchy carbohydrates. THAT is what is best explained by the Carbohydrate Insulin Hypothesis.

      • Mike Ellwood says:

        “even the strictest Atkins dieters eat sweet potatoes, carrots, peas and winter squash in Phase 4 of the diet.”

        Do they? I’m not sure which version of Atkins that is, but anyway, not all Low-Carbers follow Atkinss, and “strict” low-carbers, wouldn’t be inclined to eat that stuff. I certainly wouldn’t.

        • Warren Dew says:

          I believe Atkins basically allows any carbs to be reintroduced in phase 4 until weight gain starts up again. I believe that includes bread and even refined sugar. The assumption is that people have the will power to remove whatever was the last step causing weight gain, and stay at whatever was there before that last step.

          It’s my opinion that that’s the reason many people who try Atkins eventually fall off of it. Any diet that depends on willpower to deny oneself things one wants is asking for failure. And that includes a diet of “bland” foods.

    • Sam says:

      Beth@WeightMaven says:
      “I don’t see how folks will be any more compliant on a long-term food reward-based diet than they are on a low carb diet.”

      I don’t know how anyone can compare compliance in LC with all the good tasting food, with the punishment it can be eating bland unpalatable food. I have found my LC Paleo lifestyle pretty easy to follow and keep for many years.

      • It may work for you, but in RCTs, folks on the low-carb arms typically are just as compliant (or not) as the others. Most folks don’t like the idea of giving up carbs.

        • Sam says:

          Still there is no comparison Beth. If ever the studies are made between LC and unpalatable eating, LC in compliance will win hands down.

        • Warren Dew says:

          No one has yet done a randomized controlled trial of a food reward diet, for the simple reason that the food reward diet is insufficiently well defined to do such a trial. If you define it as “tasteless food”, Sam is likely correct that the compliance will be lower than with most diets out there.

    • Mike says:

      Saying that your brother eats lots of these things is kind of like arguing that cigarette smoking doesn’t cause cancer because you know a guy who smokes and doesn’t have lung cancer.

      What the Kitavins and other populations that eat a lot of carbs points out is that the hypothesis has to be further developed to account for those carbs that are present in most if not all populations that have high incidence of obesity. Fructose seems to fill that function. Refined carbs such as flour, etc. are propbably not as much of a problem as fructose unless someone is metabolically damaged.

      • England says:

        Having just read all three of GT lastest blogs, I must say that I’ve not been this hooked on reading something since i finished the Lord of the Rings. Anyway, interesting point about fructose being the main carb that causes much (but not all) of the obesity. This sounds like Dr. Lustig. Now, what about Dr. Davis and wheat being the main culprit. I see a great movie coming, Battle of the Titan Carbs. Will sugar win with its master evil carb, Fructose, and sidekick, Glucose? Or will it be wheat with its lightening quick carb Amylopectin A and its vicious protein partner, Gluten, with its many devilish exorphins? We’ll just have to wait and see.

        This is great to have a front row seat while science searches for the Truth! Or sadly is this just a rerun from all the great science from before the 1950’s?

    • Nina says:

      ‘Secondly, I don’t see how you can hold food reward up to a standard that your carbohydrate-insulin hypothesis fails. There are many populations for whom carbs do not lead to IR and/or obesity. Wiggling out of it at by pointing fingers to fructose and refined carbs as the trigger is likewise unsatisfactory. My brother eats tons of those things and has never had a weight problem. Why not?’

      He may not have a weight problem, but that doesn’t mean that a) he doesn’t have a visceral fat problem and b) that’s he’s healthy, for example Dr Davis has a blog post on one aspect:

    • Warren Dew says:

      If you don’t believe the carbohydrate insulin hypothesis, why do you think moderating carbs will restore insulin sensitivity? You should be recommending a diet high in whole grains for diabetes.

  3. Howard says:

    I see you truly *are* making up for lost time. Wow!

    I know from my own experience that I will definitely eat more when the food is palatable, but I suspect that’s just a confounder. “Palatable” in my case usually means “sweet” (since I don’t eat anything with wheat in it because it causes joint pain), so the excess consumption is due to things like the “taste buds” in the small intestine stimulating production of excess insulin (Google “Your small intestine has taste buds!” for an article I wrote on that subject). Dr. William Davis (who is monomaniacal about the idea that wheat is the #1 culprit in obesity) observes that one of the major components of (the modern, genetically-modified) wheat that dominates the US market is gliadin, which is highly addictive, and stimulates appetite.

    So palatability may be a factor. However, low-carb works really well for me – even when I deliberately eat large quantities of fat . I’ve tried Dr. Bernstein’s suggestion of adding 900 cal/day of olive oil to my diet, with the same results he reported — no weight gain. If the macronutrient composition of my diet is mostly fat with only a moderate amount of protein, I can run the total calorie count up to around 4000 cal/day with no weight gain.

    • Warren Dew says:

      I find grass fed beef tastier than regular beef, but I eat less of it. Same with organic fruit. I don’t think palatability necessarily leads to more consumption.

      • Mike Ellwood says:

        And unpasteurised cheese tastes far better than normal cheese, but it’s so strong, I eat less of it.

      • FrankG says:

        I also find grass-fed/finished beef much tastier than “regular” and as above that does not lead me to eat more if it… as with many real, whole, foods from local sources: I find them more nutritionally complete and as such my body responds by effectively saying “thanks… I’ve had enough now.”

  4. Rose says:

    Perhaps I’m dense, but I’ve never understood how the existence of lean carb-eating Kitavans, or for that matter lean carb-eating siblings, constitutes a “hole” in the CIH. We know that insulin production and insulin sensitivity both appear in populations along a continuum, just by the fact that there are Type I and Type II diabetics. If someone produces a lower amount of insulin, or if their fat tissue is less sensitive to it, they will store less body fat. This doesn’t mean insulin isn’t controlling fat storage; quite the opposite. It means these folks either produce less insulin to begin with, or have adipose tissue that doesn’t cram fats away at every little insulin surge. Or am I missing something here?

    And it seems fairly possible to me — but again, I could be thinking with the wrong end — that insulin production varies so much among populations because an “ideal” amount was not strongly selected for in evolutionary terms. We may not have evolved, as it were, in a highly insulinogenic environment, so there wouldn’t necessarily be a “cap” on the amount of insulin a person could produce. (Note I’m not arguing for a carb-free EEA, just a relatively — to modern times — less insulinogenic one.)

    I’m certainly still open to theories of obesity outside of the CIH, but I am just not seeing why the existence of “skinny people who eat carbs” constitutes a devastating blow to it.

    • Margaretrc says:

      @Rose, “I am just not seeing why the existence of ‘skinny people who eat carbs’ constitutes a devastating blow to it [the CIH hypothesis]” Exactly. It doesn’t.

  5. Proofer says:

    “… Yalow and Berson noted in 1965, is “the principle regulator of fat metabolism?”

    Who misspelled “principal” — Yalow and Berson or Taubes?

  6. Richard Falcon says:

    “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”

    Obvious indeed. I really don’t understand how a sentence like this is considered an insightful observation. We tend to eat more of things we think taste good, and less of foods that we consider to taste bad. Therefore, to lose weight, what you need to do, is to eat less of things that taste good, and start eating things that taste bad.

    As I commented before, if the reason something is palatable is because it affects the brain in some way, it does this through an actual mechanism due to the foods chemical composition. If this is not carbs (sugar, refined grains etc) and rather salt and spices, then what is it about salt and spices that causes the brain react in this way. And if its salt and spices, then does that mean we really should be reducing salt in our diet, not because it might raise blood pressure, but because its making us fat? And also cinnamon, and paprika, and coriander….? This may be true….. but it sounds absurd.

    Without a proper measurable component of reward, its all just subjective. We are told what is rewarding is processed fast food and the like. Really? Is this universal? Because I tend not to eat this type of food by choice as home cooked foods are much better. Who prefers a supermarket microwavebale lasagne to a home cooked lasagne? Who prefers a roast beef dinner out of a packet, rather than a home cooked version made of natural ingrediants? One person may find chocolate rewarding, but another brussel sprouts. We all really enjoy some kind of food, therefore why are we all not just pigging out on that rewarding food? Does it come back to will power again?

    This really is easy to test, as Gary alluded to with a simple experiment keeping diet the same, except for something like a suagr sweetened drink, versus, a drink with artificial sweetner.

    • johnnyv says:

      “This really is easy to test, as Gary alluded to with a simple experiment keeping diet the same, except for something like a suagr sweetened drink, versus, a drink with artificial sweetner.”

      Yes like the previously mentioned monkeys feed a supplementary fructose drink in addition to chow, another group could be feed an artificial sweetener, then compare consumption of the chow between the two plus another control group of course.

      A point some people seem to miss about palatability, you may eat a large meal of a palatable food like steak with butter but generally if you eat foods that keep your insulin low you will feel full for much longer and so consume no more calories during a day than someone eating a low palatability diet.
      Not to mention that a low insulin spiking high palatability diet is easy to comply with.

  7. nonegiven says:

    I know being really hungry makes my food taste better, even my own cooking.

    That page has a whole list of studies like that.

  8. PJ says:

    I’m just a layman, I admit, but there is something I don’t understand. Two somethings. (Ok more, but that will do for now.)

    1. It seems like a given that in almost any culture, there will be foods which are more rewarding — to the brain, to the palate, whatever. Even if they had no fast food, most every culture has something. There are lean cultures with one or more carb sources for example. Why did they not eat whatever most rewarding food/s they had to excess until they were fat? Why did it not happen until refined-grains/sugar?

    2. If a person eats more calories than normal, they generally have a little more energy to burn off. Everybody knows people who eat like rhinos and are bouncing off the wall with energy all the time and don’t get fat. Can why their food becomes ‘energy’ while others’ food becomes ‘stored fat’ be explained by the fact that the brain or palate (either) though it was more fun? This is such a critical, integral part of the weight gain/maintain/regain/lethargy complex.

    It seems like the insulin theory is a good theory that also addresses this and other things. If we trade it for the reward theory, I suppose that one might explain eating more, but why isn’t the ‘more’ expressed as energy to burn? Shouldn’t the more, if there are not additional complications like chronic insulin create, just result in a much more active group of people?


  9. Jim says:

    A nice study would have 4 groups:

    1. 400 calories of sugar sweetened beverages/day.
    2. Equivalent volume of artificially sweetened beverage.
    3. Equivalent calories of sugar swallowed in gel caps
    4. A suitable control.

    Of course this study is more difficult to design that it seems, because you don’t know what substitutions in the overall diet will result from the intervention, and some thought should be given to controlling for that.

    My guess (since we’re guessing) is that you’ll see the sweet flavor having a bigger impact than the CI-only-HO would predict. That is:

    2 would gain more fat than 4
    1 would gain more fat than 3

    With that said, I wouldn’t be surprised if:

    1 gains more than 2
    3 gains more than 4

    But I’ve never denied that sugar can have independent effects over and above its role in food reward.,8599,1711763,00.html

    • Warren Dew says:

      If you predefine it as 400 kcal, you can’t test the food reward hypothesis. What you need is a study that allows the subjects to have as much as they want, and just vary what the food is. Maybe give one group New Coke, and the other group Coke Classic sweetened with aspartame to the sweetness of New Coke.

      • Jim Stone says:

        Warren, I think I see where you’re coming from on this. There are a couple different parts of FRH you might want to test. There’s the “rewarding food stimulates consumption of the same food” part. And you would need to allow additional consumption of that item to test that.

        But there’s also the idea that rewarding foods raise the set point, and more calories will be consumed of other foods because of that. That was what I had in mind to test, and I think that standardizing the doses of the treatment food item would allow for a stronger signal in the results (than allowing free consumption of the treatment food item).

        Part of the reason I think this is because I think testing the sugar without flavor (gel caps) is an essential part of this test. And that will have to be dosed out. So it makes sense to make the amount of sugar in the coke match the amount of the sugar in the gel caps (otherwise it won’t be clear whether it was the flavor that caused more weight gain with the real coke, or that they drank more sugar with the coke than was consumed with the gel caps).

        • Warren Dew says:

          I think my proposal tests both parts of the food reward conjecture at once. I agree your proposal would test the setpoint part of it, but I think that’s the less credible part of the hypothesis.

          I think the gel caps are a clever idea, but there are a couple of problems. If the gel caps folks gain weight, Guyenet can claim that the gel caps are a high reward food, which would be pretty typical of his responses to criticism. Also, there seems to be evidence that sugar in liquid beverages is much worse than sugar in solid form. For proper control, the gel caps would need to be compared to nonchewable sugar pills or something.

