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


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

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

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

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

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

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

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

Competing paradigms: 1. body rules

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

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

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

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

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

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

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

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

Competing paradigms: 2. brain rules

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

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

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

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

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

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

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

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

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

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

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

The food reward/palatability hypothesis: looking for a mechanism

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

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

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

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

A lengthy but not necessarily irrelevant digression

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

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

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

Back on track:  the mechanism of food reward/palatability

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

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

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

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

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

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

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




Speak Your Mind



  1. scott says:

    I don’t think “major contributor” (as indicated by Dr. Guyenet) = primary cause (as summarized by you). This seems to be a recurring disconnect.

    • GT says:

      Maybe so, although I would argue that “major contributor” is a way to avoid the issue of whether it is a major cause or a primary cause. Still, I’ve made a minor fix to address this.

  2. Swintah says:

    Glad you’re back!

  3. Jim says:

    Gary, I’m a big fan of yours, primarily because you have exemplified humility and the ability to entertain new hypotheses, and new evidence, even when it doesn’t fit your own reigning paradigm.

    I also greatly respect Stephan Guyenet — for much the same reason.

    I want to try to get you to understand his position better, if I can (and, if I’m right that you’re misunderstanding it.)

    Let’s distinguish two different “calories in-calories out” claims.

    A) If one loses non-water mass, one much eat fewer calories than one consumes,
    B) The best way to lose weight is to manage your calorie balance equation — focus on eating fewer calories, and burning more calories.

    Guyenet, if I understand him correctly subscribes to A, and does not at all subscribe to B. In fact, he is squarely in your camp on this issue. He does not blame the victim, just as you do not. And I wish the two of you could see each other as allies on that very important issue.

    Your debate is over a couple of other issues — 1) the mechanism for obesity (yours involves primarily carbs and insulin, his primarily food reward and leptin), and 2) what is the best way to fight obesity (your approach involves cutting carbs, and his involves reducing food reward. And on the second issue there is actually much overlap, because carbs (especially certain kinds) can play a large role in food reward.

    On a personal note. I was a long time low carb dieter. Saw much health improvement, and some weight loss. My weight loss stalled, though, and I consoled myself with the fact that I was at least not gaining weight. After trying Dr. Guyenet’s advice, and adding in some potatoes, sweet potatos and squash, and reducing the food reward of my other low carb foods, I’ve been losing weight without effort again — 22 pounds in 5 months so far, easily and without counting calories on the way in or out.

    I’d like to be able to thank both of you, and would like to find a way to get you two to see each other as being largely on the same team against the “eat less, move more” crowd– with some questions about mechanism making things interesting.

    • GT says:

      Interesting. How did you reduce the “food reward” of your other low carb foods? And why do sweet potatoes, for instance, have a low food reward value? It is certainly possible that you have lowered your food reward value and that lowered your set point and now you’re eating less. Anything is possible. It’s hard to tell, though, from a single account.
      These are serious questions, and are the kinds of questions I’ll be addressing in the next four posts.
      One reason I hesitated to write this post, as you note, is that I didn’t want to further incite the Taubes vs Guyenet nonsense that was so virulent when I wrote my last blog. But I can’t figure out how to discuss the problems with the food reward hypothesis and then address his problems with insulin/carbs without seeming to have problems with Dr. Guyenet himself.

      • Jim says:

        Gary, thank you for responding (you really are one of my modern day heroes). Here is what I typically eat now:

        Braised beef — without salt or other spices. (I’ll substitute other gently cooked unseasoned meats)
        Vegetables — without butter salt and pepper
        Plain baked potatoes — many of which I eat cold after baking and putting in the fridge.
        Plain sweet potatoes.
        Plain spaghetti squash.
        Sauerkraut (probably my only source of added salt).
        Eggs — plain, no seasoning — cooked a variety of ways.
        Occasional pieces of fruit.

        Truth be told, I’m probably only eating 100-150 grams of carbs per day even now, so I’m still lowish carb. But I’m eating more carbs than before, and the changes I made were the addition of starch and reduction of reward.

        I’m not holding to this perfectly either. I still have coffee with cream, and wine, and an occasional higher reward food (cheese on my eggs), but the trend is definitely in this direction, and those foods comprise maybe 80 percent of my calories on average.

        About sweet potatoes. I agree with you. I find them very tasty. However, I can definitely think of ways to make them more tasty — butter, salt and pepper. I leave these out.

        I think that’s the intuitive idea here. If you start with a simple whole food, and are tempted to make it more comforting, you’re probably increasing the reward value.

        Anyway, you’re right, of course. One example does not constitute proof. And your evidence from my case is second-hand to boot! But I’m pretty happy with my first-hand experience experimenting with these ideas.

        • gallier2 says:

          That is a good illustration of what irks me a lot on this whole debate, especially on the “Guyenet’s cheerleaders” side. They attack a strawman with their caracterisation of low-carb. You eat now 100 to 150 g carbs a day, my god what a concept, that is exactly a low-carb diet, that’s ultimatively Atkins maintenance level. None of the low-carb “gurus” (Atkins, Lutz, Eades) recommend ketogenic diets long term.

          • Jim Stone says:

            Gallier2, I’m not attacking low carb. I just admitted I eat low-ish carb. I was eating even lower carb — probably 50g/day. Adding some potatoes, sweets and squash, and lowering reward value got my weight loss going again.

          • Mike Ellwood says:

            @Gallier2: Don’t they? [recommend ketogenic diets long-term?] – If you look at the early 20th century low-carb pioneers, as described by Gary in GC, BC, it was basically just meat and fat, OR meat, fat and a small amount of green vegetables. Remember the guy who could put on weight with just one apple? (That would be me too, by the way). And with Atkins, as I understand it, the original guidance after induction was to gradually re-instroduce carbs until you either stopped losing weight or started gaining weight, and then back off some, to establish your maintenance level (whatever that happened to be, higher for some, lower for others). Whether this would be “ketogenic”, or not is a moot point. I can’t see any problem with living permanently on a ketogenic, since ketones are an excellent source of energy and food for the brain.

            In my case, when I went low-carb, I happily gave up potatoes (which I hate), bread, rice, and pasta, and could happily live my life without any of them (provided I can still have my meat, fat, organ meat, eggs, pasture-fed butter and raw cheese)

            Potatoes are certainly a low-reward food for me, so much so that I prefer to do without them.
            Now, if the theory of low-reward holds true, then I suppose by eating potatoes I would somehow be eating fewer calories, and therefore would lose more weight. But I’m already not eating any calories from potatoes (or sweet potatoes, or yams or squashes or bread, or pasta,, or rice), so how would adding potatoes actually help?

            Now I will admit that although I can survive happily on one or two low-carb meals a day, and am almost never hungry, I am still technically overweight. I am trying a number of ideas to see if I can lose more weight to get nearer my “ideal”, but as of now, adding starch in any form is certainly not one of them. Unless anyone here can convince me of the folly of my ways.
            (I was much nearer my ideal at one time, and “went off the rails”, primarily by starting to eat fruit again – big mistake, in my case. I know not everyone is the same).

            @To those former low-carbers who have added in potatoes etc, how many meals do you now eat, and do you ever feel hungry?

        • Jim, there are other anecdotal accounts of people who have success in weight loss after trying low carb by increasing carb consumption. These may be people who can’t fat adapt, or do so with such slowness that they don’t experience low carb as fully as those who are more rapid or better fat adapters. Those who have lost their gall bladder, for example, have a hard time getting adequate calories via fat consumption because they cannot digest large quantities of fat (except for MCTs like coconut). Interesting story, congrats and thanks. John Berardi of Precision Nutrition associates those who do better, generally, on a higher carb diet, as those who more closely match the ectomorph body type. Is that perhaps your type (thinner, taller, smaller wrists/pelvis)? Thanks, Paul

          • Also the people who see immediate weight gain after adding an extra 100 grams of carbs to their diet. They seem to forget about that initial weight loss (water weight) they were bragging about when they started their diet.

          • Galina L. says:

            Just to add to your anecdotal evidence – I lost my gallbladder, in time I adopted to a high-fat diet, good portion (may be half) of fats are from coconuts, there is no signs I don’t digest the fats. I function my best on a VLC diet, 5’6”, with big bones, muscular.

        • @Jim, re: 100-150 g carbs

          Although most people need to restrict carbs, most people don’t need to be ketogenic. Also, many people have a threshold of minimum carbs per day to convert T4 (thyroid storage hormone) to T3 (active thyroid hormone); you appear to be one of those people. Not knowing why it worked, you are susceptible to the food reward explanation, even though it is wildly un-scientific gibberish (see J Stanton’s demolishment of it at, which he linked to in this thread).

          More on the thyroid conversion thing:

          • Jim Stone says:

            So your theory (or Jaminet’s theory) is that the starch might actually be what is causing my current weight loss. I’m open to that idea (I’ll have to read more about the T4->T3 thing to see what I think of that). I’m also open to the idea that keeping my diet low carb and making it low reward would have produced the same results. I don’t know whether the starch is playing a role either way. I think I added the starch out of curiosity. If I just did low reward and low carb, I think it would have been less clear that it was the low reward producing the results.

        • Al says:

          But Jim…

          Exactly how did you reduce the food reward aspect of your diet?


          • Jim says:

            Hi Al.

            After a while on low carb/paleo, I had gotten to be a pretty good low carb/paleo chef. Making eggs I would brown the onions in butter, maybe some garlic,, dice and cook the bacon, mix heavy cream with the eggs, salt, pepper, cayenne, cook gently with a 4 cheese mix on top, and maybe a dollop of sour cream.

            Now it’s just eggs, gently cooked.

            Other examples are similar. I used to create a more classic french pot roast. Now I just put an inch of water in the dutch oven, throw the chuck roast in, and simmer for 4 hours. Bon appetit!

            According to FRH the explanation for my weight fluctuations would be that I lost weight initially with low carb because the reward value of the new diet was reduced relative to my previous diet. But then I learned how to cook low carb/paleo so it was more rewarding. So my weight loss stalled, and even trended slightly up for a while. On removing the food reward (and even adding some “safe” starch in), my weight loss has resumed, and I’m at my lowest weight in 10 years now.

            But, of course the FRH might be wrong given my own stream of experience. I’m not wedded to it. And I have a way to go before I feel like I fully understand it. I think there’s pretty good evidence that Leptin resistance is of primary concern in obesity. I’m less sure that reward explains leptin resistance. And I’m also not sure that the carb-insulin mechanism Gary proposes doesn’t play a role — especially once leptin resistance is in play. I have some more studying to do before I get a real feel for the proposed mechanism. But I’ve seen enough to want to try to learn more about it, alongside reading attempts to make the carb-insulin theory of obesity account for the data as well.

            And also, by the way, I think both FRH and LC fit well with the intuitions driving Paleo diets.

          • Al says:


          • Al says:

            Ok… @ Jim,

            I think that looking through the goggles of food reward, that is exactly what one would say had happened in your case. I’ve read what your stated beliefs are, and appreciate you just trying to figure things out.

            I work with fat people, people that need to lose a bit, and performance athletes (I also have my own experience in being obese and an athlete at one or more times). I will say this: dropping carbs works across the board for many, many people. Some can ride it down to goal weight, others get down to a weight they’re happy with, and some (few) can’t make great progress at all. This comes down to a few ideas:

            1. I hate to say it, but yeah, you may not be doing it right. There are hidden carbs everywhere, and no carb doesn’t mean pig out on processed crap (where Atkins failed, IMO).

            2. Calories DO count… after a point – after you have healed your physiology and have lost some weight, you may encounter a stall. If your processed crap intake is minimal, you’re probably eating too much. How can this be? It’s not food reward – it’s psychological oral fixation. How many ex-fatties just need to be doing something with their mouth – talking, eating, smoking, drinking…. etc. Think about it.

            I agree that we are compelled to eat by certain manufactured foods – but these foods (candy, cakes, potato chips) are advised against by even the most inexperienced dietitians and health care professionals. But I think that all you did, was proactively reduce energy intake, even though you replaced some of that energy with lower net energy carbs. I’ve seen this many times. You have to think of the CICO argument in the light of dysfunctional system regulation AND functional system regulation. In the former, the goal is food choice to heal the systems; here, conservation of energy is applied to the fat tissue and not at the mouth, as GT argues. In the latter the goal is to reduce energy intake because, guess what, you’re still eating too much; here, the laws apply to the mouth, because your system is allowing you to get at your fat stores. Does this make any sense?

            Most low-carbers fall into a group that they see success without any voluntary action besides food choice. Some have to limit their intakes (but then they realize they were eating for other reasons anyway) to see continued success. You seem to be in this latter group. Some just plain fail and I’m curious as to why.

            Great dialogue, Jim, and thanks for sharing your adjustments.


        • Keith says:

          Way back in 1991 I lost a lot of weight eating potatoes.

          I had recently been prescribed an antidepressant (Prozac) and it altered my appetite so that I only wanted to eat potatoes, buttered toast or broad beans. And I lost all taste for junk food. So I lived on these high carb, low fat foods. I ate a lot of them – maybe up to 10 large potatoes a day.

          The weight came off very quickly, it seemed like only a few weeks before I was slim for the first time in many years. I had lots of energy as well – I was walking to and from work instead of taking the bus, just because I felt like I wanted to walk.

          I cannot explain this. After having read Atkins, Eades, and Gary Taubes I understand why carbs cause us to become fat, so my experience of over 20 years ago seems impossible. Yet it happened.

      • Galina L. says:

        I prefer to think that I lost my weight on a diet based on the Insulin theory, not the LC theory, because just lowering carbs strategy doesn’t take most people who have more than 20 lb to loose far enough. I lost initial 20 lb by LC (LC diet immediately greatly improved my health even before significant weight loss happened), then stalled for 2 years. I lost additional 10- 15 lb by adding intermittent fasting (no snacks, 2 meal a day, eating window 6 – 8 hours). I think IF helps lowering insulin level as well. Attempt to re-introduce some carbs resulted in a gradual weight regain, and I stooped it.

        Sustainable weight-loss is very difficult to achieve, LC works, unlike starving, on a long run, but there more things that could be done in order to maximize the weight-loss itself, besides counting carbs, and it could be different things for different individuals. So, it is necessary to keep searching, what else could be done.

        I personally found J. Stanton’s series on hunger and food reward more substantial than Dr. Guyenet ‘s series on a FR. However, I try to avoid foods that I can’t stop eating. There are carbohydrates, of course, unadorned potatoes included, especially fruits, ice-cream, but also some LC foods – nuts, olives, pickles, prosciutto, salami.. Also, I cook my food in a simple way most of the time, I find soft-boiled eggs with butter and lamb chops to be delicious but difficult to overeat.

    • STG says:

      I don’t have weight issues, but I have had blood sugar issues. My dietary solution has been the opposite of yours: I eliminated potatoes and sweet potatoes. My HbA1c (meaningful health marker for me) has improved significantly! “Safe starches” for you, not for me.

  4. Aaron B. says:

    I thought it was quite clear that the food reward hypothesis was a calories-in-calories-out hypothesis. I see it routinely expressed as: Highly palatable foods (whatever that means exactly) cause us (somehow) to eat more of them, raising incoming calories higher than we expend, and (somehow) that makes us fat. That’s so obviously a variation on calories-in-calories-out that I didn’t even realize there was a question about it. It simply puts the blame for the extra calories in a different place — instead of eating too many calories because we’re lazy gluttons, we do it because something about the food’s palatability makes us overeat it against our will.

    To me, it seems like an attempt to have your cake (so to speak) and eat it too. You can agree with the mainstream that calories are ultimately the answer — so you don’t get called a nutter — but you can also tell fat people that it’s not their fault, because something stronger than willpower is controlling their appetites. Everybody’s happy — except the fat people who start eating bland food every day to try to bore their brain into lowering their appetite to starve themselves thin, I guess.

    • Garrett says:

      I agree. I also thought it was a restatement of calories in, calories out. Also, if we translate the phrase “highly palatable foods” as “foods that taste really wonderful,” a case could be made that the French ought to be the fattest people in the world. Perhaps the existence of thin French people disproves the food reward hypothesis.

      • John says:

        Food reward is not the same as something that tastes good. Think of a rewarding food as some thing that acts on the brain in a manner similar to a drug that causes addiction. For example, you wouldn’t tell an alcoholic that the key is to choose moderation. There is some fundamental problem in between desire and behavior.

        • Richard Falcon says:

          Then surely these foods can be explicitly stated and classified in some way analagous to a GI/GL classification ie listed in a way that directly shows how big a response they cause to some area of the brain…..?

          To me, so far, none of this food reward, high palatability stuff is explained very well. I don’t know what these foods are. For me personally, they would be stuff like Doritos, or chocolate….. But they are high carb/sugar foods anyway. To me, Gary’s explanation and the way in which he explains it, is far more convincing then Stephan’s.

          • eLynne says:

            I agree with Aaron B. that the “food reward” theory is quite obviously within the calories-in/calories-out theory, with this vague “food reward value” concept offered as the cause of overeating. I say “vague” because the language used in the Food Reward Theory posts on Dr. Guyanet’s site are maddenly shifting and inexact. The first post in the series fingers “industrially processed foods” as the culprit. Later, the term “highly palatable” shows up with no direct linking back to the original hypothesis. Most recently, “simple food” suddenly makes an unannounced and undefined appearance!

            Lastly, I agree with Richard Falcon that the theory (and theorists) need to define A PROPERTY OF THE FOOD that’s driving the effect, not a property of the person (“I can’t stop eating it”). What, precisely and exactly, are the inherent qualities of the food that are driving people to keep eating them? This is conspicuously missing, and getting harder to identify as the adjectives are constantly switching in the posts themselves.

          • eLynne says:

            Yikes – typos and I spelled Dr. Guyenet’s name wrong! Sorry.

        • David Gilmore says:

          If that is so then “highly palatable” and “food reward” food are completely different things (for any reasonable meaning of “palatable”). To brush something of a broad stroke:

          Delicious, nutritious food = highly palatable = what the French eat

          High food reward food = processed, addictive slop [high sugar/fructose/soy/wheat] = what Americans eat

        • Margaretrc says:

          If that’s really the case, why recommend eating bland, tasteless food as the cure?

    • Mike Ellwood says:

      I agree. Unfortunately, whenever anyone makes this perfectly logical and self-evident point, Dr Guyenet and supporters counter with a variation on “Oh that’s not what I mean by Reward, [or Palatability, or whatever the word du jour is]…”. Having their cake and eat it is right. Calories In = Calories Out – yes and Garbage In = Garbage Out.

      • BlueEyesSF says:

        Mike, I agree with you 100%. Guyenet and his supporters refuse to define their own terms. Reward means palatability – no, it means addiction – no it means leptin – no it means. . . . what they need it to mean at the time to get out of the corner they’re stuck in at the moment. Sorry, don’t mean to be cruel, but if they have a serious argument, they need to put it up and stick to it.

        • eLynne says:

          I have a similar problem – the nature of the food that’s considered to have a high reward value is not clearly defined. To paraphrase your statement, “It’s industrially processed, no it’s highly palatable, no it’s the opposite of simple.”

          Without a specific description of the food, the whole thing gets hopelessly circular: “Food that makes you want to keep eating it tends to make you keep eating it.”

  5. mrfreddy says:

    I’m like commenter Jim, I’ve been low carbing for ten years (thanks in no small measure to your NY Times article, it truly changed my life!). I’ve maintained a 40 pound weight loss for all these years, but I’m also still a bit chubby, I probably have at least 15 more that I need to lose.
    I took the food reward idea out for a five day test ride. It freakin worked. I managed to lose five pounds. Which is kinda scary. Could that have been water weight, even tho I’ve been avoiding carbs all this time (ok, most of this time?)
    During those five days, my diet consisted of unseasoned beef brisket or skinless, boneless chicken thighs cooked sous-vide. And some sort of vegetable, either brocolli or spinach or peas. Also cooked without seasoning. I skipped breakfast like I normally do. I ate plenty.
    I had to cut the experiment short for various reasons but I am getting ready to give another go, for a few weeks this time.
    Interesting to note that as soon as I went back to my low carb diet, I put the lost weight back on in a hurry.
    It looks like this method may work, but you’d be stuck eating this way for the rest of your life. Not sure if that’s something I’d want to do.