          • Jim Stone says:

            I’m pretty sure Guyenet would not consider gel caps to be a high reward food — not without a very strange story to go along with it. I guess if one has fond childhood memories of eating dozens of gel caps with family right before gorging on pie at holiday feasts, it might have reward implications 🙂

            I’m glad you’re on board with the idea that it would be good to find a way to get sugar in without reward (whatever the best way is to do that), in addition to testing reward without sugar.

            Seth Roberts in his Shangri La diet claims that if you drink sugar water with your nose plugged, it will promote fat loss. Haven’t tried it. Not sure how plausible I find it. But it seems relevant.

          • Warren Dew says:

            To me, a lot of Guyenet’s “modifying the hypothesis to fit new facts” looks a lot like considering gel caps of sugar to be high reward – for everyone – would.

            Keep in mind that the food reward conjecture is supposed to be a physiological theory, not a psychological one. That allows for the gel caps to be digested and the sugar to stimulate the brain in some way that triggers the posited food reward circuits.

          • Jim says:

            Warren, I’ll have to think about this some more.

            Two things. First, the psychological vs physiological distinction:

            Physiological vs psychological were Gary’s categories, and I thought it best to put FRH on the physiological side, because that’s where FRH people put the blame — on the physiological effects of the of the specific foods being eaten, not the psychological weakness of the victim.

            But, of course, unless you’re a Cartesian Dualist or something, psychology is ultimately mediated by physiology. And many physiological processes have some noticeable psychological effects. So we’re going to have to be more precise at times when making that distinction.

            The key here is how much the obesity triggers are under conscious control. How much good does blame do. I think we all agree that blame does little good and potentially much harm in most cases.

            I’m saying this because I don’t think FRH is saying that reward factors aren’t related to psychology in any sense. The question is whether the behavior is under reasonable conscious control or not.

            I had thought the physiology/psychology distinction was an improvement over the even cruder brain/body distinction Gary started with. Now I think both are too crude. I’ll try to avoid using the simplistic physiology/psychology distinction going forward (and hope Gary does as well).

            My instinct is to say Guyenet would not expect the gel cap sugar dose to be AS rewarding than taking in your sugar in such a way that you can taste it.

            The question for the FRH is whether a factor triggers the reward pathways (dopamine, opioid, etc.) and then that causes leptin resistance, and then that increases appetite, and that leads to increased consumption and that leads to fat gain and that leads to insulin resistance (as opposed to the CIH model of how it happens).

            And you’re right. Sugar delivered via gel caps could conceivably affect the reward pathways in the brain — though it seems more likely that the sweet taste is typically part of what triggers these regions.

          • Warren Dew says:

            I’m pretty sure Gary never used the psychology/physiology distinction. He used a brain driven versus body driven – or more specifically, centrally driven versus peripherally driven – dichotomy. It was the food reward proponents who used the psychology/physiology distinction, which I was accepting for the sake of argument.

            Perhaps Gary’s distinction was more accurate in the first place.

          • Jim says:

            No. I think Gary’s central/peripheral distinction is even worse.

            What matters (as far as blaming the victim goes) is what is under conscious control and what is not. Brain/body, central/peripheral, psychological/physiological all fail to make that distinction, because only a part of the brain/CNS/psychology is responsible for conscious behavior.

            If the effect is partly caused by brain events, but does not depend on conscious control, then it confuses matters to say that it’s a brain theory as opposed to a body theory. The relevant distinction is that both CIH and FRH are not “conscious control” theories.

            BTW, Gary did use the psychological/physiological distinction in the first post in this series:

            “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.”

          • Warren Dew says:

            Okay, valid point on the earlier post. I’m glad Gary has gotten away from that and focused more on the brain/body dichotomy – or the central/peripheral dichotomy, which is another way of saying the same thing. And it is a valid and important difference between the carbohydrate insulin hypothesis and the food reward conjecture, even if you personally don’t like that way of framing things.

            With regard to blaming the victim, while I think the food reward conjecture can take forms that don’t blame the victim, I do think that the closest thing to a recommendation it can currently make does. The current interpretation is that one needs to eat bland food and avoid tasty food, which of course takes will power.

          • Jim Stone says:

            Eating low carb takes will power, too. Maybe not much once you’re used to it, but at first it certainly does.

            Similarly, low reward isn’t as bad as you might think from reading all the negative reactions in these discussions. You get used to it, too. Potatoes, eggs, meat and vegetables are not bad fare all on their own.

            And you don’t have to hold to it perfectly to see results. I sometimes put cheese on my eggs. I sometimes drink wine or eat chocolate. I put cream in my coffee. But I’ve cut way back on doctoring up my food, and it’s working.

            The thing about both approaches is that they radically reduce the amount and kind of will power needed.

            With the standard advice you need to use will power to not eat when you’re ravenous and to exercise when you’re feeling sluggish.

            With lower reward you only need to use will power to buy the right foods and make the right food choices. You’re free to eat when you’re hungry, and not move when you don’t feel like it.

            Much better.

            Both low carb and low food reward work in my experience. Eat less, move more doesn’t.

          • FrankG says:


            After 25+ years of constant struggle with excess fat mass and “diets” that left me hungry and deprived, low-carb was a revelation in that I was NOT HUNGRY ALL THE TIME… it did NOT require willpower! There was a conscious choice to change the quality of the foods that I ate perhaps but that is not the same as constantly fighting to stay hungry; for days, weeks, months or years.

            The Carbohydrate + Insulin hypothesis is about managing a disordered fat metabolism — excess fat storage is driving the over-eating.

            The FRH (so far as I can gather) is about overeating driving excess fat storage — which immediately opens the door for those who still hold fast to the “Eat less, move more” AKA “Calories in vs. Calories out” paradigm — as I’ve said before, NOT HELPFUL.

            I know what a low-fat/high carb diet looks like… AKA the “Western diet” or SAD — lots of sugars and refined starches… the cause of disordered fat metabolism and several other ills as well.

            I know what a low-carb/high-fat diet looks like… AKA LCHF — very little sugar or refined starches, but plenty of tasty and varied, real, whole, food.

            Despite reading Stephan’s blog and your frequent comments here I still don’t know what a “low reward” diet looks like — I have the impression that is “bland” which makes me scratch my head; as what I eat could never be described as “bland” and yet I have lost significant excess fat mass (100+ lbs) and maintained that loss for over 3 years already, with no reason to suspect that I cannot effortlessly keep this up for life.

            I can accept that having lost significant excess fat mass with an LCHF and then having “stalled” one might look around to try and “fine tune” it — perhaps at this stage it is worth taking a look at total calories (perhaps not — I don’t count anything), perhaps there are “trigger” foods which tend to be eaten out of boredom rather than physical need (perhaps not) — but I’d suggest that a well sourced and nutritious LCHF diet would minimise any such effects.

            Still, accepting that we are “only human”, I can see how there may be other approaches which might help you along the way BUT I’d ask that you point me towards folks who have STARTED their path to fat mass loss with a “low reward” diet, lost significant fat mass and maintained that loss — on the same diet, for several years — AND to really convince me of its merit, I’d need to see that the “low reward” diet is NOT a low-carb diet AND yet it could still manage my Blood Glucose to normal levels. Remembering that in my World the BG acts as a measuring stick for insulin levels.

          • Warren Dew says:

            Jim, I actually agree that eating low carb requires some will power at first, in order to change one’s habits. For most people, for example, throwing out all the packaged cereal or other high carb foods takes some will power, if only to overcome the “don’t waste food” habit that most people have ingrained. But yes, once you’re used to it, that changes – if anything, it takes less willpower than a standard American diet, because one needn’t feel guilty eating all the steak and eggs one wants, for example. Once you get used to it, it isn’t a diet of deprivation in any sense, or at least my form of low carb – high animal fat paleo – is not. A “bland foods” diet, in contrast, is still a diet of deprivation, even if mild – I can recommend my diet as much more delicious than a standard diet, but you can only say yours is not “as bad a you might think”.

            I do have to say that potatoes, on their own, are in fact a disaster for me. Indeed my primary benefit from low carb came when I eliminated the potato, which had been causing me perennial painful gas, back aches, constant tiredness, and various other problems. I know it was the potatoes specifically because they were eliminated a month after I went paleo, of which there are moderate carb rather than low carb forms.

            I think it would help this discussion if you could say what specific changes you made with regard to food reward. No butter or salt on the potatoes and eggs? Boil your steaks instead of frying them? Start adding cream to coffee even though you preferred coffee black or with only sugar? Or was it just eliminating cheese, wine, and chocolate?

            Specific examples would help illustrate how food reward principles can actually be put into practice, at least for one person, something I can’t figure out from Guyenet’s blog posts. It would also help us figure out if, possibly, you ended up doing the right things as a result of reading about food reward even though it isn’t actually food reward that makes those things the right things – which is also a possibility.
            The reason that would be helpful is

          • Warren Dew says:

            Oops, last line in that last comment was just a stray line that should have been deleted.

          • Jim says:

            Warren, first let me say that if potatoes don’t work for you, then you shouldn’t eat them, and nothing I’m about to say should be construed as saying otherwise. My examples come from my own experience.

            You asked for some details about the changes I made to my diet. I posted most of my changes in the comments section of Gary’s first post in this series. I can elaborate/restate here a bit, though.

            Basically, I cut back on dark chocolate — which I had started eating too enthusiastically with Mark Sisson’s permission 🙂 I cut back some on red wine. I stopped doing elaborate spicing of my meat. I stopped chewing on cinnamon sticks (don’t ask). A pot roast for me is now just a chuck roast and a little water in the bottom of the pan and a 4 hour simmer time — no spicing/browning, etc. I now eat my eggs without cheese (most of the time, and little to no salt, no pepper/cayenne, browned onions, bacon, sour cream, etc). I added plain baked potatoes, sweet potatoes and squash. I eat plain whole fruit from time to time. I cut back on the complexity of my dishes (e.g., not putting eggs and cheese in the same dish, but eating the eggs plainly.)

            In fact, my current diet plan goes something like this. It has three levels, depending on how quickly I want to shed fat (these are similar to, but a bit different than Stephan’s 4-5 levels).

            1. Increase the quality of my diet (i.e., go paleo, or at least ancestral — whole foods, not junk food, get rid of NADs like fructose, linoleic acid and gluten.). [This was already pretty much my baseline 5 months ago]

            2. Decrease the complexity of my dishes. Eat plain whole foods, pretty much as they come, with minimal doctoring (avoid increasing the “comfort” level of the food beyond what it naturally has. E.g, for me adding cheese, bacon, and onions to eggs raises the status of eggs to a “comfort food”.) Really try to avoid combinations containing starch combined with fat and salt. Eat these components separately, but not mixed together.

            3. Decrease the variety of my diet. (instead of eating 20 different kinds of food in a week, try just 4 or 5.(A decent goal for this phase is to pick one meat, eggs, a vegetable and a safe starch)

            Now, this is a progressive thing. If you’re not terribly broken or grossly overweight, level 1 might be all you need. And, in that case, feel free to “go gourmet” and doctor up your dishes as much as you want, as long as you’re sticking with whole foods. But watch to make sure you’re not crossing the line into addictive comfort feeding.

            If you’ve got a little to lose, you might try to go to level 2. (eat simple whole foods, but feel free to have a wide variety in a given week).

            If you’ve got a lot to lose, then give level 3 a try, and limit yourself ot 4-5 types of whole food for the week.

            I’m mostly at level 2 now — though I lower my variety when I want the weight loss to go faster, and I sometimes “cheat” and have higher reward dishes, too.

            Here’s the intuitive (and very Paleo) idea behind what counts as a “high reward” food. Normal food has normal reward. It is rewarding, but not too rewarding. We’re supposed to be motivated to eat normal foods as we would find them naturally. (In fact, instead of aiming for a “low reward” diet, it might be better to think of it as aiming for a “normal reward” diet.)

            Our restaurant industry and industrial food complex has been on a quest to find ways to make food that people get addicted to, and will consume well beyond normal amounts. These foods are called “hyper palatable” (though that invites some confusion), “addictive”, or “highly rewarding”. These are to be avoided.

            This is also why I think that, while low carb food can be very tasty, if it’s made of natural whole food ingredients, it’s going to be much closer to “normal reward” than “high reward”. That’s why low carb food can taste good and still lead to weight loss. It tastes good, but it’s not activating the addiction circuits that the food industry has learned how to tweak.

            So a low carb diet can be a “normal reward” diet. And it can be quite tasty. If you’re not eating industrial junk, you’re probably close to “normal reward” in your low carb diet.