    • GT says:

      Again, interesting. You told us what you did, though, now what you were doing? How did this change? Yes fIve pounds in five days suggests a lot of water weight. So what did you stop eating? Is the only difference the seasoning? The skin on the chicken? Unlike Jim, you didn’t add starchy vegetables back. More detail would help understand exactly what’s happening plus, as you say, a longer time period (not to mention a few hundred people doing this in a randomized controlled trial).

      • mrfreddy says:

        Hmm, only thing I can think of from my normal diet that I wasn’t eating during my little experiment is dairy (no cheese and left the cream out of my coffee) and nuts (I normally have a handful or so of raw cashews every day.) And yeah, the chicken skin. Hard to believe that would make a big difference but maybe. Everything else was about the same, including a few glasses of scotch on a couple of those nights. As per usual.
        And yeah, no starchy vegetables. Can’t see the point in doing that!
        I think I’ll record what I normally eat during a normal week, and what I eat while “food-rewarding” (This thing needs a better name!).

        • Ken says:

          That sounds like you made your diet more “Paleo”, so that could be the alternate explanation – which still has nothing to do with the brain.
          So, you eliminate dairy (and by the way, cashews are legumes, not nuts, so another non-Paleo food eliminated) and so you eliminate some sort of physiological reaction that contributes to obesity (just as insulin-resistance is a physiological reaction).

          • Mike Ellwood says:

            …..Alternatively, he, in-effect, cut his calories. As I understand it, people on “Low Reward” diets minimise their fat intake, since fat makes food more attractive (I have no argument with fat making food attractive). Since carbs were already low and starch wasn’t added, he must have cut his overall calories.

            A “starvation diet”? – Well, as Gary demonstrated in GC, BC, it’s perfectly possible to live on a “starvation diet”, provided that there are no carbs, or not too many carbs. Whether he felt hungry initially might depend on to what extent he was hyperinsulinemic.

            Whether this diet is sustainable in the long-term is an interesting question.
            I’ve personally found a low or very-low-carb diet to be quite sustainable over several years, and people I talk to on LC forums seem to as well. We might of course be a self-selecting population.

            Now the Carbohydrate-Insulin thesis can explain why neither he, nor we who are still low-carbing don’t feel hunger, but Dr Guyenet does not subscribe to this theory. I don’t see how or where he explains this lack of hunger on a reduced-calorie (low or lower carb) diet.

          • @Ken

            No, peanuts are legumes, not nuts. Cashews are nuts and are healthy (if dry-roasted).

        • moreporkplease says:

          I just struggle to understand this. Ok – so I don’t salt my beef steak. I eat 2 pounds of it. And I lose weight.

          I salt my next 2-pound beef steak and gain weight. That’s the food reward theory. Bland food makes you lose weight.

          Please can anyone explain any kind of plausible mechanism? Because Guyenet hasn’t, nor has any of his coterie, and I sure as heck can’t think of any. I’m with Garrett – how on earth could French people ever be thin?

          Is someone going to seriously argue that baguette with butter, onion soup, steak with Bernaise, pomme frites, and chocolate mousse are somehow mysteriously “unrewarding?” Salt will make you fat, but not the sugar in the chocolate mousse? I struggle, I struggle.

          • Gretchen says:

            It’s not my theory, but I think Food Reward would say that without the salt, you’d eat only 1 pound of the beef because it isn’t as tasty.

          • Geoff says:

            To your question of mechanism, see Stephan’s response to my question here:

            “Food reward is heavily intertwined with the dopamine-secreting regions of the brain, the VTA and substantia nigra. These regions project to the hypothalamus, the region that seems to encode the setpoint, and we know that dopamine modulates the activity of that region. Reward is not inherently short term, although it has a short term component. Reward-related behaviors change over time as an animal becomes habituated to highly palatable food, and they end up resembling a drug addiction state in some ways.”

          • alacrity says:

            The issues with regard to salt intake I consider very transparent. Salt causes the kidneys to retain water. Less salt = instant water weight loss. That’s why so many over the counter weight loss pills contain diuretics. It’s the oldest trick in the book.

          • bopes says:


            All due respect to SG, but as a description of a mechanism that aint exactly precise or illuminating. So there are dopamine-secreting regions that project into the encoded setpoint region where “activity” is modulated by dopamine, which causes us to engage in reward-related behavior . . . hmm, you mean we eat too much? So we still get fat because we eat too much but it’s not us it’s the addiction.

            I’m like . . . what? How exactly do all these regions, projecting regions and encoded setpoints affect or control what is going on at the cellular level, where (and while) fat is being deposited?

            Peter at Hyperlipid on the other hand will tell you straight up what he thinks is going on, mechanically, at the cellular level:

            “as adipocytes swell they become progressively less able to respond to insulin. This obviously translates in to insulin resistance of adipocytes ultimately limiting fat gain within the limits of the pancreas to secrete or hypersecrete insulin. That is if you accept that insulin is in any way involved in fat storage.

            Now. What does this mean for the carbohydrate hypothesis of fat gain?

            It is the RESISTANCE of adipocytes to insulin which limits fat gain.

            And the corollary is??? Sensitivity to insulin drives fat gain. You can’t have one conclusion without the other.

            Anyone telling you that adipocyte insulin resistance limits fat gain and yet insulin per se has nothing to do with fat gain… Well, you decide. I have.”

            Peter, among others, will even tell you about impaired mitochondrial fatty acid oxidation as a mechanism of obesity. Helpfully, he even spells it out:

            “Mitochondrial dysfunction leads to cytosolic fatty acid derivative accumulation.
            This leads to chronic hyperinsulinaemia via insulin resistance.
            This leads to adipocyte distension.
            This leads to adipocyte insulin resistance.
            This leads to increased plasma FFA delivery at a given level of insulin.
            This leads to increased cytosolic FFA derivatives.
            This leads to mitochondrial ATP production being normalised.

            The cost is increased insulin resistance. Oh, and the MECHANISM for improved ATP production is OBESITY. Call this a cost if you wish.”

            Whether he’s right or wrong, what Peter says is at least comprehensible.

            I’d like to hear the FR response to what he says.

          • Geoff says:


            “‘Anyone telling you that adipocyte insulin resistance limits fat gain and yet insulin per se has nothing to do with fat gain… Well, you decide. I have.'”

            I feel like I am going to have to keep stating this until I am blue in the face, so I’m going to try to be as explicit as possible on this point. Your argument that insulin clearly has something to do with fat gain is a straw man argument. We all get that insulin plays a critical role in fat storage, no one is disputing that, especially not Stephan. However, the role that insulin plays is a slave role, it takes its orders from upstream. Insulin is the wheels on a car, not the driver.

            Sensitivity or insensitivity to insulin on the cellular level appears voluntary. When the cell feels that it has an energy excess, it makes itself insulin resistant to prevent energy from entering the cell. In other words, the excess energy, the overeating, the caloric surplus, whatever you want to call it, that binge eating that is driving obesity is causing insulin resistance, it is not the insulin resistance that is causing the obesity. The question is, what is causing the binge eating in the first place.? My belief is that it is the reward value of the food; the unnatural combination of flavors, smells and textures that is scientifically optimized for reward signalling; that is causing the brain to compulsively seek these foods.

            I can see how the above can be misconstrued as being in the calories in-calories out hypothesis, but it is not. We are not saying that the overeating is a conscious, voluntary choice. It is not a conscious choice any more than breathing is a conscious choice. Like breathing, which is controlled by the medula oblongata, reward happens in a lower brain structure as well, the hypothalamus. This is the same part of the brain that regulates body temperature (metabolic rate), hunger (satiey), thirst, etc.

            On the flip side, if you say that insulin resistance causes obesity, which GT basically does, and I prove to you definitively that insulin resistance is caused by the cells trying to prevent excess energy from entering, then the chain rule would dictate that it is the overeating that causes the insulin resistance, which causes the fat gain. That, my friends, is a calories-in/calories-out explanation. And no, I am not actually saying that GT is a proponent of c-in/c-out, I’m saying that without that alternative explanation for why the overeating occurs in the first place, that is where you are left, because the empirical evidence largely suggests that this is the chain of causality.

        • Laura says:

          Dairy is insulinogenic, so it would be hard to tell if reduced reward or reduced insulin were the causitive factor in the weight loss.

          • BlueEyesSF says:

            Geoff, that isn’t a mechanism. A mechanism is a set of coherent slides like Lustig has that shows the biochemistry, the interactions, and the pathways – and he’d better have a pile of human clinical studies to show that it works in real life too. To say “well, dopamine affects the hypothalamus somehow through some time. . . in rats” isn’t a mechanism. The hypothesis just isn’t good enough to argue. Sorry.

          • Geoff says:


            Admittedly, I don’t know enough about Lustig’s work to comment specifically on his mechanisms, but what I do know about Lustig is that 1) he thinks fructose causes obesity and 2) he thinks that fiber prevents it. My totality of knowledge on the subject, which is considerable, suggests that these are both indefensible positions

            It should also be noted that there are specific findings in the literature that don’t really have any explanation other than food reward. For example, rats get fat on chocolate Ensure but not vanilla or strawberry, even though they have almost identical nutritional profiles. They have the same carb content, and if anything, it should be the vanilla that is fattening since vanilla has an extra gram of sugar in place of a gram of fiber. Yet that is not what happens.

        • gallier2 says:

          Nuts, cheese and chicken skins, all calorie dense foods. What happened imho, you reduced you overall caloric daily intake, nothing fancy, just restarting the weight loss. That it was blander is anecdotal and not the cause imo.

          • PEK says:

            Sounds like calories in calories out to me.

          • mrfreddy says:

            It might very well have been calories in-calories out, but I was eating plenty. Two meals a day (my normal routine) and I was eating as much as I could, often leaving a bit of meat on the plate because I was just too full. So, it seems to me that, if you want to restrict calories, this might be a pretty good way to go about it. When eating this way, hunger – the usual downfall when people try to simply eat less via willpower – is never an issue.
            Someone mentioned that lack of salt might have been causing the weight loss. Could have been in the first couple of days, but around day 3 I started adding salt to the water I drink all day long. I did that because I was concerned about leg cramps-I woke up one night with a serious one, which hasn’t happened in awhile. Long story short, even with the salty water I still lost a few pounds.

        • @mrfreddy

          You normally skip breakfast and eat cashews raw? I am not at all surprised you have had a hard time losing “those last 15 pounds.” Cortisol naturally rises in the early morning – to help you wake up and get up – so by skipping breakfast, you are extending that high-cortisol state by hours each day, which limits your muscle and makes you hold onto.. those last 15 pounds. A better way to do IF may be to eat breakfast every day, and one or two days a week (but not in a row) eat nothing (water only) after noon.

          Nuts contain natural anti-digestion chemicals; like vegetables, they should be cooked (nuts should be dry-roasted, not cooked in oil; can take some effort to find).

          • mrfreddy says:

            I’ve had a hard time losing that last bit of weight for ten years now. The no breakfast thing is only fairly recent, started that about three years ago I think. The cashews thing even more recent, and is on and off. I eat them when I have them around, and I might go months without having them around. My weight was running around 195 pounds for years and has recently settled down to around 187 – 189. So, I don’t think the breakfast skipping and cashews have much to do with my inability to drop those last few pounds. My fondness for single malts just might tho…

  6. Gary,

    Glad to see you continuing this series. Hope you don’t get discoraged by some of the thin skins that have become apparent in the “Taubes vs Guyenet” discussions that have set the Paleo/LCHF sites aflame. It’s valuable to have this discussion, if perhaps this much debate happened earlier in the career of, say, Ancel Keys, we micht have a healtier populace today.

    Remaining silent servers no one’s interests.


  7. Kelly B says:

    After seeing a number of blog posts on the “spectacle” at the Ancestral Health Symposium, I read through Dr. Guyenet’s posts as thoroughly as I could – I, too had a really hard time with them, starting with how he defined “rewarding” food – and not only am I not an expert in this world, I never stay at Holiday Inn Express.
    However, it occurs to me that he may be describing a scientifically verifiable phenomenon: consumption of rewarding food (however it is defined) provokes an addictive sort of response in the brain, leading to more consumption of that food. Where his hypothesis breaks down, or stops, it seems, is in what happens next. Could it be that, if the rewarding food is of a sort that kicks off the body’s fat-storage cycle, the person eating it gains weight, and if the rewarding food is not of that sort, the person eating it is able to use it as an immediate energy source, and doesn’t gain weight?
    I guess what I’m saying (none too clearly), is that his hypothesis, and the hypothesis you have laid out in your books may both be at work in the weight gain experienced by some people, that they operate independently of one another, but that both mechanisms are present in that situation. And that, for people not consuming food that prompts that addictive response, weight gain might still occur, if what they eat is of a type to prompt fat storage by the body.

    • Warren Dew says:

      The problem with this idea is that you have to define some highly palatable foods – notably full fat meat – as somehow “unrewarding”. Ultimately that comes down to a circular definition of “addictive foods are addicting”.

      • Jim says:

        Warren, the food reward hypothesis doesn’t say that full fat meat is “UNrewarding”. In fact, if all food were completely unrewarding we would probably starve to death. We are supposed to find food to have a normal level of reward value. The problem is that in our current food culture we have made things *hyper*-rewarding. Think of all the things you could do to make plainly cooked full fat meat MORE rewarding (salt, sugary glaze, browning to get the malliard flavor enhancements, and so on). It’s all the reward-accelerants that cause the problem according to the FRH. And it’s not just meat, of course. In fact, what we do to meat might be the least of our problems.

        • Warren Dew says:

          I’m already making my meat maximally rewarding – salting to taste, browned, even a honey glaze on some forms of meat. If I could afford it, I would eat this and nothing else. And yet eating large amounts of this does not result in gaining fat – quite the opposite.

          • Jim says:

            Good. Keep eating your honey-glazed meat. I still eat some higher reward foods at times myself. The FRH might predict that weight loss would be faster without the steps taken to increase the reward value, but, if you’re satisfied with your situation, don’t change. I don’t take Stephan to advocate extreme austerity just for the sake of it.

            Even with the honey-glazed meat (which is probably not the worst of anybody’s problems), an important consideration is how rewarding your overall diet is compared to the SAD. If you’re not eating pizza and doughnuts and cake and ice cream and chips and so on, you probably have a fairly low reward diet in relative terms. And if you ate “nothing but” honey glazed meat, your overall diet would be EXTREMELY low reward (variety seems to be one of the main reward factors).

            This is where people naturally ask how Stephan’s advice is any different from Gary’s. Both say to avoid doughnuts and pizza and cake and ice cream. One difference is that Stephan permits plain potatoes and sweet potatoes and squash (as much as you want pretty much), and Gary would say to avoid those.

            Plain, whole-food, “safe” starches (there may be some problems with gluten grains and such for other reasons) provide a good practical test between the two hypotheses.

            If you are worried about adding in plain potatoes, worried it will kick of an addictive carb binge or something, then don’t add them in.

            Another prediction of the FRH would be that low reward low carb would work better than high reward low carb. So, if you stall on your current version of LC, and there’s something to the FRH, then it gives you an additional lever to pull.

  8. J. Stanton says:

    GT: “I confess, though, that I find the hypothesis [FRH] surprisingly difficult to understand…”

    That may be because it is, in my opinion, poorly specified. Basic terms like “palatability” aren’t defined until the very end of the series (in a comment, no less), and they’re used inconsistently with the existing, accepted scientific concepts and terminology.

    Anyone who wants to understand the state of the existing science might be interested in Why Do We Ever Stop Eating? Taste, Reward, and Hyperpalatability. (And, perhaps, the other articles in the series, in order to understand its context.)

    Note that acknowledging the existence of hedonic impact and incentive salience does not, in itself, explain why they exist. Both “body rules” and “brain rules” hypotheses are capable of producing hunger. I believe the evidence is that hunger is primarily nutritionally driven, and the ability to burn stored fat for energy is part of that – but I leave the details of the hormonal and neural signaling involved to those more qualified than I.


  9. Jim says:

    Gary, I’m starting to see the problem here.

    There are two important questions here:
    1. What causes obesity?
    2. What’s the best way to treat it?

    Let me first say that I’ve always had a problem with you calling your main foil the “calorie in/calorie out” view. There are two reasons this frustrates me.

    First, I think it invites critics to think you don’t understand that physics dictates that ultimately mass gain/loss requires an energy imbalance. You, of course, do understand that, but the terminology invites misunderstanding, I believe.

    Second, I think it might be causing you to confuse cause with best treatment. And I think that’s part of why you’re not able to understand how the Food Reward Hypothesis is not just another “calorie in, calorie out” view.

    Here is a high-level gloss of the mechanisms of adiposity according to Taubes and Guyenet:

    High carb diet –> fat storage –> lean tissue starvation –> increased appetite –> energy imbalance.

    Highly rewarding food –> behavior of eating more of those high reward foods –> energy imbalance –> fat storage.

    So, in this sense you claim that fat storage is a proximal cause of energy imbalance, and Guyenet claims that energy imbalance is a proximal cause of adiposity.

    So far so good. There is a legitimate empirical disagreement there.

    However, here’s where we get off track.

    Just because Guyenet can be framed as saying that a calorie imbalance is a proximal cause of adiposity, that does not mean he thinks that the best treatment is to manage the calorie balance directly.

    In fact, he does not. Guyenet is as opposed to the “eat less, move more” advice as you are. To him it is very important to recognize what causes the energy imbalance in the first place. It is not moral failure (in most people). It’s not that they’re paying insufficient attention to calories in and calories out. It’s that they are unknowingly eating foods that reinforce their own consumption.

    I would guess that Stephan would say that if you try to “eat less and move more” while eating the same high-reward foods, you are highly likely to fail. (just like you would say that if someone tries to “eat less and move more” while still eating a lot of carbs, they are doomed to fail).

    And, on the other hand, if you switch to low reward foods (largely plain, gently cooked or raw whole foods – animal and vegetable), then you can reverse the flow of energy from going into your fat cells to going out of your fat cells without having to tend to the energy balance equation at all.

    So, you’re right, when it comes to the cause of obesity, the food reward folks can be thought of as saying that energy imbalance drives adiposity. But this does not put them in the “gluttony/sloth” or “moral failure” or “eat less/move more” camp.

    They are on the same side of that issue as you are. And their advice is very similar to yours. They reject the “eat less move more” and claim that the key is to find out WHAT you’re eating that’s making you fat, and to get that out of your diet. And I think that that area of agreement is way more important than the disagreement over proximal causation — at least as far as public health goes.

    “Eat less (of your current crap) and move more” is the enemy. And you and Stephan are both on the right side of that battle.

    • Jim says:

      Of course it’s not enough just to think the quality of our calories matter. You also have to be right about the particular foods you recommend. But I think the list of things both of you would take out of the standard diet is a large part of the problem — processed grain products, sugary snacks, liquid sugar drinks.

      And to be clear about the calories in/calories out thing. I’m suggesting that we need to distinguish between A) views that take energy balance to be a proximate cause of adiposity, and B) views that take direct management of calories in and calories out to be effective for weight loss.

      Commitment to A does not imply commitment to B.

    • GT says:

      I would agree with most of what you say here. I’m also fighting, though, as is Dr. Guyenet, for clear scientific thinking in obesity research and nutrition. The problem is we don’t agree on who’s doing the clear thinking. I do feel a little bit like Rodney King wanting to say “can’t we all just get along”, after all, the problem we all agree is the establishment’s position. (And I say this realizing that’s precisely not what this post and the ones that follow will be doing.) In this sense, these kinds of disagreements are counter-productive. Ultimately I would like to induce establishment researchers to test these ideas rigorously as none of us can. We should all be working toward that, but then that’s not what these blogs are about. They’re about elucidating ideas, challenging ideas and, yech, maybe demonstrating, or not, how smart we are. As I said, I thought about ignoring my previous post and moving on to other subjects. I’m not sure this really is a case of better late than never, but I chose to follow through with it. I hope it doesn’t do more harm ultimately than good.

      • Jim says:

        I’m glad you’re following up on this. I think you and Stephan got off to a bad start with each other, but there seems to be a lot of overlap in your audiences, and there are a lot of us out there who respect both of you (and have seen benefits from applying both theories). We need to clarify the individual theories, and the points of agreement and disagreement, figure out what experiments would shed light on the areas of disagreement — and THEN (the hardest part) figure out how to get people with resources to fund the studies!

        I”m eagerly anticipating your next post.

    • Elenor says:

      Jim wrote:
      Guyenet: Highly rewarding food –> behavior of eating more of those high reward foods –> energy imbalance –> fat storage.
      “It’s that they are unknowingly eating foods that reinforce their own consumption.”

      Does this mean if you locked some fat folks in a cage, and fed them highly rewarding food, but did NOT let them eat ad libitum, they would crave those rewarding foods, and not all foods? Or they’d eat smaller portions of not-so-rewarding foods because they were craving the highly rewarding foods?

      It sounds to me like this idea is: if you take away good-tasting food, then fat people will eat less and lose weight. (I mean come on — ‘stop salting your steak and you’ll lose weight’?! Feed people bland mush and they’ll quit eating?!? Maybe y’all DO want to lock fat people in a cage so you can feed them mush and nothing else?!)

      And he wrote:
      And, on the other hand, if you switch to low-reward foods (largely plain, gently cooked or raw whole foods – animal and vegetable), then you can reverse the flow of energy from going into your fat cells to going out of your fat cells without having to tend to the energy balance equation at all.

      What?? Why? How? Because the fat cells don’t LIKE undercooked bland food?!

      • Jim Stone says:

        Elanor, I was probably a bit sloppy with that. According to some, eating palatable foods often leads to a craving to eat more of those specific foods (in an addiction-like manner), but part of the theory is also that the set point is raised, which would predict that one would eat more of other foods as well.

        Also, I never claimed that removing salt was a major factor. It’s just one factor among many. I doubt I would start gaining weight if I started salting my meat and made no other change. Though I might lose a bit more slowly. Adding salt makes the meat a bit more palatable. Adding butter might make it even more so. Adding a sugary barbecue sauce even more. I think you could follow a fairly low reward diet while still salting your food. But removing salt might speed things up a bit if you’re looking for faster weight loss.

        Also, I want to make it clear that I’m not committed to the FRH. I’m experimenting with it. And I’m seeing good results. That’s all.

        • Jim Stone says:

          Sorry, I should have addressed you as “Elenor” not “Elanor”.

        • BlueEyesSF says:

          “I’m experimenting with it. And I’m seeing good results. ”

          Jim, have you ever heard of the “placebo effect?” It’s real, and it’s powerful. I think your “results” are from auto-suggestion brought about by your belief in Guyenet. Seriously.

          • Jim says:

            Hey Blue Eyes.

            You don’t know nearly enough to make a diagnosis like that. Seriously.

            I don’t have a “belief in Guyenet”. I’m a fan of both Gary and Stephan, but not a “fanatic” in either case. I read GCBC two full times, and many chapters a third time. I greatly appreciate what Gary brings to the table, and hope Stephan can come to be more appreciative of the contributions to the public discussion that Gary has made.

            I am open-minded toward both theories, and skeptical toward both theories — simultaneously. And I’m personally experimenting with both ideas. I’ve had some success with low carb. I lost maybe 15 pounds and kept it off. I’m having even more success with low reward (plain, simple whole foods) slightly higher carb fare.

            I’m not committed to either theory. I think both have some problems. Low carb has some problem accounting for people like the Kitavans and some New Guinea highlanders. They eat very high carb diets and have great health markers — until they start eating western diets, then they get the western diseases. I also think that if you lock someone in a room and feed them nothing but bread, or nothing but sugar water, they will lose weight quickly. So it’s not as simple as “carbs make you fat”. I think low carb has its place. I just think it can’t be the whole story.

            Similarly with the Food Reward theory. I’m not committed to that either. In fact, I’ll fully admit right here that I don’t fully understand what exactly the theory is. It’s a little difficult to find an easy-to-visualize toy model that illustrates what’s going on with the set point idea (though there is good evidence that something like a set point comes into play in some circumstances).

            And “food reward” is a bit nebulous. Which food constituents are rewarding? Are they always rewarding, or does context matter? For instance, if you add a sugary glaze to meat, I think it probably makes it more rewarding. But if you lock someone in a room and feed them only sugar water ad lib, it’s pretty clear to me that they would drop weight very quickly. So context seems to matter a lot for reward, but it’s very difficult to specify exact mechanisms.

            Because neither theory seems to explain everything, I’m left with no choice but to try them both, and bracket my confidence in each while I wait for more experiments to be done, more data to come in, and more models to be spun so I can hopefully one day have a theory that does explain everything.

      • John says:

        The idea of the food reward hypothesis is that foods can act in the brain through the same mechanisms that cause drug addiction. The implication is that, yes, if you locked people in a room and gave them a choice between rewarding foods and non-rewarding foods they would ignore the non-rewarding foods (nearly-absolute conditioning of the choice takes time). I’m not aware that this has been tested in humans, but this holds true in animal models. As Jim stated, salt is not the only thing that makes foods “rewarding.” And, in fact, there is no consensus to date on what exactly the criteria would be, but suffice it to say that most fast food qualifies. It is worth noting that there are several studies in which people placed on very-low variety, very low calorie (e.g., ≤550 kcals/day) diets have significantly decreased appetites and lose weight successfully, but when allowed to return to a normal diet, appetite increases and weight gain occurs.

        • BlueEyesSF says:

          “Low carb has some problem accounting for people like the Kitavans and some New Guinea highlanders.”

          I wanna see the DNA here, I really do. These are small, remote, isolated populations that probably have very special genetics. To argue that human genetic variation in metabolism doesn’t exist is foolish. I’m Russian, not a New Guinea tribesman. To say the whole human metabolic situation must be judged by 150 remote islanders is really poor science.

          Obviously there’s a wide variety of human metabolism. Some folks clearly have the genetics so that the Mediterranean diet works for them. A special few can eat literally anything at any time as much as they want and stay rail thin. Both of these groups appear to be in the minority. The majority or a near-majority of people of African, Asian and European descent seem to find success on low-carb.

          And we are pointed to that conclusion by the famous Stanford A to Z study. Or so the head researcher from Stanford himself said in his youtube presentation on it.

      • STG says:

        Totally agree! My problem with the food reward theory is that it does not relate to my experience with food. I find all food rewarding! I don’t eat processed or fast foods, but I can over-eat whole, bland foods. Fortunately, I don’t have a weight issue.

  10. Mary says:

    Don’t know if you’ve seen this EXCELLENT video: Dr. Listig explaining insulin, leptin and obesity:

  11. bopes says:

    You go, GT.

    Kenneth, what is the mechanism? . . .

  12. Martha says:

    As far as your CAVEAT goes, I think you might find this useful…

    Instead of thinking of fat tissue and the brain as primary cause and secondary effect, think about it like this: The brain may be exacerbating the situation.

    If palatibility is a direct stimulus to the brain (via taste buds and other stimulii like smell and texture), and if it is paired with a post-prandial hormonal/neurochemical response, then weight gain may–if only in some (very) small and (very) secondary way–become a sort of Pavlovian response to palatable/rewarding foods.

    To put it another way… Can the brain be conditioned into producing a response (post-prandial hormonal/neurochemical environment) that produces an effect (weight gain) that is greater than what the original stimulus (food) would have called for had that pairing never been made?

  13. Niki I. says:

    Gary, thank you.
    Anyone’s degree of ability to resist food reward as an explanation for weight again and obesity seemed logically faulty to me too and I thought I was somehow missing the argument (and me a scientist, for shame! ). Personally, I find I am much more easily satisfied (eat less, feel happy) the stronger the flavor of my food, whether from spices, vinegars and mustards, or mayonnaise and olive oil. Anecdotally, this is true of everyone I know. So fine, the food reward hypothesis doesn’t rest so much on taste itself, but specifically sugars (including converted from refined grains) and fats that create the ‘reward’ in the brain, stimulating certain centers. But then, grains and fats have been around for an awfully long time and cheaply too (unlike table sugar) – deep fried dough, found across many cultures, comes to mind. Why are we eating more of them now/in the last 30-40 years or so? Or in food reward terms, why are we so much less able to resist them now (or the reward centers in our brain so much more stimulated)? Could it be that the fault lies neither in our stars nor in ourselves (our brain) but because we were steered away from fats/meats and towards grains, which started us on the weight-gain process that reinforces itself, with grains and sugars stimulating greater insulin secretion, which regulates, among other things, directly fat tissue, which is a secreting organ itself, which….and there we are right back to your argument (please excuse the grossly imprecise summary!).
    The same ‘initialization’ in the last 30-40 years (when we were steered towards ‘healthy grains’ ) could also serve of course as the start of a sugar/grain ‘addiction’ or food reward hypothesis, but doesn’t address any fat reward (we were steered away from fats too). However, with or without fat reward, the initialization of the grains/carbs reward path had hundreds of years to happen – you don’t need to eat more of it or start gaining weight to trigger the hypothesized reward pathway to obesity, you just need to have available grains/carbs to trigger it, which we always did….yet our grandparents clearly weren’t addicted to fried dough or corn cakes (and of course most rich people weren’t overweight either).
    Does my reasoning make any sense? Do we need both a historically -differentiated trigger and a self-reinforcing mechanism to explain the Current epidemic? In which case, the reward hypothesis fails on the first alone? As I said, I don’t understand it actually, so my argument could be missing something substantial. Help?

    • John says:

      Food reward is more like drug addiction than just something that tastes good. The mechanism has always existed, but foods that are typical of the American diet have changed dramatically over the past 25-50 years. No one is waking up in the morning and cooking eggs and bacon (and maybe even toast and orange juice) and getting fat; they are going to McDonald’s or Starbucks and consuming foods that are highly rewarding not specifically because of sugar content or because they are fried, but because of a variety of factors and ingredients for which there is currently no consensus. Again, the concept of food reward is related to that of drug addiction, not just to something tasting good.

    • Margaretrc says:

      i would agree that the efforts to steer us away from fats, and therefore toward more grains and, especially, sugar–which was put into processed foods to make up for the fat that was not in there–definitely plays a part, a huge part, in leading to the current obesity, type 2 diabetes, and heart disease epidemics. Countries (France comes to mind) and peoples who did not buy into the fear of fat and stuck with traditional natural whole foods while staying away from processed foods and beverages high in sugar and grains, have not, by and large, had to deal with any of the chronic disease issues that plague modern western society. That is easily explained by the CIH, but I don’t see how it is by the FRH. As you say, @Niki, our grandparents had rewarding food, but most weren’t fat, diabetic or prone to heart disease. The French, the Thais, and many other peoples eat very rewarding foods, no matter how you define the word, without getting fat on them.

  14. FrankG says:

    Many thanks Gary.
    I particularly appreciate your discussion of the “brain rules” vs. the “body rules” concept — I think that this is an area were we humans tend to fall into conceit of thinking we are somehow “above the rest of the animal kingdom” — “masters of our own domain… we are fully in control of all our own conscious actions!” In this model the brain is the overall conductor that says to the body “OK, first do this and only then do the other” — for example “once we have extracted the required nutrition from this meal, then any excess will be carted off to be stored as fat” This is partly why many people seem stuck with the idea that: “only excess calories are stored as fat” — which as you and Dr Lustig and many others now, explain is not the case… fatty acids are constantly cycling in and out of fat tissue and it is only the external sign of which (in or out) is happening at the greater rate, which we see as increase or decrease in fat tissue.

    I do not accept the “brain-rules” paradigm: much like any well rehearsed orchestra or choir, the body can still make “beautiful music” even when the conductor is absent (as in a coma for example). Much like an orchestra is made up of relatively simple units (musicians) each with their own skill-set and functionality, and each capable of “doing their own thing”; so the body is made up of multiple relatively simple systems that give the outward appearance of working together as single organism… when in reality each sub-system is simply “doing its own thing” — in much the way that you describe the sometimes “anarchy” of fat metabolism.

    We like to think we are in control and obviously we can (in the short term at least) consciously override many of the body’s drives — holding our breath for many minutes with practise — but I am willing to accept that my physical body is run by biochemistry and not governed by external behaviours, by physiology rather than psychology.

    • Geoff says:

      The brain is not absent in a coma. The prefrontal cortex is, but not the brain. The brain is absent in “brain-dead” patients, but they can’t breathe on their own. I find your discussion of the hubris of humans to be quite ironic given that you seem to think that the brain is only involved when you’re awake and making decisions.

      • FrankG says:

        The conscious brain that we like to think makes all the decisions about what and how much we should eat IS absent when we are unconscious. I am not so naive as to be unaware of the difference between voluntary and involuntary control, or that our highly evolved brain is built around a very ancient “reptilian” brain. My intended point — for those who did not dissect every word I wrote too literally — is that we may not be as much “in control” as we like to think we are.

        It has been suggested that we choose to eat food because it is palatable — so take the example of a person who has been physically active such that they have “worked up an appetite”. This person is attracted into a restaurant by the smells, sights and tastes on offer. They eat enthusiastically until satisfied. We might assume all kinds of conscious choices and food preferences being involved here, but offer those same preferred foods again after satiety has been reached and they no longer hold the same attraction… is that brain or body? Hunger is what ultimately drives us to eat, not the smell, sight and taste of food — starving men have eaten their own shoe-leather, but once our bodies are satisfied, a cordon blue meal is unappetising.

        Another example would be a pregnant woman waking at 3am with a craving for what would otherwise be seen as an odd mixture of ingredients. Would you tell her to go back to sleep as it is “all just in her head”? Not if you value your life or at least your manhood! Or would you accept that it is a clear sign of her body communicating the need of specific nutrients for the growing fetus?

        So much processed and packaged food these days may be high in energy but low in other nutrients… so in the midst of apparent plenty, we can remain hungry… our body unsatisfied — remembering that we don’t just eat to fill the need for energy.

        I am convinced that we are born with an innate ability to judge “what” and “how much” of any nutrients our bodies need — just as any other animal on its natural diet does. If we look to animal models we can apply them to ourselves because we are animals.

        • John says:

          Caged animals will choose to eat highly processed, highly “rewarding” foods making themselves obese while leaving other “natural” foods untouched. Animals similarly caged with free access to only “natural” foods will not become obese. This is despite the fact that the “rewarding” (e.g., high in refined carbohydrates, high in saturated fats, high in salt, consistent in texture) food is low in nutrients.

          • FrankG says:

            Thanks John. This goes to reinforce my conviction that our natural adaptations work their best when we eat real whole foods; as provided by nature rather than by big business. If palatability or reward has any part in this scenario — and I suspect it has some role — it is in allowing us to determine when we have eaten “enough” of any given nutrient… try eating a pound of butter and your body will soon signal you that it is replete, but try drinking cans of cola and the body is fooled into thinking it is water; because we are not adapted to recognise this as a concentrated energy source. Beyond that I can see the addictive quality of sugars and refined starches — again from an evolutionary standpoint these would have been rare finds ( a wild beehive or field of ripe berries) that it makes sense we would want to fully exploit any such source.

            Having said that, I agree fully with what I read Gary as saying: that to focus on calories is misleading and unhelpful — this is an issue of primary biochemistry and not of secondary behaviours.

            And although I hesitate to exclude anyone from obesity research, I also agree with the sentiment of Gretchen’s remark below “I do think that progress in obesity research would be faster if we didn’t permit genetically thin people to do the research. They simply don’t understand the problem.” As a person in my 50’s with 25+ years of struggle against excess fat mass “under my belt” — literally and figuratively — I’m pretty tired of being told how “simple” my “energy imbalance” problem is, by young guns in their 20’s who have all the answers. 😉

          • GT says:

            This is a point I’ve always wanted to make to Kurt Harris and some of the young paleo types as well — understanding obesity and weight regulation without having a weight problem yourself is like trying to understand parenting without having children. You might think you get it, but when the children arrive, you will learn differently.

          • Whoa!! Gary, have YOU ever been significantly overweight? I don’t recall you sharing any such experiences.

          • @GT

            “This is a point I’ve always wanted to make to Kurt Harris and some of the young paleo types as well — understanding obesity and weight regulation without having a weight problem yourself is like trying to understand parenting without having children. You might think you get it, but when the children arrive, you will learn differently.”

            This is not only annoyingly condescending, it is just outright stupid as an argument about whether I or anyone understands something in the scientific or medical realm.

            Firstly, I am a 50 year old physician, so hardly a “young paleo”. I did in fact weigh 20 lbs more than my current weight when I was on the SAD. Now I weigh exactly the same eating 30% carbs as when I ate 5%, in direct defiance of the CIH predictions. My wife’s experience is exactly the same. None of her 18 lbs weight loss was regained with addition of potatoes and other whole foods starch sources. The only difference for both of us is in food reward effects and in wheat and linoeic acid consumption.

            Stephan is a PhD researcher and whatever his age, also should also not be dismissed as a “young paleo”.

            Must one be overweight by some particular amount before weight loss maintained is meaningful? Why does my 20 lbs not mean as much as 100? Please explain physiologically why 20 lbs is not significant. I think metabolically the last 20 lbs may actually mean more than the first 20, especially if you were obese or IR. Otherwise why is the last bit of weight the hardest to lose? I think there is more energy balance delta going from BMI 23 to 21 than 28 to 23.

            Must all diabetes researchers have diabetes? Or psychiatrists have schizoprenia? Or must all OB/Gyns be females who have given birth or had cervical cancer?

            What nonsense.

            My opinions on what makes us fat may be buttressed by own experience keeping weight off eating a moderate carbohydrate diet, as well as many of my readers who have reported exactly the same thing – namely maintained or even accelerated weight loss with INCREASED carbohydrate consumption – in direct contradiction of the CIH.

            It ultimately has nothing to do with whether I have been fat, any more than a pediatrician’s knowledge would depend on experience with his own children being sick.

            My ideas are based primarily on four years of reading the medical literature and on the direct clinical observations of patients who FAIL despite or even because of consumption of very low carbohydrate diets. FAIL by staying obese and regaining like Jimmy Moore despite VLC because they think, absurdly, that you cannot get fat eating fat, or FAIL by suffering from hypotension, mood changes or low T3 levels because your body thinks it is starving.

            There is more than one way to get fat. Eating starch and having your insulin go up is not one of them. That idea should be put to rest.

            There is no convincing scientific evidence that insulin is the primary driver of obesity via consumption of carbohydrate. Insulin is necessary to maintain and store fat, but the CIH as stated in WWGF is false.

            I don’t “think I get it”. I do get it.

          • GT says:

            Hi Kurt,

            We discussed this in the two hours we spent on the phone together a month ago. I think there are many points you’re missing here. One key question is whether you could have lost the 20 pounds originally with the starches in your diet. Maybe so. But you don’t know. You didn’t try. That’s the problem with anecdotal accounts. And could a 400-pounder lose 200 pounds while keeping starch in the diet? Maybe so. But you don’t know.

            One obvious possibility, as we discussed, is that by removing sugars and refined carbs, you became metabolically healthy — in effect, you resolve your insulin resistance. Now without sugar and refined grains, your body can tolerate the starches. That’s a different issue. And no it doesn’t disprove the insulin hypothesis. And we discussed this at length when we spoke. If the insulin resistance is caused by the sugar in the diet — as I suggested in my NYT Magazine cover story and my AHS talk — then that explains why populations without significant sugar in the diet can do fine on starches. Populations with significant sugar become insulin resistant and now all the carb-rich foods can be problematic. And the same for individuals. You get rid of the sugar and refined carbs, and your body can tolerate the tubers too.