            Now, which things do people do to increase the addictiveness of our foods? Well, sugar, starch and fat — especially in combination, and combined with salt and a strong flavor delivered with uncanny consistency seems to be one formula that works very well. That’s probably a good paradigm case. And one way to think of it is that things are less rewarding as they fall away from that paradigm. I’m sure that’s not going to completely stand up to scientific scrutiny, but I think it conveys something of the gist. Again, this is an active area of research, and the list of high reward factors is an open question.

            It might also be that none of those elements consumed all by itself would cause addictive eating. (Again, my instincts tell me that people locked in a room given nothing but sugar water to drink ad lib would not gain weight.) But it’s the ways we have of combining these elements into “comfort concoctions” that triggers the reward/addiction pathways.

            A CIH inspired Low Carb diet can be consistent with food-reward-based advice, especially for those doing paleo versions of low carb. That’s a nice area of agreement between us here. But it’s still important to remember the differences between the two approaches (CIH low carb, and “normal reward” diets).

            1. The biochemical explanation of adiposity is different. (the topic of Gary’s series here)

            2. A food-reward paradigm alerts us to the possibility that low carb foods can be made high reward through engineering. I think I remember 10 years ago getting semi-addicted to Atkins bars or something like them. And let’s just say that didn’t promote weight loss. Artificial sweeteners might also be a problem. And if someone is having problem losing weight on a low carb diet, it might be because that person is allowing food company shenanigans and industrial engineering to creep into their low carb diet. (This might be part of Jimmy Moore’s problem, as he has been addicted to artificial sweeteners and processed low carb fare.)

            3. A food reward paradigm suggests that effective “normal reward” diets DO NOT HAVE TO BE low carb. If you eat undoctored natural high carb foods they might be just fine for you. For instance, I have found that adding what Paul Jaminet calls “safe starches” works just fine for me. I’ve also found that when I eat plain potatoes, I don’t have the sugar highs/crashes and binge triggers I was afraid I might have. I seem to handle them just fine, and don’t at all recognize a high blood sugar –> high insulin –> hypoglycemia –> hunger –> more carbs vicious spiral happening at all. I do remember something like that feeling from my early low carb days when I would fall off the wagon and eat donuts or breakfast cereals.

            With that said, I think from a practical point of view we’re on much the same page. I’m very happy telling someone to just start with low-ish carb paleo. I think that’s a very good diet, and is, in fact, “one way” to do a “normal reward” diet very well. I have no problem whatsoever with that way of eating, and that’s probably still where my diet fits much of the time (though some days are higher carb than others, and I probably range between 20 and 30% of calories coming from whole food carb sources).

          • Warren Dew says:

            Did you change all these things at around the same time, or did you change them at a rate of, say, one isolated change per month? From someone reading your post, it’s quite possible that the only thing that actually helped was the cutting back on dark chocolate – candy can definitely cause stalls, even in small amounts – and all the other stuff that you think is helping might actually have had no effect.

            With respect to moving towards paleo, I don’t see it. Sure, getting rid of candy and cheese is more paleo, but potatoes and sweet potatoes are every bit as much neolithic agricultural foods as wheat and rice are. However, I don’t think that paleo is the one true way, even though I do practice it myself.

          • Warren Dew says:

            Also, “a food reward paradigm suggests that effective “normal reward” diets DO NOT HAVE TO BE low carb.” That, to me, is the real test. I am extremely skeptical because based on your description, it was eating a normal reward high carb diet that caused me to get prediabetic and start gaining weight, but if someone pipes up that they lost 50 pounds on a 60% carb normal reward diet at age 50, that would go a long way to convincing me.

          • Jim says:

            Warren, thanks for following up with this.

            About the chocolate . . . it was 88% dark chocolate. I’m not sure what I think of classifying that as “candy”.

            Here’s what I know. When I made those changes, all at the same time, I started losing weight again, without any concerns about calories at all. It’s been the easiest weight loss I’ve ever had. I’ve felt more energetic than I have in years as well. I’ve definitely experienced a spontaneous increase in calories expended, and probably also a spontaneous decrease in calories consumed, though I don’t know for sure, because I haven’t been measuring. Not sure which of those two has been the biggest factor.

            The phenomenon is a fact. The explanation is up for grabs. Was it due to lower food reward? Or something else? I think lower reward is the most plausible explanation, but my Bayesian priors on that are higher than yours, so I can understand if you want to look more closely at the other factors.

            Are my results explained by my taking out the 88% dark chocolate.? I think partially, but not primarily due to its carb/insulin effect. As I reduced chocolate (and wine), I increased fruit, potatoes, squash and sweet potatoes . That amounted to a big net increase in carbs, and I’d even guess I’m getting more fructose than before (from increased fruit and the sweet potatoes than were in the chocolate and wine). And fructose isn’t the only reward factor in chocolate (or wine) by any means (especially 88% chocolate).

            Less wine? Sure, that’s probably part of it. But is it because of the carb-insulin effects? Or because drinking wine makes me want to eat cheese, and the combination is a major comfort food? Or is the alcohol itself a reward factor?

            Is it eating less cheese? Perhaps. Paleo might predict that, but traditional low carb might not. Cheese is a traditional low carb staple, so it seems like it cuts against CIH more than food reward (though I am aware of some evidence that whey is insulinogenic). The thing is, I rarely ate cheese alone. It was usually with my wine or with my eggs. In both cases they increased the comfort value of the other food.

            And let me reiterate that I do still sometimes consume cheese and wine. I’m not following my own ideal fat loss prescription perfectly. The neat thing is that I don’t feel like I need to. That’s another benefit. With a low carb diet guided by the CIH, I always felt like, if I got off the wagon, I was risking ruining the whole diet. Now I don’t feel that way at all. If I comply 80% with a “paleo-normal” food reward diet, I still see good results, and I’m not sweating it. I’m losing 3-4 pounds a month right now. Could it be 5-6 if I ate more strictly? I think probably, yes. But I’m happy being less strict and losing 3-4/month.

            I do expect the weight loss to slow down sometime soon if I keep my diet the same. I’m about 25 pounds from goal now. As I continue to lose fat I will have less circulating leptin. So, even though I’m more leptin sensitive right now, there will be less to sense, and the commands to shed fat will become less urgent. At that point, if I still want to lose that last 10-20 pounds, I might have to tighten things up a bit.

            While compliance might be a concern on a strict low-reward diet, and while it might become more difficult for me if I have to tighten things up as I get closer to goal, it’s actually been very easy to this point.

            So, that’s my story. I think it provides some evidence for the FRH. But it’s by no means the perfect controlled experiment, and I can’t rule out other explanations completely.

            In the end I lowered reward and increased carbs, and started losing more weight without attending to calories in or out.

          • Jim says:

            Of course, mind you, when I “cheat”, I’m not cheating with industrially processed foods. My “cheats” are things like putting salt on my meat, cheese on my eggs, or having some wine, or even wine and cheese. And those cheats satisfy my cravings enough to allow me to get back on track without taking things further than that.

          • FrankG says:

            Jim said: “…a food reward paradigm suggests that effective “normal reward” diets DO NOT HAVE TO BE low carb.”

            The FRH can “suggest” anything it likes, but unless you are now eating an high carb diet Jim then you are not proving anything other than the Carbohydrate + Insulin hypothesis.

            I accept that you are now eating more carbs than when you first went low-carb to start your weight loss… in the meantime (by your account) you have lost excess fat mass… which will have also reduced your Insulin Resistance (IR). I see this all the time on the Diabetes forums… when folks lose excess fat mass, IR is reduced, carb tolerance is increased. No big surprise there.

            With your increased level of carbs could you tell us how many grams per day they amount to? What percentage of your daily energy intake comes from carbohydrates? How much for sugars and refined starches — rewarding or otherwise? Are you now eating an high-carb diet (expressed as a percentage of daily energy).

            Once again I think you are confusing “low carbs” with NO carbs”. We can all tolerate some level of carbs… for many of us it is lower than for others.

            Your description and your conclusions take a great deal for granted and make several assumptions based on “feel” whereas I can show detailed logs that tie my Blood Glucose and Insulin levels together.

            You say “…which things do people do to increase the addictiveness of our foods? Well, sugar, starch and fat — especially in combination, and combined with salt and a strong flavor delivered with uncanny consistency seems to be one formula that works very well.”
            I agree that the food manufactures know how to increase the “addictiveness ” of their foods and use this knowledge to full advantage. But can you please provide an example of this kind of “food engineering” that uses only fat and salt without any sugar or [refined] starch? Even the store-bought bacon I looked at recently had sugars in the list of ingredients… that’s why I buy mine from a small local butcher who uses no additives or preservatives. Whereas I have no doubt that we can can think of many “addicting” foods that contain sugar and refined starches without any fat or salt.

            I’ve not seen or read anything here to change my default position (null hypothesis) that: carbohydrates (especially sugar and refined starches) tend to raise Blood Glucose, which tends to raise insulin levels, which leads to fat storage — this is all perfectly normal BUT repeat this often enough and at high enough levels until Insulin Resistance ensues (as a down-regulation mechanism) and you end up with a vicious downward spiral into metabolic disorder. For many (but not all) this results in obesity, for another group (that may overlap) Type 2 Diabetes etc… etc… Reduce the need for insulin by cutting the carbs and we start going in the opposite direction… hoping that the damage was not irreparable.

            This physiological ( and peripheral) mechanism makes so much more sense to me that some vague idea (heck even the terminology keeps changing) that by eating “rewarding ” foods my brain decides to increase my fat storage “set point” and stimulates me to eat more.

          • Jim Stone says:

            @Frank, I’ve already reported about 100-150 grams of carbs/day. That’s rough, though. I know some days have been over 200, and some under 100. I haven’t really made a point of being consistent about it. I probably eat between 2000 and 2200 calories per day (though I don’t really measure, so it probably varies a bit from day to day). so, that’s roughly 20-30%. I don’t know the ratio of glucose to fructose. Just making an educated guess, I’m probably getting 20-30 grams/day of fructose, though I’m sure that varies outside those bounds on both ends from time to time as well.

            I’m not holding myself up as the ultimate test here. The Kitavans and some New Guinea highlanders seem to be better tests of high carb normal reward diets than my example. Mine is a low-to-moderate carb version with a traditional low carb diet as baseline. So it represents a higher carb diet than my baseline, but certainly not high carb.

            No one seems to think that the Kitavans and New Guinea tribes are relevant here. I can’t see why not. They seem to be very good test cases in this debate. Better than my example. Though at least you know my baseline and which direction I went with the carbs.

          • Warren Dew says:

            Jim, thanks for the additional information.

            I’d certainly consider 88% chocolate to be candy; for a while I was having 85% chocolate regularly, and it certainly had the same effect as other candy on me, specifically including the immunosuppressive effect and the effect of stimulating cravings due to insulin cycling. However, that was just an example, chosen because it was the first thing you mentioned. The cheese or the alcohol in wine might also have been part or all of the reason for the stall.

            To be honest, if I were to venture a personal guess, I would guess the cheese was the biggest problem, because I’ve repeatedly seen people stall on low carb pseudopaleo as a result of eating cheese – stalls which were fixed by cutting the cheese and making few or no other changes. Nor is it a comfort food issue, as I’ve seen it happen with people who eat it straight, on salads, on hamburgers, or what have you – though this is the first I’ve heard of eating cheese with eggs.

            As you note, that isn’t a point in favor of the carbohydrate insulin hypothesis. I don’t think it really favors the food reward conjecture either, though, because for most people cheese does not seem to be the kind of food where you eat one bite and you can’t stop. I think it’s some issue specific to milk proteins, as I’ve never seen evidence of a stall as a result of butter or heavy cream.

            I’ve also seen repeated examples of men – albeit not women – who lost large amounts of weight on paleo despite significant fruit intake. That, again, doesn’t support the carbohydrate insulin hypothesis – but it also runs contrary to the food reward hypothesis, because fruit is the kind of food that can easily trigger a binge. On higher carb paleo, which is how I started, I often had half a dozen bananas in a day, probably half my calories or more, because once I ate one banana I’d be eating them all afternoon. Tonight was grocery night for me, and soon after eating a few strawberries, the entire one pound carton was gone. It would be very difficult to define fruit as a low reward food.

            But these are all secondary effects – stalls rather than the initial weight gain and loss. The carbohydrate insulin hypothesis still explains 80-90% of what’s going on. Food reward, thus far, doesn’t seem to explain any without a lot of additional assumptions.