            I find it fascinating that some people can add starches back to their diet when they’ve plateaued and go back to losing weight. I’ll buy that that happens because one of the commenters on the blog described it. Although he doesn’t know if his weight loss would have happened anyway without the starches. That’s always possible, unlikely as it seems, and that’s why researchers do randomized controlled trials to assess the value of interventions. So I’d like to see this documented in something other than anecdotal reports. What you might consider doing, if you haven’t already, is compiling the data on these patients and posting it. Then we can get a real feel for the strength of this evidence and what to make of it.

            Amusingly enough, after I first went very low carb I added back toasted pumpernickel and other low GI breads to my diet. My problem was postural hypotension and the added carbs took care of that immediately. My weight is stable also. But not with starches; with low GI wheat.

            All of this could be tested with well-controlled RCTs. In fact it would be pretty easy to do so because the only thing that would have to change is the carb source. At the moment, such RCTs don’t exist, or not that I know of, so your confidence in the beneficial effects of tubers is admirable but hard to understand.

            And why you think that the presence of starches in your diet one way or the other has any thing to say about food reward effects is also something you’ll have to explain to me. Maybe I’m just dense. But it seems like you’re conflating your beliefs about the healthfulness of some starches with your desire to believe or support the food reward hypothesis.

            As for whether all diabetes researchers need to have diabetes, no, I think that’s not an issue. But you’re missing the point here, confusing the ability to treat a disease with the ability to understand the experience and whatever that teaches you about the disorder.

            It’s not about what it takes to treat or cure a disorder, but to understand it on a fundamental level. So I would argue that a pediatrician who never got a cold in his or her life would be unable to understand the experience of a sick child, even while he or she might be perfectly capable of taking the kids temperature and swabbing their throat. Would psychiatrists benefit from having had schizophrenia? I’d say absolutely, but regrettably the schizophrenia would impair their ability to function as a psychiatrist.

            And I think Susan Sontag, author of Illness and Metaphor, would have said that it would help doctors understand cervical cancer if they had it themselves. Could they treat it anyway, sure. Can ob/gyns deliver babies without having had one? Sure. Can they understand the experience of child birth without having had a baby themselves? Not on some fundamental level. Could a grief counselor understand grief without having grieved? I very much doubt it. Can an economist understand poverty without having been poor? Not on some fundamental level. No. I’m a big fan of book learn’n, but some things benefit from first hand experience.

            As for you getting it, I have questions about your ability to reason clearly as you have about mine. I don’t question your getting it about obesity because you, as you say, had 20 extra pounds to lose. You had a weight problem. It wasn’t the kind Jimmy Moore had, but it was a weight problem. My question to you, as we discussed a month ago, is whether your experience as a marathon runner (am I right in remembering that you ran marathons?) who had gained 20 extra pounds is immediately translatable to someone who is 50 or 100 or 200 pounds overweight?


          • Warren Dew says:

            Gary, Kurt Harris is hardly paleo; quite the opposite, as illustrated by the potatoes. He explicitly dissociates his “archevore” ideas with any connection specifically to the paleolithic period.

          • Speaking of Jimmy Moore: Gary, are you aware that he lost 170 lbs in 9 months back in 1999 on a very low fat diet? He doesn’t give details about the weights, but at 410 lbs in 2004 he was his heaviest all time weight, so 170 lbs in 9 months from a lower weight vs. 180 lbs in 12 months on Atkins doesn’t look too good anecdotally for your hypothesis (oh, and he was exercising up a storm during the 2004 weight loss too).

        • Geoff says:


          We’re very clearly not in as much control as we think we are, but that doesn’t mean that it’s the body dictating things. It’s all about the hypothalamus. That’s the point.

          • FrankG says:

            @Geoff Is that “the point”?!? Thanks for telling me what to think. OK with you if I apply critical thinking and make up my own mind once in a while? Many Thanks 😉

            Even accepting that it is “all about the hypothalamus” — and assuming by “all” you mean appetite and weight control? — then are you suggesting that the hypothalamus is under our conscious control? If it is not, then surely you are adding to the position (which I share) that we are dealing with biochemistry as opposed to behaviour?

            Perhaps I misinterpreted Gary’s “Brain rules” vs. “Body rules” concept to mean “voluntary control” vs. “involuntary control”..?

          • Jim says:

            Geoff, I don’t see why the distinction between body and brain is important here. The distinction is between the conscious mind and the unconscious processes that drive behavior — whether those reside in the brain or in the rest of the body. In other words, would it make any difference if the hypothalamus were located next to the pancreas instead of being in the brain?

        • Margaretrc says:

          @Frank G., that is.

    • Margaretrc says:

      Well said.

  15. Alex says:

    What I don’t get is how ‘palatable’ or ‘highly rewarding foods’ differ from the high carb foods, that low-carb dieters avoid, in any way?

    Stephan on his blog cites the studies involving the ‘cafeteria diet’, which he describes as is “palatable food” and “remains the most rapid and effective way of producing dietary obesity and metabolic syndrome in rodents using solid food”.

    He then lists the foods found on this ‘cafeteria diet’:
    “English muffins, French toast, pancakes with syrup, scrambled eggs, chicken pie, cheeseburgers, margarine, white sugar, various cakes and puddings, apples, jelly beans, Doritos, M and M’s, apple juice, 2% milk, sodas and several other foods.”

    Am I missing something here? Aren’t ‘highly rewarding” and “palatable foods” just high carb foods (junky ones at that)? The only food listed there that would have minimal carbs is the scrambled egg! Even cheeseburgers (often cited as a ‘high fat food’) are probably almost as high in carbs (if not more so) than fat – check McDonald’s own website for the nutritional breakdown of one of their cheeseburgers (when the bun is included).

    Also, some people find very savoury foods most palatable, while others like sweet foods. Yet, if the ‘savoury foods’ have minimal carbs (unlike Doritos), do the people who find them ‘palatable’ always get fat? On the other hand, how many people who find things like pancakes with syrup, various cakes and puddings, jelly beans, M and M’s and sodas ‘highly rewarding’ remain thin?

    • Geoff says:

      You are missing something. First, you’re missing the important distinction between “high reward” foods and “hyper-reward” foods. High reward foods are healthy, as they are the foods that our reward circuitry evolved to steer us toward. Hyper-rewarding foods are foods that are more rewarding than anything within our evolutionary experience. They are designed, by scientists, to spike motivation centers and cause people to eat more of them, even when they are full, and buy more of them.

      The other thing you’re missing is that it’s the “junky-ness” of the foods that makes them high reward, not the carbohydrates. Doritos are hyper-rewarding, corn on the cob is not. French fries are hyper-rewarding, baked potatoes are not. Pasta made from wheat flour is hyper-rewarding, while pasta made from rice flour is not. There is clearly a disconnect between the carbohydrate content of the food and the reward value.

      Also, reward value and taste/palatability are not the same thing. Reward is more along the lines of psychological addiction. Something can taste completely bland and still cause one to munch it for hours on end on an already full stomach.

      • Alex says:

        Hmm! Let’s see – 100g of corn on the cob (with butter) contains 22g of carbohydrate while 100g of Doritos (Cool Ranch flavour) contains 64g of carbohydrate. Am I missing something?

        As for their being a difference between ‘high reward’ and ‘hyper-reward’, this is not something that Stephan seemed too bothered about in his blog post (which I quoted). I will further quote him:
        “…he gave his rats access to a variety of palatable human foods, in addition to standard rodent chow. They immediately ignored the chow, instead gorging on the palatable food and rapidly becoming obese…”

        Why is it that so many of these so-called ‘palatable’ or high reward’ foods are high in carbohydrates – starches and/or sugars – if it is something other than carbohydrates that make them ‘palatable’, ‘high reward’ or ‘hyper-rewarding’?

        And it is not always a combination of fat, salt and sugar. Most of the foods used in the studies, mentioned by Stephan, contain nearly all starch and/or sugar and hardly any fat or salt – for example: white sugar, apples, jelly beans, M and M’s, apple juice and sodas. Even English muffins are quite low in fat – 2g per 100g.

        • John says:

          There is currently no consensus on what makes something high reward. Keep in mind that this mechanism is similar to drug addiction. An alcoholic and non-alcoholic regard alcohol in very different ways.

          Highly refined carbohydrates are more likely to be “rewarding” than unrefined carbohydrates. Corn on the cob is an un-refined carbohydrate, corn syrup is a refined carbohydrate. Additionally, saturated fat can be rewarding as can sodium or any other seasonings. These effects of rewarding foods are likely cumulative and dissimilar in magnitude between foods (refined carbohydrates are likely to be more “rewarding” than salt).

        • Geoff says:


          What you’re missing is that it’s not the carbohydrates. Eating a diet of 20 potatoes a day causes dramatic weight LOSS. It’s about a combination of factors, including flavors, textures, smells, colors, etc. What you’re missing is that Gary’s proposed mechanism of carb –> insulin –> fat is bunk; it doesn’t explain the empirical data, and as such can be ruled out as wrong. The real mechanism is junk –> reward signaling –> setpoint increase –> brain interprets blood leptin as being too low –> brain downregulates metabolism and upregulates fat storage –> insulin –> fat.

          • GT says:

            Hi Geoff,
            One guy eating 20 potatoes a day and losing weight is certainly an interesting phenomena, but I’m not sure I would base an entire theory of obesity on it. My question to you is this, when is the last time you changed anybody’s mind in an argument by repeatedly making dogmatic statements repeating your point? It seems kind of counter-productive in healthy social discourse, but maybe you know something about people that I don’t.

          • STG says:

            Can you provide references of empirical research that measure, demonstrate and define experimentally and physiologically the exact mechnisms and pathways (physical and neurological) of the food reward theory? It would be helpful. For example, where in the brain is the “set point” located and how do researches know this? How do they determine or measure its function?

          • For Guyenet’s Sycophants (TM) to come here and lecture and condescend to GT – as though GT’s problem w/ SG’s food reward BS is that GT doesn’t understand the science – is beyond ridiculous.

          • Geoff says:

            Gary, there is a large body of evidence of people losing weight on high carb diets, and a large body of evidence of populations eating high carb and remaining lean; I am not basing my entire theory of obesity on one guy, he is just the black swan that pokes a gaping hole in your theory that all swans are white. I don’t appreciate the ad-hominem statements about my “dogmatism,” particularly since it would appear to me to be the pot calling the kettle black.

            Below, I offered up 3 specific, repeatable empirical phenomenon that cannot be explained by your mechanism as I understand it. If you want to avoid dogmatism, it may be worth addressing these concerns directly rather than ignoring them altogether.

  16. tabatha1970 says:

    Being of the fluffier body type, and being aware of misconceptions or prejudices of thinner people, I feel there’s an extra layer of misunderstanding about the obesity issue that’s simply unavoidable. If I had never been overweight, I think I would be mystefied as to why someone would allow themselves to become overweight or obese, and would automatically conclude that there was some emotional or mental problem going on. (Actually, I’m pretty sure I’d be less judgmental, but I’m playing devil’s advocate with myself.)

    What I’ve learned though is, the struggle with weight will leave you with emotional scars – just the battering it can do to your confidence and self-esteem due to failure after failure is a doozy. Yet another chicken and egg scenario.

    I guess what I’m saying is, this will forever be a preaching-to-the-choir kind of issue. Those of us who have struggled with weight will always be intellectually and emotionally curious, and open to new ways of trying to understand it. I also include anyone who is just fascinated by the science of the subject. But people who are thin, and will always be thin, will find it easy to scoff at anything other than, “For God’s sake, put the pizza down and go for a walk.”

    I don’t think this is Gary’s area, and he seems to have been reluctant to get into it, but I would love to know how the so-called “carbohydrate addiction” and just addiction in general, plays into this. After all, even after arming ourselves with the fact that lowering carbs will help us lose weight, most of us STILL find it extremely difficult to do – emotionally and physically. Induction Flu is not for wussies!

  17. Steve O says:

    The Ornish Diet is considered a tasteless bland diet devoid of grains and fat right? Why is it that this diet doesn’t beat out the Atkins diet when it comes to weight loss and maintenance? What about full-on starvation diets, they seem to be pretty unrewarding too.

    I just find this whole food reward thing weird to me at least. When I started to low-carb, my food was actually tastier than the processed stuff from frozen or fast foods. Since I started cooking foods my way, I dabbled into my own favorite spices, artificial sweeteners that are many times sweeter than sucrose (sucralose), and even mono-sodium glutamate. I started to excessively salt my food since I also learned around the same time that the whole sodium causes massive high blood pressure thing to be wrong also. I also wasn’t afraid of cooking things in saturated fats like tallow, butter, and coconut oil, since that is also another nutrition myth. I even switched from regular soda to diet soda (aspartame & potassium acesulfame), yet my body fat dropped to sub 10%. Now-a-days, artificial sweeteners are consumed way less yet I am still maintaining my preferred body-fat mass effortlessly; or in this case, not losing anymore weight.

    I don’t know; maybe I’m just an oddball.

  18. Michelle says:

    I have been sort of following this debate (as in, I believe I get the gist of what each of you is arguing, and am hoping I’m not missing any important details) and I feel absolutely compelled to make a simple comment:


    I am convinced that the carbohydrate hypothesis is, if not completely correct, then at least correct in many ways.

    As for food reward, and I’m tempted to bang my head on my desk when I say this, obviously it is correct too. We eat more when we eat tasty food than when we eat bland food. And, depending on the nutritional profile of this food, this can cause weight gain to some degree (or not, if you’re lucky – depends on your set point and your metabolism).

    All of these people across the internet have the same story. Paleo and/or low carb works. Usually there’s a plateau. Or perhaps a rebound, and then difficulty getting back to the preferred lower limit. Do you know what always works to fix this? Eating less for a few weeks. What’s one way to eat less? Eat food that’s less tasty. You can go the route of eating totally bland food. OR, you can simply avoid (via willpower – rather than eating unappealing food, which I would argue also takes willpower in a different way) a few treats or simply excessively large portions (a few extra tablespoons of cream, a few extra squares of dark chocolate, an extra spoonful of that delicious dinner concoction a la shrimp cakes on spinach cole slaw with coconut dressing – all completely legitimate foods, and all delicious). Many people just cut out nuts and bam, they’re losing weight again. Yeah, you could argue that there’s a problem with nuts themselves, but I’d say the dominant factor at work is that it’s just too easy to overconsume nuts.

    It is absolutely true that, to some extent, calories matter. Even eating a low carb, paleo diet, it is possible to consistently consume too many calories. Here is my n = 1 experience. I love eating low carb because it’s easy to not overeat. And even when I overeat, I don’t overeat that much. Cravings for snacks are gone. And it’s easy to put aside leftovers from dinner. It’s relatively effortless to maintain a reasonable weight. When I really started eating clean (fairly low carb, no vegetable oils, no processed foods, high fat), I achieved a pretty low body fat set point and was able to maintain effortlessly. I was living alone. Then I moved in with my boyfriend and his kids. Then I started cooking extra delicious meals more routinely and indulging in a treat like a bowl of yogourt with a drizzle of maple syrup and slivered walnuts for desert. I still used only legit ingredients, but just started eating a bit more. I gained a few pounds, then stabilized. I hypothesize that I simply reached a slightly higher set point and that my metabolism is still working to maintain that with a more rewarding and higher calorie diet. When I make the extra effort to not go overboard on calories for a week or two, I lose a pound or two, without fail. I haven’t gotten down to my lowest set point yet, but I also haven’t really tried very hard. I’ve been happy eating delicious food and being a couple of pounds heavier.

    This is a long explanation, but I feel there’s a super simple point. Carbohydrates are super important in losing fat/maintaining weight and in controlling hunger. However, calories STILL DO matter. And it’s easier to eat extra calories (by a few hundred a day, say) when eating delicious food, low carb or not. And you probably still won’t balloon out of control eating a little extra tasty low carb food, but you also might not effortlessly drop weight to your desired point either.

    So, what I would hope is that you, Gary, would concede that food reward and overall calories consumed do play a role (you can’t just eat to your heart’s content and overindulge day in and day out), and then move on to getting to the real point, which is that it’s still the same hypothesis that everybody has been spouting and that it’s really not a practical solution to the problem. Carbohydrates play a major role and limiting carbohydrates is easy in the sense that once you stop eating them, you stop being addicted to them. Limiting the palability of food too probably works fine, but who in their right mind wants to actually do that? Yes, a few people have cut their connection with food, but I would say that most believe that eating is one of the joys of life. Also, a successful nutritional plan is about adherence, and I can’t imagine adhering to a bland diet. So the solution is to cut carbs, lose weight, ramp the carbs up to your happy level (a la Atkins), keep eat tasty food, and then watch your calories (much easier to do when eating lower carb) (or fast!!!) if you start to gain a bit of weight beyond what you’re comfortable with or have weight left to lose. I think if you admit that the food reward hypothesis is true and important, but just not all that helpful in solving the problem, then you’ll be way further ahead.

    ***Afterthought: if the argument is really that potato chips are more palatable than poached eggs with hollandaise sauce and bacon (or whatever), then I think the entire hypothesis is silly.

    • Greensleeves says:

      “***Afterthought: if the argument is really that potato chips are more palatable than poached eggs with hollandaise sauce and bacon (or whatever), then I think the entire hypothesis is silly.”

      Yes, Michelle, that is indeed the food-reward argument. Bacon is somehow “unrewarding.”

    • Alex says:

      I think Dr. Michael Eades sums up Stephan’s entire hypothesis with this: “The combination of oil and carbohydrate […] has a taste and mouth feel that humans love, and, consequently, are driven to eat too much of it. No one binges on butter (an oil) all by itself, but add some sugar to it, and you’ve got frosting, which everyone loves and eats to excess.” IMO, that’s all there is to it.

      My N=1 is that fatty starches are highly addictive… potato chips, French fries, crusty artisanal white bread slathered in butter, buttery croissants, etc. Not only am I inclined to stuff my face with them, the starch upregulates my appetite, and I end up eating more of all foods. But, if I have six eggs cooked in a few tablespoons of coconut oil or 8oz of steak with a few tablespoons of butter, I won’t feel hungry for six hours, and the hunger I do feel is the gentlest of impulses. Starch induced hunger, on the other hand, is voracious, and it drives me to overeat. It’s not a matter of palatability. Steak with butter is no less palatable than a large bag of potato chips. It’s simply that fatty carbohydrate is addictive while fatty protein is not.

      • STG says:

        Actually some of us have over-consumpted butter. I could eat a half pound of butter or drink a pint of cream or a quart of kefir. Processed or fast food has zero appeal for me, but I certainly can over-eat whole, bland real food. How does my behavior fit into SG’s theory?

  19. Donald Kjellberg says:

    I get ‘body rules’ and ‘brain rules’ but shouldn’t the real question be to as how food rules?! The consumption of food, whatever it is, entering the gut begins a symphony that acts on the periphery and the brain. Both are subject to the sequelae of food breakdown.

    Is it not possible the brain and body are both controlled by this exogenous influence and, over time digestion and its minions create a self-feeding cacophony stimulating both central and peripheral (dys)regulatory mechanisms until food selection changes or damage becomes irreversible?

    The brain and periphery both play critical roles in obesity, and both are dependent upon a much more powerful mechanism . . . food.

  20. Gary, I am so glad you are writing again in the blog. You know, I am not much of a scientist, most Plastic surgeons are simply not. We are very pragmatic (ie that nose job looks great or horrible) by nature–how you get there is essentially irrelevant. As I read this post a thought came to mind: (1) when I’m hungry, and I eat processed food, I am still hungry and I eat more (2) when I am hungry and have a glass of water nuts cheese or yogurt, I am not hungry. To me, this suggests that the brain provides motivation and continued motivation in response to the body’s hormonal signals via feedback loops. Point #2: I overeat, and I get fat. My medical student can eat ten candy bars and never gain weight. To me, that means overeat has little to do with the development of obesity. Point #3: My student is a gulf-Arab, who as you know, have the highest rate of type II diabetes because of their new western diet, we suspect. To me, calories still count, but the point isn’t obesity at all. If it were, then no skinny person would ever get type II, but they do. In fact my medical student has brother just like him (older) who is skinny and has it. I get the overeating part, but there is more to it. Thanks for such a great explanation. You have given me an excuse to get an iPad finally so I can read your posts! Look forward to the future ones!