            By the way, you may find your dietary picture changing again when you reach a stable weight. Right now, you are getting about 500 extra kcal per day from the fat you are losing – which incidentally, to your body, makes your diet look lower carb, or higher fat, than it is. When you no longer have the extra fat to provide those extra calories any more, you’ll need to do another dietary shift. My prediction is that if you make it up with more starch, ‘safe’ or otherwise, you’ll find yourself regaining weight.

        • FrankG says:

          Put simply: if FRH is to be promoted as a replacement for the Carbohydrate + Insulin hypothesis (and I don’t see Stephan or Gary as suggesting they are “complimentary”) then it has to explain my significant excess fat mass loss and BG stabilisation… as well as the now thousands of others who are eating this way.

          • Sam says:

            One think people always ignore about supposable high carb eating societies (total carbs compare with SAD diet can be lower). Is the amount of exercise they do to get food and on daily activities. We all know that exercise help dispose of carbohydrates quickly. If your level of activity from the day you were born and the way you eat, does not compare with this societies I don’t think one that diet is good for us, especially after all the metabolic damage is done.

        • FrankG says:

          Instead of calling fruit an “high reward food” you might also explain it in light of the Carbohydrate + Insulin hypothesis as an helpful evolutionary adaptation: consider a paleolithic ancestor who comes across the rare find of a wild honey-bee hive, or a field of ripe berries, surely it makes sense to maximise the use of that energy-rich resource for the short while it is available? Especially if we are in Europe between the ice-ages and the fruit is ripe just before a long-hard winter; that extra layer of fat mass could mean the difference between survival or not, breeding or not — all courtesy of raided insulin levels. Sure you might argue that “food reward” raising the “fat set point” in the brain might also explain why we’d enthusiastically go at eat such a transient but energy-rich source but why do we need to add an extra layer of complexity when we already know how insulin works in response to a carbohydrate load?

          @Jim you may be missing the point that the Carbohydrate + Insulin hypothesis describes a normal physiological (and peripheral) response that has been overwhelmed into disorder by a diet which is rich in sugars are refined starches. The secretion and release of insulin in response to carbohydrate is perfectly normal — it is just not adapted to be done at such high levels and for so much of the day… every day for weeks months and years.

          Too much insulin for too long causes the metabolic disorder characterised by Insulin Resistance (IR)… which is a down-regulation mechanism just like when folks live alongside a busy road, after a while they no longer hear the constant traffic noise — unless an emergency vehicle comes along with blaring sirens… but after a while, even those fade into the background. The body tries to compensate for the IR by secreting ever larger amounts of insulin (making more noise) in a vicious cycle that for many of us lead to beta-cell burnout and Type 2 Diabetes, and for many others leads to obesity; as insulin increases fat storage and prevents fat burning — that is its job! When insulin levels are high the body is adapted to expect high levels of circulating glucose.

          By starting on a low-carb diet you significantly reduced the need for insulin, in turn this allows fat to be burned and less of it to be stored… you started to reduce your excess fat mass — less insulin plus less excess fat mass = less IR, and less need for the body to compensate by secreting ever more insulin until it can’t keep up anymore. You effectively switched your body from energy-storage mode to energy-utilisation mode by reducing your insulin levels.

          The Carbohydrate + Insulin response is a normal response… the Kitavans etc… do not trigger it excessively by eating a diet rich in sugar and refined starches.

          • Jim says:

            Frank wrote: “Too much insulin for too long causes the metabolic disorder characterised by Insulin Resistance (IR)”

            If I understand this debate correctly, this is the point of contention.

            The CIH (according to my understanding, and correct me if I’m getting this wrong) claims that insulin resistance is caused primarily by frequent post-prandial spikes in insulin due to carbohydrate consumption. These spikes lead eventually [somehow] to chronic high circulating levels of insulin, and then the cells [somehow] start to become numb to the effects of insulin. This requires even more insulin to be secreted to try to force nutrients into the cells. And so on, in a destructive spiral. And in some cases the beta cells even become “exhausted” and stop working correctly, leading to Type-II DM.

            That’s a possible mechanism, but there are a lot of steps in that story, and my understanding is that they haven’t all been definitively demonstrated yet.

            And some things can cause us to question the story. If a Kitavan spikes insulin 3 times a day with a high carb meal, does it lead to higher chronic insulin in circulation? My understanding is that they have lower than western-normal fasting insulin levels. This suggests that the normal human metabolism can handle regular episodic post-prandial insulin spikes without it leading to high chronic fasting insulin. The nutrients get cleared, and then a normal mix of fatty acids and glucose circulate in the blood stream fueling metabolic activity between meals.

            Perhaps something else is responsible for the higher chronic insulin levels.

            An alternative hypothesis is that “something” causes us to chronically eat more calories than we are inclined to burn off. This results in excess fuel in the blood stream. And the natural response to this is to use insulin to drive the extra fuel into the muscle, fat and liver cells — over time, though, this primarily means the fat cells. Eventually the fat cells get full, and don’t want any more fuel, so they stop responding to insulin’s command to take in even more fat. This causes the nutrients to remain in the blood stream in potentially toxic concentrations, and THIS causes the pancreas to crank out even more insulin to try to solve the problem. Eventually the muscle cells also get overwhelmed and start to resist the effects of insulin. And that leads to the higher fasting insulin levels. So the higher fasting levels are caused by the insulin resistance, not the other way around.

            Now, there are a lot of steps in that story as well, and I don’t know how much of that story has been definitively demonstrated either.

            Either way, obesity, higher fasting insulin levels and insulin resistance go together. No question there. The question is the mechanism of the high fasting insulin levels and the insulin resistance.

            And there is also the question of treatment once you have insulin resistance. I’m inclined to accept that low carb diets can be helpful here. If they are helpful, though, it seems we have a range of mechanisms to consider to explain why they help. Is it because they are adding less to the chronic high insulin levels? Or is it because a quality low carb diet increases leptin sensitivity, and this reduces the level of fuel circulating in the bloodstream (through spontaneous reduction in appetite and spontaneous increase in activity), which also leads to fat loss, and, thus, increased insulin sensitivity.

            We’re definitely above my pay grade at this point. There’s a lot I don’t know. The above is mostly my attempt to make sense of the debate from the things I’ve learned from both Gary and Stephan.

            I think the best response for amateurs like myself is to catalogue the phenomena we know for sure, and remain open about which biochemical model best explains the evidence until we get some definitive evidence that decides among the proposed models.

          • FrankG says:

            Jim replied — “…some things can cause us to question the story. If a Kitavan spikes insulin 3 times a day with a high carb meal, does it lead to higher chronic insulin in circulation? My understanding is that they have lower than western-normal fasting insulin levels.”

            So not only does “a calorie equal a calorie equals a calorie” but now “a carb equals a carb equals a carb”? Are you really suggesting that if I ate 100g of carbs in the form of broccoli it would have have the same effect on my blood glucose (BG) and insulin requirements as if I got 1000g carbs form a can of cola? Really? A can of coal would send my BG (and corresponding insulin requirements) through the roof, whereas a huge plate of broccoli (even if I could finish it all — even if it were seasoned to high heaven and dripping in butter) would not. Are the Kitavans getting their carbs from sugars and refined starches? Any more straw men to knock down?

            I explained how IR comes about — it is well documented.

            The local/peripheral effects of insulin are also well documented and not only fit the research data but my own personal experience (and yours if you’d open your eyes) — if you would rather reach for a solution which requires a leap of faith into “brain control” of “set points” then perhaps you are reading at the wrong blog.

            Here’s another example of “peripheral control” from nature — a murmuration of starlings… it looks for all the world like a single intelligent organism with someone or something in overall control but in reality is hundreds of thousands of relatively simple organism that know how to fly and follow a simple set of rules, such as: stay as close as possible to the birds around you without hitting them, change direction when they do, avoid the edges of the flock as that is where the predators strike. That’s it! Simple, local rules — just like insulin — which give the impression of a brain in total control and saying “OK now fly left, now right, you guys at the back keep up!”

          • FrankG says:

            Correction: obviously this should read as “…if I ate 100g of carbs in the form of broccoli it would have the same effect on my blood glucose (BG) and insulin requirements as if I got 100g carbs from a can of cola? ”

            If only I had been offered a low-carb diet even as an alternative when first diagnosed, perhaps my eyesight would still be half decent ;-(

          • Jim says:

            Frank. I’m done here. You’re clearly not trying to understand what I’m saying. This isn’t fun any more.

          • Warren Dew says:

            Jim, I don’t think you have Gary’s hypothesis quite right. I don’t think he specifies whether chronic high insulin levels or insulin resistance comes first. Insulin resistance happening when the fat cells get “full” is perfectly compatible with his hypothesis.

            I also note that muscle cells have much less capacity for energy storage than do fat cells, so they become insulin resistant quicker, not slower. They also become insulin sensitive quicker – it can be in a matter of hours or minutes if you do some heavy exercise. It doesn’t take much to fill them up again, though.

            Finally, what’s the fascination with the Kitavans? Some of the data out there throw into question whether they were really on high carb diets, as they ate large amounts of fish with the skin and fat layer and large amounts of coconut. It seems to me that millions of Chinese on rice based diets would make a better example than a few thousand Kitavans. In absolute amounts, though, they both likely ate less carbs daily than the average American, due to lower total caloric intake.

          • Warren Dew says:

            Frank, I agree regarding fruit. The strawberries were self limiting because my stomach was getting uncomfortably full by the end. However, I think it’s easy to see how that behavior pattern could cause problems with the availability of calorie dense sweets like candy bars or bread – which suggests it may be the calorie density of the carbs, and not so much whether they are refined, that is the issue. I also agree it’s fully explained by the carbohydrate insulin hypothesis.

          • FrankG says:

            Actually Jim this never was “fun” for me… listening to Gary’s reasoning including reading GC,BC has literally saved me from a long slow death and I hope given my son the chance of a much healthier life.

            I’d draw your attention back to the opening sentences of this blog post “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?”” You have yet to present any compelling evidence. Show me many poeple who have resolved or controlled their Metabolic Syndrome by eating an high-carb “normal reward” diet and you might get my attention.

            I strive to remain open-minded but I don’t hold with the idea that every idea is worthy of equal airtime “just because”.
            Dara OBriain has some entertaining yet insightful comments on that idea…

            I suggest you read Stephan’s blog with the same level of skepticism as you are bringing to this one.

          • FrankG says:

            Warren – surely refined carbohydrates are calorie dense by definition? For example: OJ has more calories in a given volume than oranges. But it is not so much about calories as it is about carbs — remember that fat has over twice the caloric density of carbs or protein and yet we don’t get “fat” from eating an high fat diet — no matter how rewarding — now add in some sugar and refined carbs and it’s a different matter altogether 😉

            Dave over at “The Spark of Reason” has some interesting comments about what he terms “the rather poor taxonomy of nutrition”.

          • Warren Dew says:

            Polished white rice is often considered “refined carbohydrate” but is not very calorie dense as eaten.

            Dried fruit is calorie dense but is not generally considered refined, and based on what I’ve seen, does tend to stall weight loss if eaten regularly.

            Agreed that we’re talking about the calorie density of carbohydrates, not fat. Fat intake seems to be regulated rather differently than sugar and other carbohydrate.

          • FrankG says:

            Thanks Warren… I’m not sure why anyone would not consider dried fruit as refined carbohydrate? In both cases a measured volume would yield more calories pre gram than it’s unrefined version* but more importantly (for me at least) is that the measured volume of refined carbs contains more carbs pre gram AND they tend to be digested much faster, leading to a faster/higher Blood Glucose (BG) spike and increased need for insulin.

            As a diabetic myself I’d urge anyone interested in this topic to purchase a BG meter to see how different foods effect your BG and by inference your insulin levels — assuming you are able to manage your BG within the normal range. Wal*mart has a cheap but dependable meter called Relion.

            *as an aside: in any discussion of traditional diets, I think it is important to draw a distinction between the modern version of that food and what was actually eaten traditionally… I doubt that traditional Asian families ate polished white rice for example.

          • Warren Dew says:

            I think a lot of the people who consider whole grains “unrefined” think dried fruit is, too. I could be wrong as I think the whole refined/unrefined dichotomy is specious from a health standpoint.

            Having spent some time growing up in Taiwan before industrialization, I think you’re mistaken about the traditional Asian families. The Chinese have always eaten rice as free of the hull as possible. In fact, if you read a Chinese cookbook written by a Chinese person, you’ll see strong insistence on washing the rice to remove any residue of milling, even though that removes the vitamin fortification that is put on modern white rice. Westerners say don’t wash it because you want the vitamins; Chinese say, wash it. Traditional Chinese cuisine provides the vitamins in other ways .

            Carbohydrate is not the only bad thing in food. Plant proteins, especially in grains, cause various problems – for example, they’ve been linked to autoimmune disease like polycystic ovarian syndrome and multiple sclerosis. The Chinese side of me says that the reason a rice based diet is better than a wheat based diet – see Denise Minger’s debunking of The China Syndrome for details – is because the rice based diets have only the carbohydrates and not the plant proteins, and the wheat based diets have both the carbohydrates and the plant proteins.

            The carbohydrate intake from rice at a meal is limited for the same reason that it is from fruit – your stomach gets physically full before you can overdose too much on carbohydrate, because cooked rice is mostly water. In addition, stir fry is based on cooking in fat, so carbohydrate is not the only thing in a traditional Chinese diet.

            And yes, the traditional Chinese lifestyle did involve more activity than most modern Americans – or Chinese – get – I can remember riding in a rickshaw on my mother’s knee, passing fields in which peasants were working all day, planting or reaping by hand. While it’s not a simple calories in calories out equation, I do think much of the variation in tolerance for carbohydrate does depend on whether one burns off the carbohydrates specifically. A small amount of anaerobic exercise, in particular can go a long way as glycolysis is very inefficient, but does break down the glucose into lactate whose energy may be recovered the liver in the form of fats rather than back into carbohydrate.

  10. Tom Bunnell says:

    If cocaine and amphetamines, like crack cocaine and methamphetamine and other stimulant drugs, are addictive and alluring and compelling, in the reward sense, and they are. — Then why is it so hard to understand that sugars and starches and processed hybrid carbohydrates in the form of lactose and fructose and sucrose, are stimulant drugs, and equally addictive. — There is your rewards, we are addicted. — Like heroin! — Like rats!

    They do not exist in these abundant concentrations or availability in true nature. — Man’s inventions! — Like cocaine and amphetamines!

    • John says:

      I don’t disagree. But if you intend to lose weight, the cure is exactly the same whether you focus on CIH or FRH. Don’t eat the carbs. Carb withdrawal symptoms are part of both the low-carb flu many experience and the problems with diet compliance. Addiction is no reason to panic. Just make a choice and stick with it even if there are setbacks. Carb flu ain’t nearly so bad as crack or amphetamine withdrawal — I would imagine. ; )

      • Margaretrc says:

        And you can do a pretty good job of avoiding low carb flu by consuming coconout oil in the interim. It supplies the energy you are not getting from glucose, but is metabolized more quickly and in a different manner than fat. I’ve been consuming coconut oil for over 6 years and when I went very low carb 6 months ago, I had zero low carb flu from day one. zero. Now keep in mind that I didn’t eat the massive amounts of carbs recommended by the USDA or consumed regularly in this country. I lost my fear of fat long before I went low carb, so my carb consumption would have been less. Plus I ate almost exclusively home cooked or baked foods–no processed foods. But still…i was not short on carbs, either, consuming at least some at every meal.

        • Mike Ellwood says:

          My experience was similar, except that I wasn’t consuming coconut oil before low-carbing,, i.e. no “low-carb flu”. However, I dived into the saturated animal-fats with gusto, and was frankly, glad to be rid of bread, pasta, rice or potatoes – I realised I’d never really liked those things – it was the things you put on them or had with them that made them apparently attractive, and I found that fatty meat, butter, eggs and cheese more than compensated. I’d never eaten much of what most people would regard as junk food, which I suspect was a factor.

  11. FrankG says:

    Many thanks yet again Gary. Quiet, reasoned logic while allowing the reader some room to decide for themselves what is what; without having a dogmatic premise forced down one throat.

    Every time I read or hear your Rolf Richards quote from 1973 regarding Jamaica, I particularly note this sentence, “Obesity begins to manifest itself in the female population from the 25th year of life and reaches enormous proportions from 30 onwards.” As I recall: Weston A. Price describes around 20-25 years as the period of time it takes to start showing effects of ill-health in a community now eating the “Western” diet, having switched from their traditional fare. And on a personal note — although I am not Jamaican or a woman — it was in my late 20s that I started becoming significantly overweight; after being a lean child, youth, teen and young adult. I am not aware of any significant change to my diet or physical activity level — I was very active: not even owning a car and cycling everywhere. It makes me wonder if it takes that long for the metabolic damage to show itself?

    Of course, these days we are seeing harmful metabolic effects in much younger — even young children — and as I recall you offered suggestion (which made a great deal of sense to me) in an interview that we are now into a multi-generational scenario where the foetus, in the womb of an already metabolically damaged mother, is in effect given an “head start”.

    Thanks again Gary, your work has made an huge diefference to my life and health.

    • FrankG says:

      So many typos I don’t know where to begin :-0 Hopefully the sense is clear enough.

      Meantime here is an online copy of Weston A. Price’s book Nutrition and Physical Degeneration – A Comparison of Primitive and Modern Diets and Their Effects

      Be advised that: although some of his remarks may see almost racist by today’s standards, I don’t think that was his sincere intent and they may merely reflect the language of the time when this was written.

    • Mike Ellwood says:

      Similar here, except that I did start driving a car, didn’t cycle so much, didn’t walk so much, but also gave up smoking.

  12. Rocketman says:

    There may be a significant and relevant breakthrough in understanding of FAT BURNING. The Science Daily article about it is at:

    Clearly, an understanding of the details of the fatu burning mechanism may be of value in the weight issue either as a preventative means of preventing obesity or of causing weight loss to reduce obesity.

    The Fat-Burning Zone: News On Burning Fat

    ScienceDaily (Nov. 16, 2011) — Obesity-related diseases are an increasing health problem. Researchers at the University of Oslo have now uncovered a central component of fat metabolism.

    It is well known that exercise results in “fat burning.” Physical activity and fight-or-flight responses increase the levels of hormones like adrenaline, inducing the metabolism of fat. Until recently, some of the molecular details of exactly how this works have been a mystery.

    Fats are stored inside fat cells within specialized compartments known as “lipid droplets” (LD), and their metabolism requires the cooperative action of several different proteins. Not only must these proteins act together, they must also be found within close physical proximity on the surface of the lipid droplets. This clustering of proteins is achieved by what are called anchoring proteins.

    The essential role of the anchoring protein OPA1 in lipid metabolism was recently demonstrated by researchers in the Taskén group, and the study published in the EMBO Journal. Dr. Greenberg and colleagues from Harvard and Stanford University underlined on the importance of these findings in a research highlight: “The observation of [OPA1] on the LD surface provides an important step in understanding the regulation of LD biology..”

    “It has taken a long time to sort this out.” said Group Leader, Professor Kjetil Taskén. “In fact, the publication of this paper summarizes the work of two postdoctoral researchers and two PhD students over a period of more than seven years.”

    Journal References:

    Guillaume Pidoux, Oliwia Witczak, Elisabeth Jarnæss, Linda Myrvold, Henning Urlaub, Anne Jorunn Stokka, Thomas Küntziger, Kjetil Taskén. Optic atrophy 1 is an A-kinase anchoring protein on lipid droplets that mediates adrenergic control of lipolysis. The EMBO Journal, 2011; 30 (21): 4371 DOI: 10.1038/emboj.2011.365
    Andrew S Greenberg, Fredric B Kraemer, Krishnakant G Soni, Mark P Jedrychowski, Qing-Wu Yan, Christine E Graham, Thomas A Bowman, Ayla Mansur. Lipid droplet meets a mitochondrial protein to regulate adipocyte lipolysis. The EMBO Journal, 2011; 30 (21): 4337 DOI: 10.1038/emboj.2011.371

  13. The causal link between carbs/sugar and obesity is increasingly well supported and will likely become even more compelling as the detailed mechanism of sugar leading to insulin resistance is established. But it still seems that there could be an important role for the addictive nature of sugar– at least for some people. For insulin resistance to develop quickly some sort of disequilibrium needs to be created and it seems plausible that the extremely palatable nature of sugary foods could be responsible. If the nature of the food increases the propensity to binge uncontrollably over short periods, it is more likely that metabolic regulation would break down even if energy balance is maintained over a longer averaging period. Once the damage is done, the carb-insulin vicious cycle can take over. It also seems undeniable that the availability and creativity being put into desserts has increased dramatically in recent years– note the cupcake and doughnut shop proliferation in metro areas. Of course this could be a side-effect of the epidemic but it seems possible there is some more complex feedback occurring.

    • Adam says:

      Hi Krista,

      What you say sounds totally plausible. I believe Taubes even talks about the addictive nature of sugar in WWGF. It seems like some body/brain feedback thing — that squares with everything he’s been writing about with these posts and also adequately explains the stuff that the Food Rewardees want to explain — can live within the framework of the carbs/insulin theory.

      My personal beef with all this chatter about reward versus carbs is that we’re all focusing WAYYYY too much on food quality and quantity, when what we SHOULD be discussing is the totality of the forces at work on the fat tissue.

      What does that mean, why is it important? It means we need to look at ALL the possible hormones, enzymes, growth-factors, and other such stuff. Because if we don’t, we may miss critical clues.

      LPL, for instance. What might impact that? GT says nicotine, menopause, and lots of other things can influence the enzyme LPL, which directly impacts the fat tissue. This “stuff” that is making us fat (or lean) has NOTHING TO DO with food quality or quantity. Or even insulin, for that matter.

      So in our obsession with vague concepts like “reward” we miss the bigger picture and we miss hugely important possible solutions.

      Say you’ve got someone on a LC diet who “can’t lose those last 15 pounds” or who experiences weird weight re-gain. Traditional LC will tell you “just cut more carbs, fool!” Food reward is even less helpful. “Eat blander foods, fool!”

      NO. At least, we shouldn’t assume either solution will work. What about the countless other factors that could influence the balance of forces on the fat tissue:

      * medications (many have been clinically shown to cause WG, I believe)
      * change of life (menopause, puberty, male menopause, subtler “changes”)
      * smoking/drug use
      * sickness/injury
      * some allegry/inflammation thing
      * stress or lack thereof
      * sleep or lack thereof
      * etc etc ad nauseum

      These factors are probably not trivial, especially when you consider them in the context of GT’s idea about “20 calories a day” (i.e. 20 kcals a day “overeaten” = obesity in 2 decades).

      • Jim Hippard says:

        Your list, with emphasis on etc., etc, geometrically multiplied through the prism of genetics.

      • FrankG says:

        Sure there may bother factors to explore but it seems to me that the quality of our food is one of the biggest determinants of our fat metabolism and one over which, we have the greatest control. Try using a Blood Glucose (BG) meter to see how various foods (at different times of the day) influence your BG — and by association your insulin level — and you quickly gain sense of how much control we really have.

        • Adam says:

          Agreed, Frank. Have enjoyed reading your comments, btw. I haven’t read em all, but every time I read one, I’m like “yes, yes, listen to this guy.”

          Agreed that the quality of food is almost assuredly both a) the biggest deal and b) easiest to influence.

          My point was that there are secondary, tertiary, quaternary factors that probably become non-negligible, once you’ve become metabolically damaged. Are these trivial when compared with food quality? Sure. Totally. And if obese/overweight Americans bought into the ultra-simpified version of what Taubes is saying — “count carbs, not calores” — would that basically lead to the eradication of chronic disease and save America? I’d bet money on it.

          The trouble is, whenever “experts” point to non-carbs/insulin factors that MIGHT influence obesity, people view this evidence as somehow refuting what Gary and Lustig are saying. As refuting the “paradigm shift” they’re trying to push.

          Their loopy thinking goes somthing like this:

          1) Oh-ho! These (non-carbs/insulin factors) might be important!
          2) Therefore, Taubes is wrong, he’s oversimplified it, and the only thing I know that REALLY matters (ultimately, at the end of the day, because it “has to be” true) is Calories-In-Calories-Out.
          3) Ergo, no need to do Low Carb, after after. I’ll just “watch what I eat” and renew my gym membership, so I can burn a few more cals.
          4) The poor fool then loads up on 100 calorie junk food snack packs and gets sicker and fatter.

          That scenario is what worries me. That people will momentarily get excited by GC, BC or WWGF or Protein Power or Atkins or Paleo or what have you. But then they will read these long, complicated debates about biochemistry on the internet, think to themselves “well, shucks, everyone’s confused, no one REALLY knows what’s going on, I’ll just count calories, because that’s what everyone says to do” and they’ll miss out on this opportunity to fix themselves.

          Veteran LCers make this error, too. Whenever something “goes wrong” (or “not right enough”) with the diet, they immediately default to thinking that “calories might matter, too.”

          They might. Food quantity MIGHT influence fat tissue metabolism. But HOW? Again, it comes down to questions of mechanisms.