    • dlm says:

      Re ten candy bars: I was a sugar-holic since birth and ate the equivalent of at least ten candy bars for over 20 years and did not gain weight. Then I quit smoking, gained weight, was diagnosed hypoglycemic and later diabetic type II. The weight fell off on a low carb diet (no starch, no sugar). I’m still addicted to sugar/starch and fall off the wagon with binges, regain some weight then have to lose it again with low carb. If I eat a slice of bread, I gain a pound. I was slim (with a thick waist) until the insulin could no longer handle the high glucose from the massive amount of addictive carbs I ate. Keeping relatively low carb keeps me diabetic drug free with HbAiC at 6 rather than 12 when diagnosed.

  21. Laura says:

    Unfortunately it seems to me that the food reward theory of obesity is being proposed without any real understanding of obese people – those with real weight problems and food issues. There is a real difference between those who want to lose a few lbs (whether they need to or not), and those with a significant amount to lose and other issues such as insulin resistance and food addictions.

    Regardless of whether food reward theory works for weight loss – for most people, the advice to ‘eat only a few bland foods for the rest of your life’ is simply unrealistic advice and impractical and unsustainable in the real world. Its like asking people to eat a low calorie diet long term – its very, very difficult to maintain.

    If obese people have difficulties sticking to the myriad of more palatable diets that are out there, including low carb, do we really think it is realistic to believe that in a world surrounded by palatable food, that an obese person with a carb addiction is going to be able to eat just bland foods – not just for the length of time it takes to lose the weight, but also after that for maintainence? In my opinion, this is just another example of a scientist being so very caught up in the science, that they forget that their supposed subject – the obese person – may have more than a little difficulty actually sticking to such a limited diet. And if a diet is not sustainable, its pointless – whether it works in theory or not.

    Anyone who has the willpower to stick to a bland, low reward diet, long term, either has no food issues at all, or has a drive and iron determination that most of us don’t have.

    As a very obese person, I believe that insulin is the major problem for me – eat low carb and I lose weight. However, I do think that there are addictive processes regarding foods such as sugar and flour which inhibit many obese people’s ability to sustain a low carb diet, and that some assistance with dealing with these addictive processes, in combination with a low carb diet is the key to weight loss.

    • John says:

      The food reward hypothesis addresses those who are significantly overweight and those who “want to lose a few pounds.” The problem that it addresses is appetite and food cravings. This has been shown in obese people who eat a very low variety (i.e., low reward), very low calorie (≤500 kcals/day) diet; these people both lose weight and report a decrease in appetite.

      The problem that you mention is the real problem of obesity and the one that Michael Pollan attempts to address. These highly processed foods (the same ones that are most likely to fit into the high reward category) are the predominant foods in our society. They are so difficult to avoid that, as you said, you need an iron will. Or you can do a form of low carb diet, which is “doable” because it allows you to eat some of the things that you enjoy (fats) but eliminates some of the things that are the most “rewarding” (refined sugars).

  22. Amber says:

    Thank you for the post, I found it very clarifying. Unlike Aaron B., it was not immediately obvious to me that hyperpalatability implies that excess calories are the culprit, but it is very clear in retrospect. As always, the real problem is what makes the body do what it does with a given amount of calories, and in my view this must be hormonally decided.

    MrFreddy’s experience is interesting to me, because I know of many people, myself included, who simply cannot lose weight, or often even maintain weight loss, while eating nuts or cheese. I believe Dr. Eades has addressed this point, and his take on it was that even on a low carb diet, calories count, and that these foods are particularly calorie dense. ( I don’t buy that explanation, though. For one thing, other, equally calorie dense foods, like rib eye steaks, for example, don’t seem to cause this problem at all. Second, some people have demonstrated that they can continue to lose weight on extremes of what should be excess calories, as long as these foods aren’t included. Finally, it begs the question of why eating these foods seems to break the normal, natural response to a LC diet of feeling satiated on an appropriate amount of calories.

    I don’t know an answer to this puzzle. I would be willing to entertain a reward-type hypothesis to explain it, but only if the mechanism involved a hormonal response. That they simply make one eat more doesn’t resolve the contradictions listed above. Someone else, and I apologize for forgetting who, once suggested in some blog comments somewhere, that it may have something to do with the chemical combination of starch and fat together in these foods — something that may be different from eating steak and a potato separately, for example.

    • BlueEyesSF says:

      gallier2 has your explanation, Amber – pasteurized, homogenized dairy increases your insulin. Raw dairy seems to do this less. Are you sure you’re not lactose intolerant or allergic to casein? Have you been tested? Have you eaten conventional dairy products and then tested your blood sugar? You should, you will find it enlightening!

      • gallier2 says:

        No, it was not me with the dairy explanation. I had a stab at the caloric density of cheese and nuts, that makes it easy to still overconsume. But one remark I would like to make to Amber anyway, she says “For one thing, other, equally calorie dense foods, like rib eye steaks, for example, don’t seem to cause this problem at all.”. That is imo erroneous, because steak is not very calorie dense, fresh meat contains a lot of water. J. Stanton of had an insightful article on that, not long ago.

  23. Geoff says:


    You’re really grasping at straws here. “Now, the brain could regulate fat mass directly by increasing, for instance, insulin secretion via increased stimulation of the vagus nerve, but Dr. Guyenet would like to dismiss the role of insulin in excess fat accumulation.”

    This is a straw man, Gary. Stephan’s point is not that insulin plays no role, his point is that it is a slave in a master-slave relationship. Stimulating the vagus nerve could be one of many mechanisms by which the brain drives up fat storage, but the point that it is the brain driving the increase in insulin, full stop. The analogy that Stephan has used in the blogosphere is that if body fatmass is a car, insulin is the wheels, not the engine, and certainly not the DRIVER; those would be leptin and the hypothalamus respectively.

    Of course insulin plays a role in fat storage, but only when the brain tells it to. When insulin is elevated by means other than the brain telling it to increase, we do not see the same effects. For example, take the LIRKO mice, who lack the insulin receptor in the liver. Despite 10x circulating insulin of normal mice, they are LEANER.

    You need to get out of here with the idea that the food reward hypothesis is in any way entrenched in the energy balance paradigm. Both your hypothesis and the food reward hypothesis are outside of the energy balance paradigm, the difference is that yours is a settling point theory and food reward is a set point theory. In my opinion, settling point theories have some explaining to do.

    While a settling point can explain how the body defends against fatmass changes in one direction, either up or down, it cannot explain how the body defends against both up and down. Specifically, your hypothesis has no explanatory power whatsoever for the observed experimental phenomenon that both lean and obese people defend against changes in fatness in both calorie restriction and overfeeding experiments. Your hypothesis explains why lean and obese people defend their fatmass in the presence of caloric restriction, and it even sort of touches the realm of plausibility as to how lean people upregulate energy expenditure in the presence of overfeeding to prevent fat gain. What it definitely does not do, however, is explain how an obese person upregulates metabolic rate to defend against gaining weight in the presence of caloric excess.

    So imagine an obese person, under your paradigm, doubles his portion size of everything without changing the composition of the diet. Under your hypothesis, the body increases the secretion of insulin as a result of this (since there are twice as many refined carbs in the diet), which then causes these calories to be stored as fat. Since the calories are not available to the body for oxidation, the body craves more nourishment, signals to the brain that it’s hungry, and causes the person to eat more, which of course is readily available to the subject since overfeeding is the goal here. What is being described is very obviously is a positive feedback loop, not a negative one. The result would be a massive increase in fat and a decrease in metabolic rate as compared to baseline. As I mentioned earlier, however, this is not what is observed. Instead we observe an increase in metabolic rate and a massive disconnect in the accounting between fat gained and calories eaten. We also see a quick normalization of the body when the overfeeding ends.

    “The alternative would be to suggest that the brain adjusts fat stores directly via hormonal and central nervous system mechanisms, and this leads to compensatory changes in energy balance. But then, as I said, we would have to discuss the direct peripheral effect of insulin on fat storage and fatty acid oxidation, and that’s not allowed.” No, that’s not the alternative, that’s the proposition. And it’s not that discussing the hormonal cascade is not allowed, it’s that it’s uninteresting because it does not sufficiently explain why we get fat or how to make us thin again. The brain is the causal agent, it regulates the hormones. When you want to build a car that goes faster, you may get a small amount of mileage from changing out the tires, but your real bang for the buck is going to come from tweaking the engine, or simply stepping on the gas pedal harder.

  24. The major disconnect in the SG description of food reward as the driver of obesity is that fat by itself, or fat and sugar, are not foods eaten in excess. It may be the case that fat+salt+sugar is the witch’s brew of obesity, but how could you prove that it’s not just the sugar? We don’t see depressed people sitting around getting fat on avocadoes and lard. “It’s the sugar, stupid.”

    The other problem I see with the palatability “conjecture” is that it does not explain the metabolic heirarchy the way the carb hypothesis does. The metabolism must deliver O2 to cells, or life stops; so breathing-distributing O2 is job one. Shortly after that in time priority is getting adequate glucose to the brain – when glucose levels get too low, the brain shuts down, life becomes tenuous at best when the brain involuntarily stops. So amongst the known variables of metabolism, I’d say that’s job two. In the event, though, that glucose levels get too high, we damage ourselves from glucose toxicity – not the long term damage of diabetes, the short term “lose your eyesight” kind of damage. I don’t know exactly where this is in metabolic priority, but it’s up there.
    My conjecture is that the carb hypothesis illustrates a system that operates well to sustain enough glucose but has an “emergency mechanism” that prevents blood sugar from getting too high. The emergency mechanism, when used chronically, makes us fat and sick over time.
    It’s possible that the palatability conjecture would also support what seems to me to be a rational metabolic priority scheme, but as yet, there’s been no effort to connect the two that I know of – perhaps because this is just another bit of speculation and there’s likely way to prove either of the two approaches without having to also prove the “glucose management priority” aspect.
    This bit of conjecture also explains why fructose may have a disparate impact on the body’s “glucose regulatory function” in that fructose consumption of sufficient quantity seems to interfere with the ability of the liver to regulate glucose disposition.
    Gary – is there anything in the literature that is relevant to the support/opposition of the above described “metabolic priority hierarchy”? In your view, is it a useful concept for framing an understanding of human metabolism?
    Thanks for taking time to post and respond to us, I very much look forward to the next post. Paul

    • Jim Stone says:

      Apolloswabbie, what’s your best guess about what would happen if you locked someone in a room with nothing but sugar water for a week? My guess is that they would lose weight (though, admittedly, I know of no studies demonstrating this). IF this guess is right, then it’s not *simply* the sugar.

  25. I wish I had a pound (dollar) for every time I’ve heard a scientist sneer at something as ‘mere journalism’. In fact, a good journalist (eg Michael Lewis on finance) can get us closer to the truth than any 100 mediocre scientists with their ‘research’ contracts funded by Big Pharma or Big Food.

    The psychology of scientists is also fascinating, in a grisly sort of way. As pre-school kids their mummies always told them they were clever little boys, and in high school they were clever little boys, and at PhD level they were the best brains in the state, or Europe, or whatever. So naturally they’re never wrong. About anything. Ancel Keys was never wrong, and look where that got us.

    • tess says:

      well said!!!

    • Jim says:

      Let’s not go the other way and claim that no PhD biochemical researchers have anything to add to the discussion either — or that they are all blinded by money or status, or locked into a paradigm. There are many good obesity researchers doing good work these days, and they are running many interesting experiments and discovering a lot of new things every year.

    • Michael Allen – the snitty research-scientist types interest me greatly, knowing as I do that the cutoff entry score for a BSc in most Western countries is significantly lower than it is for law (top percentile), medicine (top percentile) or economics (top 2nd/3rd percentile). Par contre, BSc entry routinely requires no better than top quartile. The ‘top’ students – those who go on to grad study – are brighter than the rest of the top quintile, but that’s not saying much.

      They strike me also as the type of person who derives a sense of ‘betterness’ from the acquisition of pointless but easy-to-acquire skills (e.g., chess playing – the iPad of mental acuity signifiers for the soi-disant ‘clever’ person): this also manifests itself in the tendency to stay one or two chapters ahead of the crowd in the “Important Persons’ Book of Obfuscatory Jargon”.

      FWIW (zero), I dropped out of a PhD in Econometrics (using on computer-based economic modelling and stochastic simulation to model investment behaviour… it’s even duller than it sounds.) I quit as soon as my scholarship stopped paying me to be a student, and went to work in financial markets (where the “Important Persons Book of Obfuscatory Jargon” dominates).

      Anyhoooo… I’m 46, 6’2″, 230lb, and have a VO2max of 46. I’m the same weight I was at 25, but slightly less muscular. I’m vegetarian (TEENSY dairy), relatively low-carb, quite high protein – but the turning point in my recent quest for lower bodyfat was really specifically eliminating SUGAR six weeks ago. (Bodyfat is the issue for me, not weight – I have been a six-pack lean 230lb in the past: I can lift heavy things AND do sums).

      Anecdotal evidence aside, one of the key things that this thread pints out is the tendency of people to flail around in search of some magic bullet – instead of doing the obvious (eliminating sugar, which is evil – the Lustig metabolic slides show that).

      It also seems that – in typically American fashion – a lot of folks latch on to some or other new ‘thing’ and become infused with the zeal of the converted. They get early results… then the results taper and they get disillusioned – at which point they begin to cheat. They TELL themselves they don’t… but they do. They yell from the rooftops that they don’t… but they do.

      Thing is, if you start the ‘Couch to 5K’ running plan and then stop, you can’t lie to yourself (you can also complete the Couch to 5K and still be quite fat – obviously-fit fat chicks run past me all the time). However if you start a sugar-free diet and then cheat, you can lie to yourself that you’re not cheating, or it’s only one Mars Bar. Or whatever..

      To me, the ‘new thing’ (the ‘palatability’ stuff) seems to be a moving feast (har har). It also seems – in the background – to continue to try to medicalise obesity, and to portray the obese person’s brain as somehow *different from* a lean person’s brain. And as we all know, *different from* morphs quickly to *inferior to*, and before you know it someone is offering a pill. Given the misadventures resulting from the American-led overdosing of teen males with SSRIs and other psychotropics (e.g., Ritalin), this is something about which we ought to be very wary.

  26. Jenny says:

    Does the following report confirm or deny the reward hypothesis, or is it totally unrelated?,0,5914182.story

    • GT says:

      Question is do the monkeys lose belly fat, as the LA Times says, because the cancer drug makes them eat less, or do they eat less because the cancer drug makes them lose belly fat. If the cancer drug kills the fuel supply to fat cells, which is interesting as cancer cells and fat cells have many metabolic pathways and characteristics in common, than that could explain the eating less. Something I’ll discuss in one of the coming posts.

      • Geoff says:

        The food reward hypothesis would say that the monkeys lose belly fat because the drug makes them sick, which based on very simple behaviorism mechanisms causes a dramatic reduction in the psychological reward value of the food. So foods that were previously hyper-rewarding; i.e. the combination of reward factors (various flavors, textures, temperatures, colors, etc) is such that it returns a reward value that is outside of the scope of anything that our evolved satiety mechanisms would be built for handling; are now no longer as rewarding. This reduction in the reward signaling in the hypothalamus causes a normalization of the setpoint. From there, the hypothalamus realizes that blood leptin levels are above the setpoint, and chooses to upregulate energy consumption via futile cycling, NEAT, etc. while at the same time reducing appetite. This setpoint normalization is what we see in the bland liquid diet experiments, for example. In my opinion, these experiments are first in a long list of empirical data that your body-centric view of adiposity fails to explain.

        Gary; I admit I have not read the study in full, so if they actually did accounting of fat cell numbers, this point would be moot; but I don’t think that the null hypothesis should be that it is the killing of fat cells that is causing the fat loss in this experiment, even though this is the proposed mechanism by which this drug is working. The way the weight loss is described in the article sounds like fat loss on a normal, paleoish type diet, which suggests a voluntary reduction in adipose tissue driven by the brain. The food reward hypothesis does a much better job of explaining the observed phenomena.

        • GT says:

          Well. let’s just say that we probably have completely different definitions of what is meant by “does a much better job of explaining the observed phenomena.”
          Plus we’d have to wonder what it is about monkey chow that is hyper-rewarding, assuming that’s what they got fat on. We certainly wouldn’t find it rewarding. Why would they? And if it makes them fat, for the food reward hypothesis to be meaningful, we’d have to demonstrate that it did so independent of the metabolic and hormonal effects of the monkey chow — the peripheral effects, as opposed to any central, food reward value type phenomena.
          Another obvious problem, also to be discussed in the coming posts, is the circular definition one. Monkey chow must be hyper-rewarding, right?, because these monkeys got fat on it. (Or on whatever they were eating?) And if they then lost weight, it’s because whatever drug they were given made the food less rewarding and so, what?, it lowered their set point, or it just made them sick enough to not eat it. Either way, I’m not a fan of that kind of thinking.

          • BlueEyesSF says:

            This just takes us back to the question of what makes food “rewarding” or “palatable.”

            My Chinese-born friends love duck feet. They could eat duck feet all day when we go out for dim sum. They find them rewarding and palatable. I however am of Russian extraction and duck feet freak me out. But I love the pork buns. I could eat pork buns all day. My Chinese friends think pork buns are just so-so.

            Isn’t this just cultural training and not something hard-wired into the brain?

          • John says:

            The animals were fed a commercial diet consisting of 28% protein, 12% fat, and 59% carbohydrate (LabDiet, Purina Mills).

            Part of the problem with differentiating the “high reward” from the “carbohydrate” theories is that foods that tend to be “high reward” are also foods that are high in refined macronutrients. You can’t separate these “high reward” foods from the carbohydrates that are implicated in Taubes’s model.

          • GT says:

            Just checking in quickly this morning and saw your comment John. Precisely. You may have negated the need for at least one of the coming posts.

          • Geoff says:

            “Well. let’s just say that we probably have completely different definitions of what is meant by ‘does a much better job of explaining the observed phenomena.'”

            Happy to take turns offering examples of empirical phenomenon that our respective working hypotheses do not explain. Here’s three for you to start on:
            1) Massive weight loss on an all potato diet in insulin resistant individuals.
            2) Bland liquid diets that are high carb and 20% sugar by calories get eaten at maintenance levels by lean people (2,000-3,000 calories a day) and at starvation levels in obese people (2-300 calories a day) when both are instructed to eat to satiety.
            3) Overweight “metabolically damaged” individuals defend against changes to fat mass in both directions. In overfeeding studies their bodies kick into overdrive and burn off most of the caloric excess.

            No amount of mental gymnastics will allow you to fit any of those observations into the carb-insulin hypothesis.

            “Plus we’d have to wonder what it is about monkey chow that is hyper-rewarding, assuming that’s what they got fat on. ”

            Well, that is what is interesting, and worth studying, but doing so would require acceptance of the food reward hypothesis. My armchair theory is that polyunsaturated fatty acids are inherently hyperrewarding, particularly linoleic acid. PUFA are essential fatty acids, meaning that we cannot produce them for ourselves and as such need to get them from our diet. However, they are not widely available in our environment. Ruminant fats contain only a small percentage of PUFA, somewhere on the order of 5% if I’m not mistaken. So it stands to reason that we could have evolved reward mechanisms that would reinforce the behavior of PUFA seeking without an upper limit since their availability in the natural environment is in short supply.