          And what’s probably going on with many folks who struggle on LC, in my admittedly-less-than-educated-opinion, is that they’re encountering the secondary/tertiary/quaternary constraints discussed above.

          And maybe, unless they dial into those and fix em, they’re going to struggle, even if their food quality is ideal for controlling insulin.

          • FrankG says:

            Thanks for you kind words Adam…. despite my terrible typos above :-0

            I agree that these other factors are worthy of consideration but I balk when they are brought up, as invariable it leads to other agendas — such as looking for drugs to treat obesity — that can distract from the simple message, as you eloquently put it “…if obese/overweight Americans bought into the ultra-simpified version of what Taubes is saying — “count carbs, not calories” — would that basically lead to the eradication of chronic disease and save America? I’d bet money on it.” And I agree with you.

            Leptin, or the other aspects of hormonal control in “Food Reward” I think, come under this heading and are part of the “down stream” effect which, as I recall, GT discussed in GC,BC with the analogy of hitting a person on the head with a hammer: researchers might go to great lengths to discover the minute details of the biochemical interactions that take place to translate the hammer-blow into the perception of pain — possibly with the promise of a pharmaceutical treatment to interrupt that biochemical message and prevent the pain — when the common-sense approach is simply to say “stop hitting me!”

            “Stop eating the sugars and refined carbs” is something we can all do today… it will take a societal change along the lines of the anti-smoking campaigns (remember that not so long ago Doctors advertised cigarettes?) and polices such as removing the subsidies on corn — but the payoff in public health would be immense.

          • Adam says:

            Thanks Frank. Your point about directionality is key. How about we first STOP hitting people with hammers and blaming them for when they bruise and cry? Let’s try that for Step #1 🙂

            Anti-Taubesians seems to want to take this debate 43 levels deep and showcase wonky biochemistry trivia they’ve unearthed as “refutations.” If someone cites biochemistry to prove that biochemistry doesn’t matter and CICO “really does”… well, isn’t that inherently silly and preposterous?

            This is not a level 43 discussion. It’s a level 2 discussion. It’s a debate a 2nd grader could win:

            “The Earth is not flat, professor. I have a globe of it at home.”

            “It’s not about calorie deficits, professor. Otherwise, I could sit on a snowbank and cure my overweight and diabetes.”

          • Jim says:

            Adam wrote: “Their loopy thinking goes something like this: 1..2…3…4”

            Adam, once again, this is a gross mischaracterization of the FRH. How many times do you have to be reminded that FRH is a physiology rules theory, not a psychology rules theory, and so is not a “move more, eat less” view (the sense of CICO you seem to be using here).

            How many times do you have to be reminded that FRH people do not advocate consumption of Mountain Dew or snack packs?

            Have you even read the posts on Guyenet’s blog?

            Have you even read the comments others (like myself) have posted here?

            It’s very tiresome to have you and blueeyessf continue to blatantly mischaracterize (“FRH is the view that a pinch of salt makes you gain 100 pounds of fat”).

            Please go read Stephan’s posts on this topic thoughtfully. Gary has done this. You should too. I still think Gary’s not quite getting it, but he’s not blatantly disregarding things like you are.

            I am seen defending Guyenet here, but I’m not fully convinced by any means. I will tell you, though, that I have very thoughtfully read GCBC two full times, and many chapters a third time. I read WWGF as well, and many of Gary’s articles, too. I have much respect for Gary, and am trying to reconcile what I’ve learned from Gary with what I’ve learned from Stephan.

            Please show Stephan some respect and give his view at least one thoughtful open reading.

            I’m sure there are many carb/insulin theorists here who can see when the FRH is being misrepresented. It would be wonderful if you would step in and “police your own”, so it might be more likely taken to heart.

            There are no points awarded for knocking down straw men.

          • Jim says:

            Another thing that’s bothering me is the charge of circularity that has been leveled time and again against the FRH.

            Stephan’s definition is not circular. It might be a little vague, or hard to pin down exactly. But vague and circular are not the same thing.

            If you’re going to accuse reward of having a circular definition, you have to demonstrate the circle, and show that the definiendum and definiens have the same term used *in the same sense* (and that it’s not a legitimate recursive definition).

            Circularity is not the same thing as shifting a definition here and there to accommodate new information. That practice can be frustrating, as it gives you a moving target, but it’s not circular.

            And, though it’s frustrating, someone who does shift definitions a bit over time might actually be exhibiting a scientific virtue. It’s often the humble response to changing information — an admission that the first theory didn’t quite work, and that you need a slightly different one if it’s going to accommodate all the phenomena.

            Gary has himself shifted his view some just recently (or so it seems to me). And I applaud him for this. He used to be much more against “safe starches” (whole food glucose+fiber bundles like potatoes or squash). At times he seems to be adopting a more Lustigian view, and focusing more on refined grains and sugar.

            But, if it’s OK for Gary to adjust his view of “which carbs are bad”, then why isn’t it OK for a FR theorist to stay open about which foods affect reward in which people?

            No one has a definitive complete list of rewarding factors and combinations of reward factors right now. That’s a fact. But it doesn’t make the Food Reward framework invalid. As it stands food reward seems to be more of a general framework for generating testable hypotheses, than a testable hypothesis in its own right.

            For another example of this sort of thing, Darwin didn’t offer a very detailed mechanism for how biological traits changed over time, but the Evolutionary framework was still valid and very fruitful, and helped to combine a lot of previously disjoint observations to a single theory.

            I’m not saying FRH is right. I’m just saying some people need to give it some more thoughtful consideration.

          • FrankG says:

            Why Jim? Why do we have to give FRH thoughtful consideration?

          • Adam says:

            Hi Jim,

            Thanks, and you’re right that it would serve me to read Guyenet et al’s thinking in depth. On my list!

            In my comment above, I was less aiming to diss on the FW crowd and more taking aim at the strict CICO team. I must confess, I have had some difficultly trying to tell them apart. But then again, as you write, probably worth it for me to read the “physiology rules FRH” in more depth. No disrespect intended. We’re all sincerely struggling to come to terms with this stuff, after our health “authorities” so abysmally screwed the science.

            I’m mostly concerned with LCers and Paleos who are struggling who think:

            1) Hmm, LC/Paleo is not working optimally.
            2) Must be the food is not bland enough.
            3) I’m going to blandify things and that’ll fix it!

            Instead of thinking…

            1) Hmm, LC/Paleo is not working optimally.
            2) Must be one or several of thousands of factors that could be impacting the balance of forces on my fat tissue (including, perhaps, leptin or something else as modulated by food reward or something like it)
            3) I need to embark on a serious N=1 that looks not just at food quantity/quality (and possibly reward, leptin, etc) but also at dozens of other potential culprits, including the anti-depressant I’m on, an allergy/illness, change of seasons, normal fluctuation in fatness, etc.

            I also worry — as I mentioned above — about the casual observer who stumbles into the FW/CIH turf war, gets lost in the back and forth, and defaults back to the CICO version that both you and I reject.

            Hope that makes sense, and again, I appreciate your thoughtfulness.

          • Jim Stone says:

            Fair enough, Adam. As long as you put food reward in among the “many factors” to check when the diet isn’t working, I can’t argue with that.

          • Warren Dew says:

            Adam, exactly. I’ve seen steps 1, 2, 3, 4 so many times I can’t count. Just today I saw a comment on Eades’ review of Why We Get Fat from someone who had been given a ketogenic low carb diet by a doctor, and lost 12 pounds in the first week. Time to stick with it and lose the other 88 pounds, right? But no, the person has now spent the second week experimenting with ways to cheat on the diet. So far, based on the review and the book, it’s only added protein, but one whiff of “safe carbohydrate” and that person will be ballooning up again instead of losing.

            Jim, you might want to go back and reread Adam’s comment. His steps 1, 2, 3, 4 are not his interpretation of what Guyenet says. They are his view of what a lot of people will do when they read Guyenet’s blog. And his view is correct in many cases.

          • Jim Stone says:

            Warren. You’re right. I took Adam’s steps out of context. My bad.

          • Adam says:

            Thanks guys, and no worries Jim. Any time someone says: “hey, wait, you’re overlooking XYZ, don’t be so quick to judge,” my ears prick up. Lord knows, the blogosphere is populated with more than enough folks who already know all the answers. 🙂

          • Jim Stone says:

            No, Adam. I’m truly sorry. The irony is dripping, no? As I’m exhorting people to read Stephan’s words more carefully, I’m in the process of not reading Adam’s words carefully. I will try to follow my own advice going forward — especially before commenting.

          • Al says:


            The problem with the FR theory is that it is a subset and contained within, the CIH theory, in the sense that there is a an additional, yet minor insult to brain physiology.

            Stephan is about to state that hyper-palatable foods cause overeating cause obesity cause IR, etc. This is minor in the grand scheme of things, interesting, but minor with respect to the person bogged down by an extra hundred pounds of adipose tissue.

            The fix has been seen at the practical level – remove the processed foods, and most carbohydrates. Hyper-palatable foods are contained within this prescription; so why the additional prescription of cutting back on flavor? Fodder for a scholarly article?

            I work with overweight people (and was obese myself, at one point), and can tell you beyond a doubt that 99.999% of the time, if they stall or fail, unfortunately, they are simply doing something wrong; and/or are eating some foodstuff that insults their particular physiology in a way that causes fat retention.

            I can’t tell you how many times I’ve heard how oatmeal, orange juice, or whole wheat bread doesn’t count toward their carb count because they’re healthy, right? This is after many seminar type workshops that I give, as well as some individual counseling, teaching of the opposite. It simply takes time for the education to get in the mind, and stick.

            Understand that I do not discount FR – it is certainly a actual phenomenon – but it is minor, if at all significant.

            I wonder how many obese people Stephan has/does work with.


        • Adam says:

          Ha! Would that all internet discussions be as civil as ours.

          Okay, my daughter’s begging me for blueberries and apricots. Girl needs herself some fructose, apparently. Wherefore, I do not know. :]

    • Mike Ellwood says:


      Yes,why do we have to give FRH serious consideration? I’m not doing so for several reasons, one of them being that, unlike the Carbohydrate-Insulin hypothesis, the FRH cannot apparently be summed up in a few short sentence that everyone can _clearly_ understand (or if it can, I haven’t seen it. Maybe you’d like to attempt this?).

      OK, well, maybe neither can Relativity (although actually, I think the Special Theory _can_ be summed up in a few short sentence/equations).

      If you can’t define what you mean by “food reward” in one sentence, then I think you have failed, and I have yet to see a definition of this that dozens of people will not pick holes in and argue about. As soon as one tries to grab hold of this concept, it vanishes, like an autumn mist.

      • Jim Stone says:

        Mike, I’m not asking you to find it plausible. But if we’re going to have a reasonable discussion in the comments section of a blog post that’s dedicated to adjudicating between two hypotheses, it seems we should want to have an accurate view of what the two hypotheses are — or what the two theorists are saying.

        I don’t see how one can evaluate GT’s thoughts about SG’s views unless one goes and read Guyenet’s views first hand. There are only 7 or so posts, and they’re shorter on average than Gary’s posts. It would take about 1% of the time one would spend reading GCBC. And it would prevent a lot of obvious mischaracterizations that detract from the discussion.

        • Galina L says:

          I give FR some consideration by not eating foods that I can’t stop eating. It has some importance, but a minor one, in my opinion. The bulk of benefits in my diet comes from the low carb content. In my case, the FR is the way to tune-up my low-carbing , because the carb content for me determines the force of physiological hunger which it difficult to ignore, while addictive qualities of foods are easy to overcome by just staying away from that box of chips or not buying that ice-cream, or abstaining from some culinary tricks, that can make my food irresistible. Good quality meat is great by itself, and veggies with butter taste really good, but it is not possible to stuff myself beyond satiety om such menu.
          I think it is a good idea to avoid making food too stimulating, because it could promote eating for wrong reasons.

  14. kilton says:

    Thanks so much for these posts, Gary. Really insightful stuff.

  15. Donald Kjellberg says:

    This argument is developing well. I always enjoy your writing Gary. That is probably why it only took me 3 weeks to go through GCBC (I need to reread it again BTW). Since I gave my book to a doctor, I need to get another copy.

    Anyhoo, I have been eating a non-processed diet for 1.5 years now with 135lb weight loss. My BMI dropped from 40.3 to 22.3 with no real plateauing until it reached normal range values. My body is now maintained on a very palatable diet that is basically paleoish/WAPF like. I could add much more but what I wanted to discuss was this:

    Occasionally, I get sleep deprived due to the higher levels of activities I now engage. When these activities do overwhelm me and I make it through multiple days fighting fatigue, I inevitably crash, crave some, high carbohydrate junk food (usually highly processed), eat, and catch up on sleep. This fatigue-influenced craving is completely inconsistent with my day-to-day lifestyle and am at a loss to understand why this happens. I am probably not the only one who experiences this either.

    • Jim says:

      Cortisol? I’m in the same boat. If I get behind on sleep, cravings are a bigger problem.

    • Mike Ellwood says:

      Astonishingly good weight/BMI improvement. Congratulations (and I’m envious).

      Yes, sleep is so important. Try to make your surroundings totally dark, and maybe consider use of a mask.
      (When I mentioned this to my wife, I got some funny looks, so I haven’t dared so far 🙂 ).

      (You might consider Magnesium supplementation, unless you can find good food sources, which is not so easy, or maybe “transdermally” (e.g. Epsom Salt baths or with Mg Bicarbonate crystals dissolved in a hot bath).

      • In addition to what Ellwood said, it’s important to go dim 1 – 2 hrs before bed (like the sun going down); sends a signal to the brain to prepare for sleep.

      • dlm says:

        Some people recommend a piece of tape covering any LED lights in the room.
        Also melatonin 3 mg helps sleep tremendously.
        As does natural progesterone but probably only good for women.
        And blackout drapes make a big difference.

        • Donald Kjellberg says:

          Well, my bedroom blinds leak light like sieves and its noisy at my place routinely disrupting sleep. In addition I spend too much time bedtime reading on my computer. Maybe I need to find a cabin in the country away from roads, bright lights, and electricity, LoL.

    • Galina L says:

      Wow! Somebody lost weight by just eating non-processed food! It can be that easy for some lucky ones. I have been eating non-processed food all my life! Now it has to be VLC kind. Remember, folks, we are different. That is why there are a lot of advise on internet given by naturally thin people to poor fatties to eat more blueberries, sweet potatoes and stay away from fast food.

  16. Meri says:

    Excellent post, super interesting! Thanks for upping the game, once again.

  17. John says:


    Please understand that I am a “Taubesian”. I have both GCBC and WWGF, and they were the #1 inspiration that helped me lose 45 lbs so far, hopefully with more to follow.

    I understand that your posts now are to compare CIH with FRH. You seem to want to discredit FRH. That’s fine.

    It has been suggested by others that CIH and FRH are complementary, not opposing. That there is valuable information in both that can help us to achieve our weight goals. I agree. You seem to disagree.

    So I am willing to abandon FRH completely if in your upcoming writings you can use CIH only, without borrowing even slightly from FRH, to completely explain why my attention is drawn, my eyes widen slightly, my mouth starts watering, my hands shake, and I consider jumping in my car and driving to the bakery when I simply read the words “ice cream” or “apple fritter” or “fresh baked bread” in a book, newspaper, or magazine.

    Reading–an interaction between my eyeballs, optic nerve, and brain–sets me off and makes me want to eat. Is this part of the CIH peripheral response you write about?


    • Adam says:

      Hi John,

      As a fellow Taubesian and fan of the CRH, I hear your confusion about the “fresh baked bread” siren song. What’s driving it? Could it really just be “the body”?

      Not to be a shill, but I actually speculated on this at length in my eBook,

      Here’s a snippet that I think might address this mission-critical point that you and others have been making about FRH’s appeal:

      “Many of the factors [impacting the fat tissue] operate below the conscious level. So the idea that you could control them all (including, e.g., how much you shiver or your resting body temperature) is abjectly absurd.

      Likewise absurd is the idea that you could somehow change the fat tissue (and only the fat tissue) without somehow also changing the body’s other tissues in the process, especially when you’re doing something as gross* as manipulating the amount of food eaten. (* I mean “gross” as in “untargeted” not “gross” as in “eww, gross”)

      The analogy to body temperature is useful. Yes: you CAN make yourself chilly by sleeping in a cold dank cave; and you CAN heat yourself by roasting in the Arizona summer sun. But once you leave the cave or chez lounge, your body will manage — without your conscious help, thank you very much! — to return to 98.6 degrees, due again to the magic of homeostasis. Likewise, you can “overeat” or “semi-starve” for long periods of time — possibly even gaining or losing lots of body fat in the process — but these gains or losses will almost certainly be erased after the gorging or dieting is done. Again, because of homeostasis.

      Like I said earlier: you’re trying to fix an organ. You’re not trying to burn off excess fuel goo trapped inside your body.

      We all focus too much on short term gains and losses. Some fluctuation in the amount of fat you store is perfectly normal, just as fluctuation in your body temperature is perfectly normal. What’s confusing, and I’m speculating here, is that two distinct fluctuations are probably going on. These overlap with each other, and we can’t easily tell them apart!

      1. Normal, healthy fluctuations in the amount of fat we store in our fat tissue. These are
      similar to normal, healthy changes to our body temperature.

      2. Fluctuations that indicate an illness or malfunction of some sort. These are
      comparable to changes to our body temperature that happen when we get sick.

      The SICK FLUCTUATIONS can be related to the NORMAL FLUCTUATIONS. But not
      necessarily! Just like you can get sick without getting a fever; so, too, can you probably damage your fat tissue without gaining excess fat, at least immediately. On top of all that… teasing these signals apart is super hard, if you just look at weight or fat mass alone. Think about it. A 101 degree body degree temperature might indicate fever (due to illness) or normal heating (due to an intense tanning session). You can’t know which, unless you get more info than just temperature.

      So when DO fluctuations in body fatness indicate fat tissue sickness?

      Figuring this out is trickier than you might think. Because obesity doesn’t develop overnight or over a week or two. You don’t pig out at a luau and “become obese” the next day. Obesity is a chronic disease, meaning that it develops over big stretches of time. As Gary Taubes points out in his book, Why We Get Fat: And What to Do About It, when you crunch the numbers, it turns out that, to gain 40 pounds of excess fat over two decades, you need only “overeat” by an average of 20 calories a day. That’s like three Wheat Thins. It’s nothing.

      Compare that “20 calories a day” benchmark with [a theoretical dieter named] Mary’s wild swings in food intake. Hot dog eating contest here. Break-up-induced fast there. Haagan Dazs and burrito binge here. Fresh salad there. The swings in her food quantity, day to day, totally swamp out that “20 calories a day” figure. Even if she wanted to, there is no conceivable way Mary could consciously identity
      which “excess 20 calories” on a given day will ultimately be the ones that result in her having flabby arms and thunder thighs once she hits middle age.

      The lesson is: we probably need to freak out less about short term swings in our weight/fat. Instead, we almost certainly need to pay more attention to the subtle stuff that is effectively “breaking” our fat tissue — making this organ SICK.

      • John says:


        I think you and I are both onboard with these concepts. And no matter where you look, either to CIH or FRH, avoiding carbs is the answer. Although Gary has previously written about the addictive nature of sugar/carbs, I don’t see it specifically indicated in CIH in and of itself. Maybe if we abandon the restricting term “Carb Insulin Hypothesis”, and just say “What Gary Said”, it would all be OK. Because WGS seems to include much more than just CIH.

    • Warren Dew says:

      John, I think your experience is a perfect example of what Gary is talking about in the penultimate paragraph of the post you are responding to: it’s a learned Pavlovian response, not an intrinsic food reward effect.

      • John says:


        I agree, it is a Pavlovian response. But does Gary’s “carb insulin hypothesis” explain Pavlovian responses? Carbs drive insulin which drives fat which drives Pavlovian response? Not sure that has been explained.

        I do think any reasonable “food reward hypothesis” should explain a Pavlovian response. Many versions of the FRH do (and I’ve seen several), but I can’t say whether Dr. Guyenet’s does or not. I just don’t know.

        • Warren Dew says:

          A dietary theory doesn’t have to explain Pavlovian responses, any more than it has to explain planetary motion. Behavioral theory already explains how classical conditioning works – that is, how Pavlovian responses develop and operate.

          The thing is, different people have different Pavlovian responses due to different experiences. For example, after three years on a paleo diet, the smell of fresh baked bread makes me mildly nauseated, rather than being appetizing to me. The kind of positive reaction you describe I have to foods that help me lose weight, like a rare slice of fatty prime rib. That means classical conditioning doesn’t have anything to offer in terms of general weight loss advice. “Eat the foods you really like” would be great weight loss advice for me, but might be terrible weight loss advice for you.

          In contrast, “don’t eat carbs” is good weight loss advice for everyone.

          • John says:

            Warren said: “A dietary theory doesn’t have to explain Pavlovian responses, any more than it has to explain planetary motion.”

            Warren, any comprehensive dietary theory should explain “Why We Get Fat”. Ignoring Pavlovian and addictive responses to food is ignoring a very important piece of “Why We Get Fat”. I do agree that planetary motion ain’t part of it. I also think you and I agree on what does make us fat.

        • FrankG says:

          John says: “But does Gary’s “carb insulin hypothesis” explain Pavlovian responses? Carbs drive insulin which drives fat which drives Pavlovian response? Not sure that has been explained.”

          From the perspective of a diabetic who injects insulin I can tell you that high levels of insulin lead to a desire for certain types of food — quickly absorbed sugars to be precise. Isn’t that what the body expects to be the case when insulin levels are high: that there is plenty of Glucose around?

          I look at this in the same way as Gary’s discussion above about how other metabolic abnormalities lead to a carving ( and requirement even) for slat or calcium.

          • John says:


            I’ll buy that, it makes sense. I now think part of my problem is the misunderstanding of the FRH. If I’m reading here correctly, Dr. Guyenet’s FRH discounts the overeating effect of high reward / highly palatable food. The HR /HP factor alone causes you to get fat, even if you don’t eat more of it, and even if it’s not the carbs. I don’t accept that, unless the food contains plenty of carbs. The older, much more popular FRH says simply that high reward / highly palatable will make you fat because it will cause you to overeat. Period. I do believe that, but carbs are still involved. There are no high reward / highly palatable foods that don’t contain carbs, usually plenty of them.

          • Warren Dew says:

            John, I understand how “high reward” can be defined however one wants, but how can one define “highly palatable” to exclude low carb foods like steak, bacon, or whatever meat foods one prefers?

            That’s a genuine question. It seems like some people have a definition of “palatable” that I don’t understand, and I’d like to understand it better.

          • Robbo says:

            About conditioning:
            In my view conditioning, or put another way the need to break old bad high-carb habits and build new low-carb habits, is one of the obstacles any person who seeks to lose weight has to face. In my experience it took a couple of weeks before I did not have to use conscious willpower to refuse the slice of cake, or avoid the sandwiches. Later on, I developed the opposite conditioning, so that what they served in the works canteen did not even look like food to me.

            However, this is not the same as food-reward, because it is individual – start the day with toast and marmalade every day for fifteen years and you will at first have to consciously decide to have bacon and eggs instead. Someone else will be conditioned to cornflakes for breakfast. Another to pancakes and maple syrup, etc.

            Jim says November 21, 2011 at 2:59 pm:
            “3. A food reward paradigm suggests that effective “normal reward” diets DO NOT HAVE TO BE low carb. If you eat undoctored natural high carb foods they might be just fine for you.”

            This is the crucial trial, low carb diet versus high-carb, normal reward diet.

        • Stipetic says:

          Hi John, couldn’t the thought of some Chunky Monkey cause a rapid pre-prandial insulin surge (hey, you’ve had the stuff before; your brain remembers how gooooooood it was. Hey, Pavlov’s dogs got conditioned to dog food, for crying out loud; so getting conditioned to ice freakin cream can’t be all that difficult)? Seconds later you get that immediate dip in glucose and you get hungry. Happens you’re still thinking about the ice cream or the ice cream is that last thought you had. And, hey, you even have the route planned out to the nearest Ben and Gerry depot–it’s at the store around the corner. You can squeeze on your Vibrams in time for a sprint to satisfy that surge in insulin. But what if the store was across town…would you feel the urge to drive then or just satisfy your low glucose with a home bolus of what’s available? Maybe insulin is involved, just maybe. Thinking out loud, here.

  18. Ken says:

    I was wondering when someone was going to mention the obvious “artificial sweetener versus sugar” test for the palatability/brain theory.

    While it is anecdotal and not scientific, nevertheless it is interesting to note that when Supersize Me came out (film where someone ate a month only at McD and gained weight), someone made a point of doing the exact same McD meals that were eaten in Supersize Me, except that he substituted DIET drinks for sugar drinks – and his result was that he LOST WEIGHT after eating the same McD food for 30 days.

    • Jim says:

      It is consistent with FRH that the diet soda would stimulate appetite, but that the person used will power to stick to a set meal plan and thus reduce calories. To be relevant it seems both versions of the diet would have to be done in ad libitum situations.