            “And if it makes them fat, for the food reward hypothesis to be meaningful, we’d have to demonstrate that it did so independent of the metabolic and hormonal effects of the monkey chow — the peripheral effects, as opposed to any central, food reward value type phenomena.”

            This shouldn’t be very hard to do. Swapping out saturated oils like coconut for PUFA shouldn’t cause significant changes in the metabolic and hormonal effects, particularly with regard to insulin signalling.

            “Another obvious problem, also to be discussed in the coming posts, is the circular definition one. Monkey chow must be hyper-rewarding, right?, because these monkeys got fat on it.”

            If the food reward hypothesis is right, then the fact that monkeys got fat on the chow diet would presuppose that the food is hyperrewarding. But that’s conditional on the hypothesis being correct. It’s no different from you saying that if carbohydrate content drives fat storage, then if the rats got fat then there were more carbohydrates in the rat chow. The carbohydrate content can be measured independently of the adiposity, just as the reward value can. Thus it is non-circular.

          • Warren Dew says:

            Geoff, how do you measure the reward value of monkey chow independent of adiposity?

      • “cancer cells and fat cells have many metabolic pathways and characteristics in common”

        This explains why fat tissue cancers are the leading cause of death in traditional Pima and the Japanese!

    • Mike Ellwood says:

      Oh boy. Let’s just sit back and wait for the side effects.

      Hell, I’d even go on Stephan’s diet, rather than “monkey” around with those drugs.

  27. Neil says:

    The food reward/palatability mechanism seems best explained as foods that we are very tempted to eat but will leave us hungry when our body realizes that it has not gotten the nutrients it had expected.

    You need to explain why we repetitively eat things we know will not leave us feeling full. This is where the food ward/palatability argument is really compelling. Our body should, in theory, have mechanisms that deter us from continuing to eat potato chips for supper. Yet we may be content to continually repeat that mistake. Because no one has adequately explained to the food reward/palatability community why our bodies do not learn from our repeated mistakes, they place the blame on the brain where it is easy to make an argument-from-common-sense that we confuse our wants and our needs.

    I found it illuminating to realize that this community focuses on everything that happens before we take our first bite.

    • moreporkplease says:

      “You need to explain why we repetitively eat things we know will not leave us feeling full. ”

      Ok, I will. It’s easy, actually.

      So I’ve grown up on the Standard American Diet and now have insulin on the high side, but I’m not really sick yet, so I don’t know it. Got that? Excellent. This is the majority of the American population now, apparently.

      My body wants 2200 calories a day. It tells me to eat 2200 calories. So I do – choosing the usual foods that help keep my insulin high – but because of my high insulin, 550 go straight to fat and stay there. I’m 550 calories fatter, but my body only got 1650 to burn. My body wants to access its fat stores, but the high insulin won’t let the fat out. So my body tells me to be hungry again.

      Yes, my body tells me I’m still hungry. It feels short those 550 calories. Ok, so I’m snacky and I grab 550 calories of snack food like pretzels or ice cream, which also helps keep my insulin up. But my high insulin promptly takes 135 of those calories and stuffs them into my fat.

      So now I’m 685 calories fatter, and my body only got 2075 to burn. My body wants to access its fat stores, but the high insulin won’t let the fat out. So my body tells me to be hungry again.

      Yes, my body tells me to keep eating. – it wants that last 125. This time I go for a cookie, which again keeps my insulin up. But again, the insulin stuffs 30 into my fat. Great!

      Now I’m 715 calories fatter, and that cookie wasn’t quite enough, because my body is an excellent calorie counter. It really knows how much it wants, down to a 1% margin of error.

      My body wants that last 95 calories, so I have a second cookie. My insulin’s ragin’ high. Again, I lose 24 into my fat. Now I’m 739 calories fatter, and my body got 2170 calories. But guess what? That final 30 on the way to 2200 is outside my body’s margin of error!

      So my body tells me that I want “just one bite” of my girlfriend’s cake. So finally I satisfy my body. I got my 2200 calories, and only had to eat 2939 to do so.

      Gosh, I wonder why I’m obese!?!?!? I only eat when I’m hungry, after all.

      • Neil says:

        Accepting all that as true, which I had accepted before I posed my question, it still doesn’t explain the mechanism that says “My body likes insulin, give me something that will drive insulin.”

        Having read GCBC a few times, as well as WWGF:AWtDAI, I’m still not seeing this answer, at least an answer that outlines the biochemical signaling for this behavior. If anything, I get the impression that many of the low-carbohydrate advocates have the attitude that we can just decide to stop eating carbohydrates, leaving out the discussion of what drives addiction to carbs. This seems to be the gray area that has been filled by the food reward/palatability crowd.

        I’m very interested in what biochemical signaling leads us to prefer a high-carb/low-nutrition cookie over a low-carb/high-nutrition hard-boiled egg. “Your body wants insulin” isn’t good enough.

        • Warren Dew says:

          I don’t think it’s biochemical signaling; I think it’s just habit, aside from second order effects. Once you go very low carb for a while, you do indeed prefer the hard boiled egg.

          • dlm says:

            Not me. I would and could never prefer the egg over the carb. If I could, I would probably not now have type II.

      • Geoff says:


        That would be a very convincing explanation, except that elevated insulin doesn’t actually inhibit lipolysis. Stephan offered evidence of this fact in the following post:

        • Neil says:

          Cue a Gary Taubes-like explanation that you have to take ALL data into account when coming to a conclusion. The more full your fat cells are, the less they respond to insulin. Fine. Fasting insulin isn’t a perdition of future weight gain. Fine. Omitted is a discussion of how much insulin is secreted after actually eating.

          It’s like diabetes doesn’t even exist in the world the author lives in. Fat cells become more insulin resistant, the body produces more insulin to cope, and eventually can’t produce enough to sack away blood sugar. So diabetics inject insulin.

        • BlueEyesSF says:

          “elevated insulin doesn’t actually inhibit lipolysis”

          Then please explain the widely known and observed fact that those who inject insulin gain fat quickly, often at the injection site. The insulin they inject makes the salted steak they eat later taste better? Geoff, you just can’t push up 1 study against the entire known and clinically observed understanding of diabetes. Diabetes really does exist. But you have no explanation for it.

          If the more insulin you have makes you thinner, then all the fat people and diabetics should just overinject themselves and lose weight! But we know that doesn’t happen in reality. Sorry, Geoff.

          I get that Guyenet and many of his followers scorn the fat, diabetic “broken people” but what can we do? Their issues are striking hard at your tax dollars. Guyenet’s “food reward” is no different than the scam “diet” called Sensa, where you eat “taste crystals” to supposedly change the taste of the food and thus make you lose weight.

          Except it doesn’t work. I know Guyenet would like to translate his food-reward addiction research into drugs that he can pop fat people on and make a killing. Maybe something like Naloxone.

          • Olivia Fischer says:

            You didn’t hear he’s come out with an electric shock collar that zaps fatties to recondition the reward value out of their food?!

          • BlueEyesSF says:

            “You didn’t hear he’s come out with an electric shock collar that zaps fatties to recondition the reward value out of their food?!”

            Precisely, Olivia! 1,000% agreement! Not only does the “theory” boil down to calories in=calories out, it also reeks of disdain for diabetics and the overweight. How dare those bad, lazy, nasty fatties enjoy their food? How dare they have a big body instead of focusing on their brain? The flesh and pleasure of fat people is somehow disgusting – this taint hovers over Guyenet’s work like a bad smell.

          • STG says:

            Scathing commentary–keep speaking up!

          • Geoff says:

            As I said, insulin matters, it has a physiological role, it just happens to be a role that is downstream of leptin and the hypothalamus. If we bring it back to my car analogy, cars cannot drive without wheels, period. And yes, spinning the wheels exogenously will cause the car to go faster. It still doesn’t mean that the wheels are driving the car, that would still be the driver who is pushing the gas pedal.

      • Alexandra says:

        I like this…. My personal experience shows that interrupting this process by very strickly limiting carbs works very well. I was nearly 300 lbs and stayed fat eating things considered healthy by today’s “experts”… oatmeal with cinnamon, slenda and almond milk for breakfast, whole grains, veggies, very lean meats and nearly no fats for lunch dinner and snacks. Though I would eat some candy, processed foods were mostly of the “healthy” variety: whole grain cereals, WW pastas with fat free marinara, occasional lean cuisine, etc. diet sodas only since Diet Rite, etc. appeared in the 70’s Eating out has always been a rare experience and never any pleasure in part because people tend to stare at fat people when they eat which I found difficult to ignore. I lived in a state of constant hunger and so overate these so-called healthy foods day after day with very little relief. I lost weight (tempoarily) a few times over the past 35 years through sub 1000 calorie per day starvation.
        Fast forward to a day four about years ago when I finally understood the concept of starving at the cellular level… From there I went low carb and then low carb paleo.. probably a natural progression for real food preferers like myself. 120+ lbs off in under two years which is maintained easily, I am never driven to eat between meals, I forget about food for hours and hours (bliss!) 2-3 low carb, high fat delicious paleo meals per day and I am satisfied and have no interest in the foods that are everywhere around us.
        I will follow along as the exact process is worked out, but the truth is, getting the carbs out of my diet has changed my life.. IT WORKS!

      • Warren Dew says:

        @moreporkplease – now if the Guyenet fans could come up with something equally clear for their conjecture.

  28. Gretchen says:

    Way back in the last century when I was forced to read in the history of biology in order to pass my qualifying exams, it struck me that whenever there was a big controversy in science, for example debate about spontaneous generation, it turned out that either both sides were wrong or both sides were partly right but missed the essential truths.

    Oten they missed the truths because technology was not yet able to detect the things they needed to know. For example, it’s difficult to see viruses when you don’t have electron microscopes.

    Is it not possible that some yet-undiscovered hormone or hormones will turn out to be the key to obesity? Leptin plays a role in all this, and leptin wasn’t discovered that long ago. Why do we think we know all there is to know about metabolism?

    So I it’s possible (I think likely) that both these theories are partly right.

    Also, there are different types of obesity. As illustrated in Gary’s book, the problems of a person who is skinny in the upper body but obese in the lower body are obviously not caused by food reward, or eating carby foods, for that matter. The cause of obesity in the person who has been overweight since childhood is likely different from the cause of obesity in the former athlete who stopped competitive swimming but kept eating massive meals, which is likely different from the cause of obesity in the woman who just went through menopause and puts on weight with no difference in lifestyle.

    Appetite and calorie intake obviously play a role. You don’t see a lot of fat people in concentration camps even if they eat nothing but bread. The few children who turned out to have genetic lack of leptin ate constantly until given leptin injections, when their appetites returned to normal and they lost weight without being on diets.

    Insulin also plays a role, as illustrated by the fat deposits that occur in people who inject insulin and the fact that most people lose weight on LC diets and the other arguments presented in Gary’s books.

    But some people can pig out on nothing but junky, carby foods and never gain an ounce. Obviously neither insulin nor calories are the whole story.

    And people eat for different reasons. Some eat because of real hunger; others because of appetite and access to appealing foods. Others eat more than they want because they were raised in the Clean Plates Club. I eat when I’m bored. Some people eat when they’re unhappy. Some people eat when they’re happy. And so forth.

    I don’t think there’s a single cause of obesity.

    I do think that progress in obesity research would be faster if we didn’t permit genetically thin people to do the research. They simply don’t understand the problem.

    • Mike Ellwood says:

      I agree with Gretchen that there are many reasons to eat. There is more to it than just hunger, and that is one of the few criticisms I might make of GC, BC, in that perhaps it underplays the psychological element in eating, which seems to be there to some extent (although I still think that GC, BC is essentially correct in its analysis, although I’m sure there is more waiting to be discovered). This does not mean I find the Food Reward theory convincing – far from it – but I can identify with boredom-eating, or worry-eating, for example.

      • Alexandra says:

        I used think there was something wrong with me mentally because I was ALWAYS hungry… once the carbs were gone, so was the hunger.. I am inclined to think I didn’t spontaneously become psychologically healthy in a matter of days…it was just the carbs all along. I wonder how many people, women in particular, are in counseling for their overeating problems when, for them too, it may just be a carb problem.

  29. I have lost 40+ lbs after reading GTs book ‘good carbs bad carbs’ and for the first time in my life have an ordinary B.M.I.
    My better half was sceptical but so impressed with the result that she also followed the books advice -she did not have so much to loose though. After a while it stalled until she read a book by Zoe Harcombe which suggested that if you cut out foods you crave [ low carb or not-the suggestion is that you are intolerant to those] you will loose weight. This for her has been the answer! Whether this adds to the food reward argument I am not sure?

    • Sam says:

      To me is just another version of eat less and lose weight. In essence all it is: If you have the will power to eat bland food, you will eat less and lose weight vs. if you have the will power to eat less you will lose weight. Trying to eat food with “low palatable reward” is harder for achieving long term weight loss success. Since a sustainable lifestyle modification is essential for long term weight loss and eating food you don’t enjoy for a lifetime is more a punishment that a lifestyle.

    • Olivia Fischer says:

      Yeast issues & weird appetites go hand-in-hand. I’ve witnessed it in people, cats, dogs and rabbits.

  30. Sam says:

    if one responds to a low carbohydrate diet (Gary Taubes’ diet) by reducing total caloric intake below maintenance one loses weight. Many people’s metabolisms and appetites and eating patterns respond this way.

    if one responds to a low carbohydrate diet (Gary Taubes’ diet) by increasing total caloric intake below maintenance one loses weight. Many people’s metabolisms and appetites and eating patterns respond this way.

    How is this different from the thousand books of the last hundred years that promise if one follows a set of rules they will lose weight, because following the rules automatically reduced caloric intake – and each and every one of those diets worked for at least a few people.

    While many of those diet books claimed “calories in and calories out don’t count”. In the end that’s what the rules did – they counted the calories implicitly for the people who could follow the ruiles.

    Even Taubes “supporters” like the Eades and Ferriss agree on this point: if one responds to the Taubes diet by gaining weight one must reduce calories. The diet has not worked to automatically count one’s calories, so now one must do it explicitly.

    So how is the Gary Taubes diet NOT a calories in and calories out diet?

    To say “you don’t count calories on Taubes” misses the point and severely mis-characterizes the other diets; very few “calorie counting” require one to weigh each and every ingredient and figure out the calories in the meal. Most introduce simplifications and rules and tricks and techniques to make the majority of the counting automatic.

    • Sam says:

      CORRECTION in the 2nd paragraph: replace loses with gains.

      if one responds to a low carbohydrate diet (Gary Taubes’ diet) by increasing total caloric intake below maintenance one gains weight. Many people’s metabolisms and appetites and eating patterns respond this way.

      • Sam says:

        apologies, it’s just another one of those days …

        CORRECTION in the 2nd paragraph:
        replace below with above
        and replace loses with gains.

        if one responds to a low carbohydrate diet (Gary Taubes’ diet) by increasing total caloric intake above maintenance one gains weight. Many people’s metabolisms and appetites and eating patterns respond this way.

      • Sam says:

        Some people eat more calories on low carb and lose weight others do not, but eating highly satisfying food that make you feel full for a longer period, make it easier to reduce total calorie intake and lose weight. That is a lifestyle change that can be sustained for life vs. being constantly hungry on a high carb calorie restricted diet or being hungry eating unpalatable food. Maybe all depends on how damage our metabolism is. You can lose weight no matter what the mechanism, that’s what really matter to the common folk. Taubes advice works in real life.

        • Mike Ellwood says:

          The point is, or the points are (IMHO):

          1, If indeed we do reduce calories on a low-carb diet (and I don’t count my calories, and neither does Dr Guyenet count my calories, so I’m not having him tell me that’s how I lost weight on LC), we do it unconsciously, without weighing and counting (or most of us do I believe – I certainly did).

          2. If we do indeed reduce our calories compared to our previous diets, how is it that we are accomplishing this without pangs of hunger? The Carbohydrate-Insulin thesis offers a plausible explanation for this. So far as I know, the Food Reward thesis does not.

        • Sam, nobody eats more calories on low carb and loses weight, unless they have a fat malabsorption problem. In theory this would be possible if a significant portion of fat and carb calories are replaced with protein and alcohol, but I’m thinking the compensatory reduction in energy expenditure brought about by passing out would compensate for any thermogenic advantage. 😉

          • Rose Smith says:

            Evelyn, that’s just not true. I was on a nutritionist’s 1,200 calorie a day regimen, high carb, low fat, and lost nothing. 220 when I started; five weeks later, 221 pounds. I was meticulously strict, to the point of being miserable and occasionally crying in my office from hunger. Plus working out a minimum of one hour every night. When I started the Eades’s Protein Power plan right after that, I was eating about 1,700 calories a day on average, and lost 30 pounds, while dropping my workouts to twice a week. I don’t think I have a fat malabsorption problem; I think my body handled the energy much differently. Now, I have no doubt I was “expending” more energy on the Protein Power plan, but not consciously, and definitely not through working out at the gym. Something completely out of my conscious control occurred.

          • Peggy Holloway says:

            On a low-fat, high-carb diet, I must eat at starvation levels to maintain my weight at a desired level. I did that for years, living on low-fat yogurt, salads with low-fat dressing, carrot sticks, and fruit juice and avoiding fat like the plague. I was constantly sick and by the time I was in my 40s, could not longer control my weight. On low-carb, high-fat, I eat whatever I want, steaks, cheese, cream, butter, etc. and although I don’t count calories, I guarantee I now consume higher calories than I used to eat by probably 1,000 per day. After 12 years of VLC, high fat eating, I have no trouble maintaining a normal body weight. Genetic nsulin resistance is real. It affects my family in many ways, including causing ADHD, depression, mood swings, “chronic fatigue,” and chronic high blood sugar (so-called type II diabetes) if we don’t severely restrict our carbs. Those of us who have adopted a low-carb diet (and that is most of my immediate family) have had spectacular results in terms of preventing obesity, mood disorders, and our familial “diabetes.”

          • @Rose Smith

            So.. you got enough calories to get out of famine mode, and stopped over-training? MAGIC!

            (Recovery’s where you make your gains.)

        • Alexandra says:

          I agree.. I have read both GCBC and WWGF and my take is that GT does not say calories don’t matter only that the real question needs to be: Why do we overeat beyond our body’s needs? For me the answer certainly lies in too many carbs of any sort.. That drive to overeat is gone when the carbs are kept very low. After losing over 120 lbs, I have easily stayed the same weight for two years now without ever feeling hungry and I have more energy than I have had since I was a teenager… I would enjoy knowing exactly why this is so but, luckily, it works without every detail of the process being known.

          • @Alexandra
            “luckily, it works without every detail of the process being known.”

            I agree w/ this completely. The attempt by some to require EVERYONE to be a bio-chemist is just confusing the public; everything most people need to know to be healthy is on the macro level.

  31. Olivia Fischer says:

    Yay, a post!
    The food reward hypothesis is a helpful for some/unhelpful for others….umm….(what’s a nicer word for “gimmick”?) It does not explain the world wide obesity crisis. Practically applying it to real-world experience as well as personal experience: my mother was a terrible cook, we ate terribly bland food, we were terribly poor, and we got terribly fat. Except my brother, but he was missing teeth with others cracked by adulthood . We were unhealthy; obesity was only a symptom. After I moved out and started to eat fast food everyday, I actually started to lose weight. Mcdonald’s everyday was a huge improvement over a diet based on: oatmeal/cream of wheat/toast/bread & jelly/beans/rice/pasta/tortillas/apples/bananas/flour-sugar based baked goods/sugar & corn oil. I was an adult before I ever had a steak and figured out the difference between butter & margarine and started to eat eggs again.

    Calorie count just doesn’t become relevant until grains like wheat & soy, and sugar are eliminated & nutrient dense high quality foods are added to the diet…which single handedly turns the Standard American Diet into “low carb” (normal, really). Then there are other things to address: like birth control pills, vitamin and mineral deficiencies, severe stress & sleep deprivation, and other medications. There are other foods that can also contribute to thyroid malfunction but I suspect that ties back into the leaky-gut intestinal damage by grains.

    After a period of time of eating real food — the body heals itself and the metabolism just starts working better and better and other foods can start being added back. One new food per week was Dr. Atkins’ recommendation. Speaking of someone with clinical experience who engaged in practical application of his theories…Dr. Atkins’ may not have had explanations for everything — but he recognized the wide categories from where problems could stem and provided tools to help people help themselves. (His explorations into vita-therapy were interesting too; like vitamin A deficiency & juvenile diabetes.) The system of starting off with 20g of carbohydrate a day, eating non-preservative containing meats, cutting caffeine & other drugs if possible, and eating lovely nourishing fat starts the normalizing process along. The one thing that didn’t help was the lack of warning about the severity of soy. I cut out all the wheat and replaced it with soy and ended up in almost the same boat (didn’t gain weight, but wasn’t losing it and had dry skin etc etc).

    One last thing: I think genetically modified mice can be used to prove or disprove just about anything.

    One more last thing: when are you tackling human-caused climate change theory?

  32. Mike Ellwood says:

    Hello Gary,

    As I understand it, you challenged Dr Guyenet at AHS with the charge (essentially) of only looking at evidence that supported his hypothesis, and ignoring any evidence that went against it, i.e. classic “bad science”. He should have defined his hypothesis in such a way that it could be falsified, and then gone about searching for falsifying evidence, rather than the opposite. One of the more important things to come out of GC, BC and your other writing, is your urge to overturn bad science when you find it. This is probably more important to you (I imagine) than becoming known as a second Banting, Mackarness, or Atkins.

    When Dr Guyenet first came out with this “Food Reward” hypothesis, I saw it as some kind of thought experiment – put up something for discussion – have it shot down, re-think it, refine it, etc.

    It doesn’t seem to have quite worked out that way, and it sadly appears that he has “married” it. It seems to be something he wants to make a name for himself with. I noticed he’d got a couple of volunteers to try it out. Both regular commenters on his blog, and both fairly young people I believe. I’d like to see him try it with some middle-aged and older people. I found it interesting that the one on the higher-carb diet was initially “RAVENOUS” (for about a week or two weeks, depending on which part you read). Well well, imagine our surprise! How does Food Reward explain that, I wonder.

    At the end of the day, the Carbohydrate-Insulin thesis explains quite a lot of the obesity epidemic, and your simple (if unoriginal) “remedy”, would probably help the majority of people so affected. It might not help those with severe hormonal disruption, and it doesn’t address things like dietary supplements which may or may not be relevant. But then, neither does Dr Guyenet’s. I’m sure there is still a lot to be discovered, but I’m sure that if simple low-carb were adopted throughout the western world, it would have such a substantially beneficial effect on health and weight, that it would free up a large number of resources which could then be devoted to the less tractable aspects of overweight and obesity (and ill-health).

    A good low-carb diet based on simple, natural ingredients can certainly be rewarding, and I look forward to my daily steak, butter, eggs, raw cheese, and optional organ meats, but I don’t over-eat them. I don’t go back for seconds, or thirds, as I might have done on my old mixed diet. I suspect I am still probably eating slightly too many calories though, one reason I have not yet lost as much as I would like to. As another commenter mentioned, I suppose I am a member of the “clean your plate club” – it’s how I was brought up, but I have also made myself a member of the “fill your plate” club – a bad habit brought over from high-carbing. I’m experimenting with slightly reducing quantities, and quantities of protein specifically (to reduce the insulin response). I don’t know if this will of itself help, but I am reasonably confident that I can do this without inducing undue between-meal hunger.

    I think nutritious food _is_ rewarding (in _my_sense of the word …. I’m not really sure I understand what Dr Guyenet means by that word … the goal posts seem to change on a regular basis), for very good evolutionary reasons. I’m not going to start being a puritan and I’m not going to stop enjoying my food. This (hopefully) doesn’t mean I’m going to be a glutton.


    • Alexandra says:

      Have you tested your BG after a high protein meal? I was so often reading that low carb can’t work because one gets a “massive” BG increase from eating protein too. I got a meter and tested myself under various protein alone, protein/fat combinations.. the average increase in BG was about 3 points 1 hour after eating, from around 85 to about 88.. hardly massive.
      You should try this for yourself.

  33. Jeff says:

    Some thoughts from a person while is neither firmly in the GT camp or SG camp:

    1. I think these theories are closer than we think since reward and carbs are very closely linked. While there may be many other ingredients that contribute reward I sense carbs trump the rest for the most part. Salt doesn’t hold a candle to HFCS or refined grains. Watching my children is a great example and not too far from animals. They will choose candy over bread, bread over potatoes, potatoes over veggies and veggies over meat. This is consistent withe nearly all I see. The carbs are simply more rewarding making most of this point moot in my mind whether the mechanism is body centric or brain centric.

    2. I think GT is missing the point on the reward theory. Other have said it, but no one is claiming that calories that needs to be controlled. In either case the behaviors are not voluntary. Saying it is “thinly veiled” restatement of the calorie balance theory doesn’t help the case since it sounds like SG and company are trying to slip one by us. I sense none of that and feel it is unfair.

    3. I have added back some sweet potatoes and potatoes and have experienced no negative changes in body composition. I remain at ~185# and~8% body fat as I have since getting to Paleo body comp in mid 2008. Small sample size, but works for me. It suggests that lumping everything as “carbs” and saying all is bad is reductionism. (I cringe whenever I hear “occum’s razor” for this very reason as GT did in his excellent book. It scream of naive reductionism. ) There are likely safer carbs and unsafe carbs and it could possibly be the proteins in the unsafe carbs are more of an issue.

    4. Refining and concentrating seem a major problem. Another kids example but they will prefer juice by far over real fruit and fruit strips over fruit as well. I think that we get a double whammy of reward AND higher carbs than we are able to handle with such foods and as such are problematic. Eating whole foods and avoiding the refined, processed and concentrated is a recipe for healthy living regardless the mechanism.


    • Mike Ellwood says:

      Kids preferring vegetables over meat?

      e.g. sprouts over pork crackling?

      I can remember enough about how I felt as a kid to know that I would have chosen the pork crackling (or beef, or lamb) and I still would, today.

      Body fat at 8%? Di d you get down to this from some much higher percentage?
      If not, then, sorry, we are simply not on the same page..

      Your metabolism was never broken.
      Good luck to you.

      I think Gary is writing to the likes of me, and we are (unfortunately) in the majority.

      Age, probably several decades or more older than you.

    • Margaretrc says:

      @Jeff, I don’t believe Gary or anyone else who thinks that the Carbohydrate Insulin Hypothesis is the better explanation of why we get fat is “lumping everything as “carbs” and says all is bad.” You are right, that would be reductionism. What he is saying is that some carbs–the sugary, starchy ones, are inherently fattening because of the effect they have on our metabolim–our hormonal control of adiposity. Non starchy vegetables and leafy greens have never been “bad” and no one would deny they are carbs. You are one of lucky ones to have suffered no ill consequences from adding sweet potatoes and potatoes back into your diet. Your metabolism wasn’t broken by years of eating low fat (and unrewarding, BTW) and high carb as conventional wisdom has advised. But many, many people aren’t so lucky and, for them (no, I’m not one of them, but my husband is) cutting the starch and sugar–the grains, sugar, bread and white potatoes–I believe Gary has the better answer. Eating unbuttered, unsalted potatoes is still going to send a diabetic or pre diabetic person’s blood sugar through the roof–I don’t see anyone in the FRH “camp” addressing that issue, and I believe it is a bigger issue in the western world than simple obesity. If you are just fat, you may (may) be unhappy, but you are not ill and, perhaps, you can lose weight with bland, unsalted, unbuttered, mush, though I remain skeptical. If you are fat and diabetic or even thin and diabetic (both happen), you are ill and at risk for heart disease and a host of other problems and that is not going to be cured by eating bland food–at least not bland high carbohydrate food. Bland, unsalted meat, maybe, but who needs to eat bland meat? You can eat lovely, seasoned, fatty meat and still get healthy and lose weight as long as you keep your carbohydrates low. That is a fact that has worked for countless people and is not explained by the FRH–at least not to my satisfaction–or conventional wisdom.

      • Margaretrc says:

        Sorry–a few grammatical corrections–I should have proof read better before posting: “for them (no, I’m not one of them, but my husband is) cutting the starch and sugar–the grains, sugar, bread and white potatoes–I believe Gary has the better answer.” Should read “for them (no, I’m not one of them, but my husband is) cutting the starch and sugar–the grains, sugar, bread and white potatoes–I believe is the answer, as Gary has said.”
        “host of other problems and that is not going to be cured ” should read “host of other problems and that are not going to be cured.”

  34. Hi Gary,

    The bottom line here is that Bauer was observing and trying to explain genetic obesity. He makes that very clear. How does this explain the obesity epidemic or all the observations you accuse Stephan of failing to address? It doesn’t because you have acknowledged from your earliest lectures (I’m listening to your 2007 Berkley lecture on YouTube) that there must be something environmental involved.

    From your own book, GCBC p. 362, Bauer discusses how genes act on endocrine organs and neural centers to regulate lipophilia. Sounds like brain ruling fat if anything.

    Also, in that Berkley lecture (Part 5: you discuss overectomized rats becoming obese. Either eat more or move less (when food is restricted) and become obese. You say this counters any CICO based theory of obesity. I would say the opposite, we just don’t have much if any control over basal energy expenditure. Next up you cite the case of hypothalamic lesions. These rats become fat. Talk about the brain rules! LOL. They aren’t changing up the usual high carb low fat chow fed these rats. They only took the brain regulation away.

    Ahh, things that make you go hmmmmm.

  35. Jim Hippard says:

    As a man who is down from 341 lbs (with full metabolic syndrome, type 2 diabetes, high blood pressure, popping capillaries in my retinas and taking the usual handful of medications daily) to 273 lbs over a 2 year period (no meds, good values across the board, more muscle and less fat and all systems continuing to improve) I am following this debate closely. I had tried the way of conventional wisdom (I was a Covert Bailey disciple) twice with good success but found that the dry chicken breast and broccoli with lemon juice diet coupled with 6 to 8 hours a week doing chronic cardio were unsustainable.

    Your book GCBC was part of a process that led me to eating somewhere between Atkins and Paleo, which I find easily sustainable; and I have achieved a healthy state at 59 that I have not enjoyed since I was 32. One of the big impacts of GCBC on me was coming to understand the implied response of “conventional wisdom” that my failures were a behavioral problem; that it was an emotional/mental defect on my part or that I simply lacked the discipline necessary to succeed. GCBC helped me see that it wasn’t me at all, but the fact that the King was not well dressed but indeed, butt naked.

    1. My gut reaction to Guyenet’s public presentation and blog made the basis of this debate (his challenge to the insulin hypothesis) is that his position directly follows the emotional/mental defect, lack of discipline part of the conventional wisdom paradigm of which I am an epidemiological study of one that says that paradigm is false. If I understand correctly the issue at point, the problem is caused by the impact of food on the brain versus the impact of food on insulin. Either way, my response is; show me the biological mechanism.

    2. Which in effect, Gary, is the same question you asked in GCBC and the lite version, Why We Get Fat. As you have said, and I paraphrase, there are many questions yet to be answered, but most of the answers that we have been given in the last 50 years about how and why we get fat are wrong. Guyenet says no to the insulin hypothesis but gives no meaningful biological explanation about how we get fat. Guyenet’s position does not give me answers or solutions. His is a soft fuzzy “no” to the insulin hypothesis that my own experience disputes. Do I hear the hum of conventional wisdom?

    3. Why is it that all of the people involved in this entire arena are little people, who from what I can tell from photographs are what I call lean. For years I have been directed by little people (e.g. Covert Bailey) who don’t have a clue what it is like to live in a large body. You, Rob Wolfe, Mark Sessions, Kurt Harris and Guyenet are perfect examples of what I am talking about. I have read and like all of you but you are all what I call little people. I was never sickly like Wolfe, a chronic cardio warrior like Sessions or an apparently conflicted materialist/doctor/investor like Harris. However, I was always big and eventually fat.

    4. My journey to good health began when I decided to ignore the advice of my doctors and the incessant cawing of conventional wisdom. I view Guyenet as a part of that noise; annoying sounds without offering meaningful solutions. I want solutions and I am hopeful for more information in that direction in your future responses to his position.

    Thanks for your hard work.

    a former big fat person.

  36. @GT

    “Curiously enough, I had a run-in with Professor Schwartz himself over precisely this issue back in March 2005 when I was reporting Good Calories, Bad Calories.”

    Should “reporting” be “researching”?

  37. Margaretrc says:

    The proponents of the food reward hypothesis say it’s not about taste, it’s about addictive quality of certain foods. Then they say if you don’t salt your meat or butter your vegetables, which to me means reduce the taste of the food, you’ll lose weight because you’ll eat less. Duh. Sorry, you can’t have it both ways. Either it is about taste after all, in which case, the French should, indeed, be fat, as should I because my food is very tasty–buttered veggies, meat with the fat still on, cream in my coffee, etc. Or it isn’t about taste, in which case, the “cure” shouldn’t involve making food tasteless. The carbohydrate-insulin hypothesis just makes more sense to me. As to the Kitavans and others who eat a high carb diet and do not get fat, a number of things can come into play. Genetics; glycemic index; low/no sugar or grains. All more easily explained with the CIH than FRH. But that’s just me. Until scientists get around to testing it, the only thing we can be 100% sure of is that conventional “wisdom” to eat low fat and watch calorie balance is wrong!

  38. Peggy Holloway says:

    I’ve been posting some of my family anecdotes over at Guyanet’s blog in response to his post about what causes IR, and the reactions have been interesting. The story about my sister following Weight Watchers (which is carbohydrate based) to a “T” and walking 4 to 5 miles/day which resulted in a 10 pound weight gain in 3 months was greeted with “that is impossible, so she must have actually been eating more than she claims.” I mentioned a range of mood disorders (depression, insomnia, chronic fatigue, bulemia, ADHD) that have been almost eradicated by family members who have gone low-carb/paleo which elicited a “mood disorders are related to IR?” Gary’s readers might be interested in going over there are seeing my posts and the “cognitive dissonance” they have engendered.

    • Margaretrc says:

      @Peggy Holloway, ““that is impossible, so she must have actually been eating more than she claims.” Isn’t that the usual reply by adherents of the calories in, calories out paradigm to anyone who follows it and is unsuccessful? It couldn’t be metabolic disorders brought on by too many carbs, oh no. It must be the person’s own fault somehow. That’s one of many reasons why I don’t buy the FRH. It is still a round about way of saying it’s the fat person’s fault. Sure, they pay lip service to addictive behavior and the person not being able to help it, but in the end, it’s about addictive foods making you eat more than you should and the way to solve the problem is to suck it up and eat unappetizing foods for the rest of your life. No thanks. Not when I can eat delicious high fat, low carb foods and lose weight or maintain!

  39. Elisa says:

    I’m really glad to see GT bring up the discussion about perspectives here. I agree that it’s difficult for genetically lean people to understand why other people can’t stop eating certain foods. I’d also like to bring up the importance of cultural perspective.

    I am Mexican-American and my culture is centered around food. My family gets together often and when we do, it is to eat. Most of those foods, I’ve come to realize, are proportionately high in sugar or carbohydrates. As a result, my family has a history of insulin resistance, PCOS, and diabetes. In May, I was diagnosed with hypoglycemia, which was causing me anxiety and depression. Although I was a healthy weight, it was a sign to me that I was becoming insulin resistant. It also made me realize the role of sugar and carbohydrates in mental health problems (which are also present in my family).

    Although I agree with the CIH, I think its implications are difficult for Latino – and other food-centered – communities. I’ve experienced this first-hand. For example, some of the staples in our family meals are bread and fried rice. It was easy for me to cut them out of my every day meals because 1) I was exposed to other foods after I moved away to college, and 2) carbs made me sick. But it’s been a struggle to convince my parents, aunts and uncles, and other members of my family to stop eating them, even temporarily until they become metabolically healthy again. Because not only are these foods addicting, but they’re also the center of our traditions.

    So, understanding obesity and weight regulation will also require a culturally-sensitive dimension in addition to the biology.

    • Warren Dew says:

      Maybe – or maybe we just have to suck it up and realize that eating correctly will require some cultural adjustment in the way of food. Certainly anyone who goes paleo, for example, is going to have to give up some culturally central foods – bread for Europeans, rice for Asians, sweet potatoes, potatoes, corn, beans, whatever.

  40. Jim says:

    I’ve seen at least three uses of the term “calories-in/calories-out theory”.

    A. A view that holds that in order to gain weight calories in must be greater than calories out.
    B. A view that holds that a calorie surplus is a salient proximal cause of gaining fat.
    C. A view that holds that the best way to lose weight is to try to reduce calories consumed and/or increase calories expended.

    Three things to note here;
    1. Almost everyone, including GT, holds a type A theory.
    2. SG and others hold a type B theory, but do not hold a type C theory.
    3. The type C theory is the real enemy.

    I loved many of the ways GT framed things in WWGF. His 20 calories a day thing is brilliant. However, the one thing that frustrated me most about the way Gary argued in that book was that he positioned himself against the “calories in/calories out” view. That choice of framing has led to a lot of unnecessary misunderstanding.

    I want to encourage all commenters to try to be more precise when using the term ‘Calories in/calories out view”. Otherwise we’ll be moving in circles, and failing to distinguish our friends from our enemies.

    • Martin says:

      >> A. A view that holds that in order to gain weight calories in must be greater than calories out.

      It’s not exactly what Gary says in his books. His main point is: carbs drive insulin which than makes fat cells accumulate free fatty acids and so other organs, including muscles, become undernourished. If you then stop eating, you’ll be hungry, but you’ll grow fatter. What will happen next is you’ll either eat more or reduce the activity level which will result in a positive calory balance.

      Hence fat tissue storing energy (fatty acids) and getting bigger comes BEFORE positive calory balance. You’ll get more calories in than out AFTER you fat tissue gets bigger and the rest of your body (musles, organs) become undernourished.

      • FrankG says:

        ANY focus simply on calories is redundant and unhelpful. The laws of physics require that in order to gain mass we have to be storing more mass/energy than we expend — not a theory… for all intents and purposes a FACT!

        BUT so what?!?

        It tells us absolutely nothing about WHY… and as generally interpreted, it is overused to berate those of us who are overweight… to beat us about the head with behavioural dogma and moral judgments that we are failing in the exercise of our will-power. Again NOT HELPFUL… other than perhaps allowing those genetically lean folks to feel smug and morally superior to the rest of us.

        It is ONLY when you start to look at the biochemistry driving what along the way is expressed as overeating behaviour that we can start to make some headway and help folks.

        “Calories in vs. Calories out” in ANY form is talking about behaviour — we need to focus on the biochemistry be that Refined Carbs + Insulin (which currently makes the most sense to me), Leptin + “Reward” or something else completely. So long as we stay focused on calories we are not asking the pertinent and (impertinent) questions needed to get to the root of this problem — questions for which the answers will allow us (as a society) to formulate a practicable solution.

        • Jim says:

          The reason I make these distinctions is because, in point of fact, they are causing confusion in this thread.

          And what I’m saying is that you should not take a Type-B theorist to be “beating you over the head” or blaming you for being fat. They do not. It’s the Type-C theorist who does that.

          Only type-C theorists blame the problem on conscious behavior. The other two are concerned with the biochemistry that leads us to eat more calories than we consume.

          I’m not advocating “focusing on calories”. But here’s the deal. Gary has framed the issue as “Guyenet advocates a CICO view”. If by that he means that Guyenet is a type-B theorist (which is the only plausible accusation in this context), then it does not imply that Guyenet is a type-C theorist.

          And that means that EVEN IF Gary is right that Guyenet has a CICO view (in the type-B sense), that does not mean that Guyenet is trying to blame the victim or that he is avoiding the biochemistry.