      • FrankG says:

        Jim… when you say “the person used will power to stick to a set meal plan and thus reduce calories” is this part of the FRH reasoning or is it unrelated to FRH?

        • FrankG says:

          …as I recall in SuperSize me there were a set of rules to be followed about what to eat… so it was hardly “ad libitum” and reportedly he was getting through about 5,000 calories per day… so while the “diet drinks” version may have been fewer calories than the original, I doubt it would be seen as “calorie reduced” by comparison with a normal diet.

          • Jim Stone says:

            OK. So there is reason to expect Ken’s “anecdotal” diet drink version was calorie reduced compared to Morgan Spurlock’s version. But there’s still the question of whether the diet coke version was calorie reduced compared to some baseline or “normal” diet.

            Fair point.

            I guess I’d have to see more about the second study to know what to think about that. If they didn’t measure baseline numbers, then we’ll be in the dark, though, right. It was just one guy after all, and we’d have to know HIS baseline.

            Maybe Ken has a reference we could follow up on??

            I’ve also seen studies showing artificial sweeteners cause weight gain — and there’s much anecdotal evidence among low carbers that this holds as well.

          • Elenor says:

            Geez guys– just go WATCH Tom Naughton’s movie “Fat Head” on Hulu for free, or order it for less than $20 and get the info straight, eh?! Morgan Spurlock has refused to give out his food logs to prove he actually followed his own rules (which he couldn’t possibly have, if he (allegedly, unprovably) reached anywhere near 5,000 calories a day!) . Spurlock, his idiot doctor, and his vegan-chef girlfriend blamed his weight gain on the “fat” he ate — while ignoring the pound of SUGAR Spurlock ate (and mostly drank ) *every day* of the 30 days, and the carbs from buns and hash brown and the like.

          • FrankG says:

            Thanks Elenor _ I’ve watched “Fat Head” several times and am a big fan of Tom Naughton.. he also has an informative yet entertaining blog : 😉

          • Jim says:

            Ditto. I’ve seen it a couple times as well. Naughton does not address food reward or any experiment done with a diet-soda version of Spurlock’s experiment.

            This whole part of the discussion is probably beside the main point, though. There were problems with Spurlock’s experiment, and there would be problems with the experiment Ken points out as well. I doubt either experiment has much to teach us about CIH vs FWH.

        • Jim Stone says:

          Frank Wrote: “Jim… when you say “the person used will power to stick to a set meal plan and thus reduce calories” is this part of the FRH reasoning or is it unrelated to FRH?”

          I didn’t say the person did have to use will power. I don’t know. I was saying that IF they did, that would allow weight loss on the plan to remain consistent with FRH in spite of the fact that we would normally expect increased food reward to lead to weight gain. If calories were restricted, then the food reward led to an increase in unsatisfied hunger instead of to an increase in fat tissue.

          • FrankG says:

            Sorry Jim but I don’t see the word “if” anywhere in your comment that I referenced?

            My concern is that whenever you attempt to phrase things in FRH — which you have frequently reminded us is NOT just about how food tastes, and is most assuredly NOT about “Calories in vs. Calories out”… that is in fact a physiological effect not a psychological one — having reminded us of this and even reprimanded us for not reading Stephan’s blog nor fully understanding his position… despite ALL that you still end up using words like “willpower”, inferences to consciously reducing calories in (or out) and food palatability.

            In order to convince me of something, the position taken needs to stand up to scrutiny… and so far I agree with others above that FRH does not even seem to have a clear definition that can be tested. Even those above who see an overlap between “FRH” and CIH” I suspect are basing that on the idea that FRH has to do with how food tastes… which you tell us in not what it means. And yes I have visited Stephan’s blog — you may see some of my comments and questions over there as well — I do not find his position convincing or balanced and in my view it does not stand up to scrutiny.

          • FrankG says:

            I screwed up on the html tags above… I did not mean for most of the comment above to be in bold — mea culpa.

            Any chance of a preview window or even a limited time to re-edit comments Gary? Please 😉

          • Jim says:

            Frank. I used the word ‘willpower’. But I did not say that losing weight on a low reward diet requires willpower. I was saying that if you were to lose weight on a high reward diet it would probably require will power.

            And I didn’t use the word ‘if’, but it was implicit in the statement I did make. My original words were: “It is consistent with FRH that the diet soda would stimulate appetite, but that the person used will power to stick to a set meal plan and thus reduce calories.”

            I take that to be equivalent to “If the person used will power to stick to the plan, then they could lose weight with a high reward diet, even if FRH is true.”

            Also, palatability IS one reward factor. I don’t think anyone has said it’s about taste at all. In fact, palatability is probably a big factor. It’s just not the only one.

            And, Frank, I wasn’t exhorting you, personally, to read Stephan’s blog. I have seen you over there. In fact, when I wrote the exhortation to Adam I had you in mind as one who was making some effort to understand the FRH as Stephan has laid it out.

            (Also, as I’ve already admitted, my exhortation to Adam was partly misguided as I had taken some of what he said out of context. I’d been growing more and more frustrated by having to repeat things and having things mischaracterized, and I’d grown impatient and took it out on Adam. I have now taken a chill pill, and I’m good now)

          • Jim says:

            That should be: “I don’t think anyone has said it’s NOT about taste at all.”

  19. Peggy Holloway says:

    I have little doubt that even a sweet taste causes my pancreas to release insulin. I have very strong symptoms in response to surges in insulin levels, and I experienced the “too many carbs” symptoms the first time I tried a commercial stevia-sweetened soft drink. Gary’s explanation of why consuming artificially sweetened soft drinks may cause weight gain is the only thing that makes sense to me.

    • FrankG says:

      This makes sense to me also Peggy, and as I recall there has been a study showing that drinking diet soda can lead to increased consumption of energy at the next meal — perhaps as you suggest, the extra insulin secretion leads to a net loss of energy into the fat cells that has to be made up for sooner or later.

      Jim Stanton over at GNOLLS.ORG has series of blog posts where he discusses terminology such as satiety and satiation. As I recall his discussion: satiation is the body’s initial response to food, the expectation of how nutritious it was — if you like — before we have digested it. Whereas satiety is achieved only after the food has been absorbed, maybe hours later. Presumably in our evolutionary past, these two would always have been in sync but modern “franken-foods” have confused these systems.

      Why Are We Hungry? Part I: What Is Hunger? Liking Vs. Wanting, Satiation Vs. Satiety

      I’ll see if I can find a reference for the diet soda study.

      • FrankG says:

        I still can’t find the published diet-soda study (it was presented earlier this year at an ADA conference and made the news. Perhaps has not yet been formally published? But here is a press release from The University of Texas Health Science Center at San Antonio…

        “Epidemiologists from the School of Medicine at The University of Texas Health Science Center San Antonio reported data showing that diet soft drink consumption is associated with increased waist circumference in humans, and a second study that found aspartame raised fasting glucose (blood sugar) in diabetes-prone mice.”

  20. Rocketman says:

    Earlier Gary T wrote:
    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.

    Notice how much similarity there is to the following from “Evolution For Everyone” by David Sloan Wilson
    page 57 in dealing with examples of early life experiences “Switching basic behavior” of animals, including body sizr.

    “…Of course, they are not thinking at all, because they are still embryos, but some physical system is functioning as a calculator to mipliment metabolic plan A or metabolic plan B depending upoon the environmental signal (body size). Once the decision is made, there’s no going back any more than a dung beetle can reconsider his horn. [Dung beetles deprived of nourishment early in life will develop limited energy demanding body characteristics, such as not having a fighting horn].

    This kind of adaptive flexibility evolved because fetal body size was a reliable indicator of the adult food environments for many thousands of generations, even before our appearance as a species, since other mammals such as rats have the same adaption. WE CAN PLAY A CRUEL TICK ON A RAT BY FEEDING ITS MOTHER A RESTRICTED DIET DURING PREGNANCY AND THEN SWITCHING THE ENVIRONMENT BY GIVING THE OFFSPRING AS MUCH FOOD AS IT WANTS. THE RAT BECOMES OBESE BECAUSE ITS METABOLISM IS DESIGNED TO SQUEEZE EVERY CALORIE AND NOT THERE ARE SO MANY TO SQUEEZE. In just the same way, if you are obese, it is likely that you were underweight as a newborn. You are “Dancing with ghosts” in a surreal dream.”

    I was reminded very much of the phenomena of impoverished settlements having obese mothers and really skinny children and the skinny children growing up to be obese. As in WWGF.

    There are multiple reasons for getting fat other than overeating fatally attractive foods.


    This is part of the other problem I have had with the food reward model – in that what is rewarding changes over time depending upon what response the eater associates to the food. After a long enough period of carb restriction, fat/sweet/salt has a much lower appeal to me now. I’ve gone from near uncontrollable sweet tooth to nearly not enjoyed sweets at all. IOW – in my experience, food reward is not as compelling a model as sugar “addiction” with physiology as conceptualized in the post above.

    This was a great post, Gary, thanks. Paul

  22. One’s perspective governs one’s argument and mine is no different. After going through a heart event myself and having 2 stents fitted I eventually became very focused on finding a solution especially after having to dismiss my doctor’s advice on the grounds that the pills weren’t working and I felt shocking. The conclusion I came to was that I lost control of my normal bodily needs due to what seemed inescapable stress from family problems. I was consumed by this stress. It had been going on for more than 10 years and the way I saw it it had taken it’s toll. Quick fixes for food had become the order of the day – and yes I suppose that meant carbs! Preferences and palatability didn’t come into it. Food became a simple quick fix. Now thanks to my personal research, and I must say the most helpful was Diet Delusion AKA Good Calories Bad Calories. My only point here (and I wish to return to this) is that the basic premise of cutting down carbs has been central & crucial to my recovery with improvements wholesale within weeks if not days of a number of health issues. I found the results nothing short of astonishing. I continue to study but it is easy to get diverted my many, even by your friend Gary, Mr Lustig. The enemy seems as much to avoid one’s ego and sensationalism as much as carbs. I digress. I am indebted. Thankyou

  23. Martin says:

    The distinction between physiological and psychological is an artificial and problematic one. There is obviously an interdependence between brain and body.

    What the “brain rules” hypothesis essentially says is that someone is hungry without there being a physiological need for food.

    Let’s compare this with some highly addictive drug. Someone is curious and he trys the drug. He feels fantastic but is not yet physically addicted to the drug. (1) He comes back for more. Now he is physically addicted. (2) He comes back for more …

    Now let’s see: The drug causes (1) AND (2) but through different pathways.

    Maybe there is psychological food reward – but only until a point is reached, where there is actually a physiological need.

    It is conceivable that the “brain rules” hypothesis is basically right, before the physiological condition sets in.

    • Martin says:

      *tries the drug

    • Jim says:

      Yes. I like this distinction. However, if the person doesn’t know that their psychologically driven response will lead to the physiological addiction, it’s still tough to blame them. It’s only if they know about the slippery slope that we can blame them for taking the first (or second) step.

  24. Ryality34 says:

    Thanks Gary for the free and well thought out writing as always. Its clear to me you are playing a very important role in this discussion and one frankly that I’m deeply grateful for.

  25. I don’t see how your carbohydrate-insulin hypothesis explains this obesity dichotomy. Perhaps one day you can explain how carbohydrates make Jamaican children undernourished and the adults obese. Obesity researchers have answers to this mystery. You might just have to look at something newer than the 1960’s.

  26. brd says:

    So I’m curious about the times GT mentions children. There’s the paradox of the under-nourished child with the overweight mother, and then there’s the growing child that’s eating a ton because they’re growing (not growing because they’re eating). At what point do these lines cross? Somewhere, the under-nourished child’s body is sending growth hormone signals that make it grow and then would uptake more food, were it available. At what point is that over-ridden? Or is the malnutrition he speaks of a matter of nutrients and not a lack of calories?

    I ask this as a father of a child who is 0% on the weight/age charts. She is not malnourished from a vitamins/minerals standpoint, but possibly from a caloric restriction (due to medical issues) standpoint. So reading about these things in his books and articles makes me wonder, why doesn’t her body just signal her to grow, like a caged hibernating animal that will still put on weight even if starved?

  27. Dan says:

    Didn’t taste evolve as a marking system to find nutritious food? So over time in mammals the tastes for Umami, Fat, Sweet? Modern production of food has hijacked these developed tendencies. When you are a lean hunter-gatherer and come upon an apple that is one thing but being a overweight, stressed out city dweller drinking 12 oz pasteurized Apple juice is another.

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