          This is an important distinction to take note of. I would guess a majority of the putative disagreement in the comments on this post have been due to people not understanding this distinction.

          • FrankG says:

            “…a majority of the putative disagreement in the comments on this post have been due to people not understanding this distinction.”

            Exactly… “Calories in vs, Calories out” has become a meme or a sound bite that everybody already understands as a behavioural dogma… so whenever it is brought up there is no distinction made — obviously we are overweight because we eat too damn much! You may see distinctions but you cannot arbitrarily list them and expect them to to be accepted by everyone one just because you say so… and why even try? How does it help to even talk about calories? What does it gain us? Accept the 1st Law of Thermodynamics as fact and lets move on to the real issues here, which are do with the mechanism(s) of abnormal fat storage — calories are just one of many other factors to be considered… they are not the most important.

          • Jim Stone says:

            Frank wrote: “You may see distinctions but you cannot arbitrarily list them and expect them to to be accepted by everyone one just because you say so… and why even try?”

            My distinctions aren’t arbitrary. I’m reporting on the ways people are already using the term in this thread.

            When Sam above asks: “So how is the Gary Taubes diet NOT a calories in and calories out diet?”, he clearly has sense A in mind.

            When Gary argues in his post that Stephan’s view is CICO, he clearly has sense B in mind.

            And when people talk about how CICO is a way of blaming fat people, they clearly have sense C in mind.

            And much confusion comes from not realizing that these three senses do not have the same meaning.

            For instance, the mainstream media accuse Gary of not understanding Physics, because they confuse his denial of type-B and type-C with a denial of type-A.

            Many people in this thread think Stephan Guyenet blames the fat person, because they confuse type-B with type-C.

            I typically tolerate vague talk — until it leads to confusion. Then it is time for distinctions.

      • Jim says:

        In writing this, you’re disagreeing with Type-B theories, not type-A.

        Type-A is indifferent to the causal order of things. It just says that, at the end of the day, mass gain (that isn’t due to water retention) will require that there is a calorie surplus as well. Gary does not disagree with this, and says so in WWGF.

        Gary does, as you say, claim that the causal order is that fat is stored first, and then this drives hunger or lethargy, leading to the calorie surplus. That is, he does deny that a type-B theory accounts for obesity.

        This is exactly the kind of confusion I’m trying to clear up.

      • Jim says:

        The comment immediately above is in response to Martin, not Frank B

        • Adam says:

          Hi guys,

          I’m a blogger and friend of Gary’s. My new blog, caloriegate, is precisely about this problem: i.e. how do we collectively move beyond the traditional (Type 3) CICO theory. Doing so does NOT require you to buy the CIH. You guys are right: we need to focus on MECHANISM(S). Non carb/insulin things can matter. Fine. Great. Bella! Food QUANTITY may play a role, too (as long as it indirectly or directly impacts the health of the fat tissue).

          We can kill the beast that is CICO without accepting CIH as the cure-all or even replacement. The “Lipophilia” hypothesis is an entirely different animal than the carbohydrate/insulin hypothesis. ENTIRELY DIFFERENT!

          And I think that’s why people like Gary are so perplexed and annoyed with this debate. It’s why I am.

          “Lipophilia” should not even be considered a hypothesis, since all lipophilia tells us is that we need to count all the different forces on the fat tissue, be they direct forces, like insulin or leptin or what have you, or indirect forces, like behavior. (for behavior to “count” as you’ve mentioned, it must ultimately translate into biochemical effects that change the fat tissue itself).

          It’s time for everyone in the Paleo/low carb community and beyond to awaken from the fever dream that is CICO and accept lipophilia.

    • Warren Dew says:

      The type B theories are the enemy, not just the type C theories.

      Why? Because you get the situations like Peggy Holloway alludes to above, when someone points out that they are on a starvation diet and still gaining weight, and Guyenet comes back with, essentially, ‘you must be cheating on the diet’.

      Now, if the type B theories were actually correct, this problem wouldn’t arise, except where the person was actually cheating on the diet, in which case the theory would imply that willpower actually was the ultimate problem. Since they aren’t actually correct, though, they just reinforce the prejudice against fat people.

      • Adam says:

        Agreed. Warren, your comment rocks.

        Type B and C both suck.

        CICO is a fever dream that makes as much sense as “The Earth is Flat” or “the stars are painted on a sphere around the Earth.” It sounds good because it seems to make sense, because we’re using caveman brains to intrepret phenomena. But apply just a WEE bit of logical thinking, and the entire superstructure collapses.

        a) It is PREPOSTEROUS and SCARY to me that people in the low carb / paleo world haven’t en mass accepted that CICO is complete insanity.

        b) If the low carb/paleo “community” ever wants to make any meaningful progress against the status quo (e.g. fighting back against “eating cholesterol gives you bad cholesterol” and other preposterosities), then it is ABSOLUTELY ESSENTIAL for us to destroy CICO ASAP.

        CICO is the Emperor to the Food Pyramid’s Darth Veder. Recognize that. And then ask yourself: do we want to destroy the Death Star that is the Food Pyramid/Plate or not?

        If the answer is Yes, then CICO must be your target.

      • Jim Stone says:

        Warren, it is not common for people on starvation diets to gain weight, regardless of which theory is true. If someone told you they were on a starvation diet and gained weight, wouldn’t you want to ask a few follow-up questions? Or would you just take their report at face value? I think it’s fair to question that claim — even if you’re ultimately open to it.

        That’s really beside the point here, though.

        Cheating on a diet isn’t the problem either. Cheating doesn’t imply that will power is to blame. The question still arises about why the person cheats.

        Either way, we who reject Type-C CICO want to find the biochemical cause of the eating behavior associated with calorie surplus (or, alternately, the sedentary behavior, or down-regulation of metabolism). Whether it’s the hypothalamus (as per FRH) or cellular starvation (as per CIH) providing the impetus to eat more calories than are expended (or to expend less), the point is that something outside conscious control is driving the behavior.

        Guyenet and Taubes are on the same side of that issue. Neither blames the victim, and both want to understand the biochemistry of the entire system that regulates adipose tissue (perhaps including brain circuitry).

        I get the feeling that many people here are in tribes, and one tribe must win and the other be vanquished. Why can’t we all be on the same side — the side that aims to get a full understanding of all factors at work, and that tries to come up with hypotheses that account for as much of the phenomena as possible — adjusting as new considerations come into play. The biochemistry of metabolism and human behavior is immensely complex. We aren’t required to pick sides before we fully understand the situation.

        I don’t see why the FRH threatens any low carber. In fact, it seems to me that it actually gives you a new option to try if you’ve stalled on your low carb diet. Just try a lower reward version of low carb, and see if it does anything.

        • Adam says:

          Hi Jim,

          Your posts strike me as really thoughtful. Your last 2 paragraphs, in particular, define a sentiment that I find beautiful.

          I was trying to sound a similar note when I wrote the mission statement for Caloriegate:

        • FrankG says:

          Jim said : “…it is not common for people on starvation diets to gain weight, regardless of which theory is true. If someone told you they were on a starvation diet and gained weight, wouldn’t you want to ask a few follow-up questions? Or would you just take their report at face value? I think it’s fair to question that claim — even if you’re ultimately open to it.

          That’s really beside the point here, though. ”

          This is precisely on the point I have been making above and a prime example of the wrong thinking that results from buying into “Calories in vs. Calories out” AND how such wrong thinking leads to value judgements about people such as “they must be telling lies, because obviously if you eat less you will lose weight… how could it possibly fail?”

          Now let’s look at the biochemical explanation for why yo-yo dieting leads to long-term weight gain; where a person finds they have to eat less and less simply to stand still, let along lose weight — and I use the term “weight” rather than “fat mass” because when calories are restricted we tend to lose both fat and lean mass… which just adds to the problem…

          NY Times – Study Shows Why It’s Hard to Keep Weight Off

          original study… The New England Journal of Medicine – Long-Term Persistence of Hormonal Adaptations to Weight Loss

          • Jim says:

            Frank. I understand that caloric expenditure can fall in response to starvation. And I’m even willing to grant, for the sake of retuning to the main issue in Gary’s post, that Peggy’s sister gained weight on the “starvation diet” (though I think it’s completely reasonable to dig deeper on that one as well).

            My point is that Gary’s “Body rules vs. Brain rules” dichotomy is causing confusion.

            The question is not whether the organ that drives adiposity is in the body or the brain. The question is whether it’s reasonable to expect people to lose fat with will power while eating the same foods they are currently eating.

            Both Gary and Stephan say “NO”. You have to fix the diet and/or the food environment before you can expect people to have success losing weight.

            If you move the hypothalamus to the pancreas, and keep its function the same, does the food reward hypothesis suddenly become a “body rules” theory?

            If Gary had stated more clearly that the distinction was between “physiology rules” and “psychology rules” (instead of “body rules” and “brain rules”), then I think people could see that the FRH primarily seeks a physiological explanation, not a psychological one.

            This distinction corresponds to the one I’m trying to make with the three senses of CICO. Type-C is a “Psychology Rules” view. Type-B views like Guyenet’s are “Physiology Rules” views.

            The only reason I’m even bothering with calling Guyenet’s view a Type-B CICO view is because that’s the way Gary framed the debate.

            I don’t want to naysay Gary’s claim that FRH is a CICO view, because there is ONE sense in which that is accurate. Guyenet does claim that a calorie surplus precedes adiposity in the causal chain.

            But, in the most important sense, Guyenet’s view is NOT a CICO view. He does not claim that trying to cut calories while moving more is an effective treatment for obesity. Like Gary he thinks you have to understand the biochemical factors driving obesity before people will have a fighting chance.

        • Warren Dew says:

          It is quite common for people on starvation diets not to lose weight even though they are overweight. It has been known that failure to lose weight on starvation diets is actually a typical result since Ancel Keyes’ experiments on conscientious objectors in WWII. It’s legitimate to ask follow up questions in specific instances, sure, but it’s not legitimate to judge such assertions “difficult to believe” before asking the question, as Guyenet does.

          With respect to “sides of the debate”, Taubes and Guyenet are on opposite sides with respect to the key question: whether calorie surplus precedes adiposity in the causal chain. And on that question, the existing data largely backs Taubes and the carbohydrate insulin hypothesis. Guyenet’s food reward conjecture, in contrast, is so incomplete we can’t even tell what the relationship is between “rewarding” foods and “palatable” foods. At this point, he’s basically just speculating.

          Now, speculation would be fine if he didn’t use his speculation as a basis to attack successful low carb dietary regimens – but he does. Those attacks make it more difficult for those of us who try to help people understand how to implement these successful dietary regimens, because we have to waste time debunking Guyenet’s half baked speculations.

          As for the idea that everyone should be on the same side – if that’s the objective, go with the mainstream fat heart hypothesis and you’ll be on the “same side” as 90% of the population. Me, I’m going to go with what is supported by data and logic and actually seems to work – and from that standpoint, Taubes’ carbohydrate insulin hypothesis is useful and Guyenet’s ideas are counterproductive distractions.

  41. Edward Vytlacil Sr. says:

    Perhaps Jack Kruse’s blog post discussion of Reward Theory might be helpful:
    particularly his experiences with “WHY NEUROSURGERY DOES NOT SUPPORT REWARD THEORY?”

  42. Warren Dew says:

    Gary, if you are interested, I think I can explain some of what frustrates you Guyenet’s theory and its reception.

    There are actually two paradigm clashes at work here. One is the one between the calorie balance paradigm and the hormonal insulin paradigm. On this one, Guyenet is stuck in the “establishment” calorie balance paradigm, and you have the “new” paradigm. This part I think you already understand.

    There’s another paradigm clash in this community, though: between the biological mechanism paradigm and the evolutionary diet paradigm. And on this paradigm clash, your explanations are solidly in the “establishment” biological mechanism paradigm, while Guyenet draws a lot of support from people who are using the “new” evolutionary diet paradigm, who read his theory as a form of ‘we get fat today and not before because historically lean conditions have caused us to evolve to overeat when food is not in short supply’, – an intellectually very seductive point of view, albeit, in my opinion, mistaken.

    At an “ancestral health” symposium, the deck is going to be stacked against you with respect to the second paradigm clash. I think that may be part of what’s irritating you. I’m not saying you should change – I think we do need investigation into biological mechanisms, and not just an evolutionary diet analysis – but perhaps understanding that clash will help you understand what irritates you about the situation.

    On a separate topic, with respect to adding carbs back in, as mentioned above, I’d point out two things.

    First, if you eat a lot of meat, and it’s not overly fatty, you’re going to be eating a lot more protein than you need for tissue maintenance. Where does that extra protein go? Well, the liver processes into glucose. My bet is that people who add some carbs back in are actually replacing some of the protein with it, and from the point of view of the bloodstream, it doesn’t change the effective dietary glucose load.

    Second, relatively small amounts of anaerobic resistance exercise can consume relatively large amounts of glucose in the form of glycogen. The lactic acid thus produced is reprocessed in the liver, but may well be processed back into fatty acids rather than glucose. Thus, anaerobic resistance exercise, like weightlifting, can substantially increase the amount of carbohydrates on can consume without prolonged insulin elevation.

  43. xMenace says:

    I’m a body rules guy myself, and I’ve not been swayed.

    Might I propose another hypothesis; I promise I’ll keep it clean. I’ll call it for now the “submissive priority hypothesis.” One has to place the general conditions of western disease in the context of public policy; that is, ask what our leaders think is best for us. One could argue it’s what we think is best for us, and strangely, I think if a sensible person looked at all the issues, he or she might agree that living with obesity, diabetes, heart disease, cancers, and other western diseases might very well be acceptable. They are, after all, later in life developments, for the most part.

    Let’s face it. Healthy nutrition is not a high priority with our governments. You might think it should be, but there are trade-offs. In 2009 American governments spent $388.8 billion on food, through subsidies and programs. That’s over $1,100 a person. For a family of five, that’s $5,500. That money needs to be spent. If they don’t spend it on food, you do. Are you willing to spend an additional $1,100 per family member on food? The real fear is if governments don’t spend this money, people will go hungry. They’ll starve. People will die. That’s not good policy for a party trying to win elections. But now let’s say we leave these subsidies alone. Let’s focus on food quality. No more grains, no more sugars, no more junk foods. Where’s the food going to come from? Are we even able to convert many millions of grain fields into grass-fed animal farms? How many decades will that take? And if we do, you can count on prices rising. Let’s double that $1,100 a person to $2,200 a person. Your family of five now spends $11,000 more a year on food. World recessions, increasing energy costs, increasing pollution costs, decreasing standards of living. Where do we place food nutrition on teh policy totem pole? Obviosuly very low, and of course big business, the food conglomerates want it kept there.

    Whether you believe in body first or mind first, it makes little difference to most. Public policy that pushes cheap and plentiful food is the main driver of our problems. We are not going to fix anything until we overhaul the back-end systems.

    • Warren Dew says:

      I’d be thrilled to spend the extra money on food that is actually healthy, and have my taxes reduced rather than used to subsidize politically powerful agricultural interests that produce the unhealthy food that is subsidized.

  44. Peter says:

    But clearly it’s not just insulin release, it’s how your cells react to the insulin too. It’s insulin sensitivity and the amount of insulin released in response to a certain amount of glucose increase in the blood. We’ve all met a hot chick who eats whatever she wants and stays thin. We all know of a skinny guy who struggles to put on weight. I suggest their body is dealing with the carbs and insulin differently from others. Even though they are eating carbs, their insulin efficiently packs away the glucose and then drops, then between meals their insulin is low enough to release ample fat into their blood streams. So when people add back carbs when they have stalled on low carb, perhaps these extra carbs and extra insulin causes a hormesis response, as if they are a brief stressor such as exercise, in turn actually benefiting the way the cells release fat between meals by becoming more sensitive or by some other mechanism. Perhaps, the best thing to do when you stall on low carb is to increase your carbs for a month put on a little weight and then go back into low carb. At least, this is what I’m currently trying to test on myself. I stalled for two months so I decided to lift weights and eat more carbs for a few months. By having more muscle weight, i’ll look better at the same weight next time and hopefully my fat mass continues falling past the original point. If the guy who added 150g of carbs to his diet but lowered food reward had simply stayed low carb and lowered food reward and then lost weight, those would be more controlled variables than adding some carbs, lowering food reward and then losing weight. He did both simultaneously so it’s impossible to tell if the re-adaption to extra carbs has made his cells more efficient and releasing fat between meals or if his brain is now regulating him to eat less food and release more fat from fat cells somehow.

    Carb refeeding isn’t a new idea. Body builders have been doing cyclical ketogenic diets for years. Perhaps what they didn’t realize was the full extent to which they were benefiting fat loss from the short spike in carbs. The other thing is they have depleted glycogen when they eat the carbs meaning most of them will simply be converted into glycogen and stored in muscle rather than fat and stored in fat cells.

  45. Neal Paisley says:

    Good to see you updating your weblog. Had a doctor’s appt, and am down 25 lb, with bloodwork at excellent levels. Told doctor that I had stopped the statin meds 3 months prior, and he was of the mind I could discontinue them. Off one BP med as well. 15 more # to go. Thanks for the book, Gary.

  46. Daniel says:

    Okay this is how I see things panning out: susceptibility to food reward drives overeating past normal satiety signals initially (leptin and dopamine both interact at the level of the hypothalamus, probably can influence each other as Guyenet indicates). you get slight leptin resistance as food reward seeking behavior continues in our modern hyperpalatable environment. leptin resistance and growing fat cells’ inflammation begins to sustain your adiposity in a vicious cycle leading to obesity and more. in other words, your fatness partially sustains itself. leptin resistance (as written by Byron Richards in Mastering Leptin) precedes and causes insulin resistance leading to Taubes’ research on carbs. in other words, once (and ONLY if) you’re metabolically broken, then the amount of carbs may scale your weight up or down. but you’re already a hormonally “obese” person.

    despite many factors, the initial cause was the food reward susceptibility + hyperpalatable food leading to a chain reaction of leptin resistance/inflammation + altered dopamine functions in hypothalamus, sequentially then to insulin resistance (where carbs matter on the scale/severity of obesity). Does anyone think parallel to this?

  47. Jose Marti says:

    Only now I have been able to follow all this debate, but reading the lucid explanations provided by Mr Taubes I am stunned by all the publicity and relevance given to this Theory of Palatability. Guyernet with all his degrees notwitstandiing is no match for Taubes.

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  50. Greg Boles says:

    I am living proof that Taubes is correct. I ate whatever I wanted, including lots of carbs, but stayed lean. I went on prednisone for an illness and quickly gained 20 pounds, despite a vigorous exercise program and no change in diet. I read Taubes, watched my carbs and lost the weight in short order eating a high calorie meat-based diet while I remained on prednisone. An alternate hypothesis-I exercised less or ate much fewer calories-is exactly what the calories in, calories out crowd would posit. I know exactly what happened to me and Taubes easily explains it.

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  1. […] I am still in the GT corner. The food reward of SC just doesn't match up with my own experience. Catching up on lost time Dr K has said they have it both partially correct, but I suspect GT is closer to Dr K's with his […]

  2. […] In one of his recent posts, Taubes makes the distinction between body-centred and brain-centred theories of obesity (or you can think of it as physiology vs. psychology, one of his commenters points out). Taubes believes obesity originates in the body: In this paradigm, specific foods are fattening because they induce metabolic and hormonal responses in the body — in the periphery, as its known in the lingo — that in turn induce fat cells to accumulate fat. The brain has little say in the matter. […]

  3. […] and Stephan Guyenet replied. The sentences that struck me most strongly were offered by Gary, in this comment: [A]fter I first went very low carb I added back toasted pumpernickel and other low GI breads to my […]

  4. […] lays out a masterful defense of the Food Reward theory at his blog.  Mr. Taubes presents his side here, here, here, here, and here.  If you have a couple hours to wade through this, I’d start […]

  5. […] Catching up on lost time – the Ancestral Health Symposium, food reward, palatability, insulin sign… […]