Gary Taubes and Stephan Guyenet: Three Views on Obesity

In a post titled “Ancestral Health Symposium Drama”, Stephan Guyenet begins to expound his scientific differences with Gary Taubes.

Since my views differ a bit from both Stephan and Gary, I thought readers might enjoy a third view.

My General Perspective on Obesity

My view is that obesity is caused in the first place by malnutrition, toxins, and infections. Each can contribute in multiple ways:

  • Malnutrition can affect appetite and energy utilization. Micronutrient deficiencies will increase appetite, regardless of energy balance. Macronutrient deficiencies may also do this. The resulting increased calorie intake may be only partially balanced by increased activity and thermogenesis; fat gain in caloric surplus tends to be more weakly opposed by brain regulatory circuits than muscle loss during caloric deficit. Malnutrition can impair energy utilization by several pathways: for instance, loss of mitochondrial antioxidants may lead to oxidative damage that impairs mitochondrial health. Choline deficiency induces metabolic syndrome and obesity (see Choline Deficiency and Plant Oil Induced Diabetes, Nov 12, 2010). Long-term, malnutrition may induce methylation defects which affect epigenetic regulation of metabolism. These can be passed on from mother to child.
  • Toxins also have multiple pathways by which they induce obesity. For example, diets that combine fructose or alcohol with polyunsaturated fats are very effective at producing metabolic syndrome and obesity in animals, and food opioids affect the endocannibinoid pathways which can be important in obesity and appetite regulation. See Why We Get Fat: Food Toxins (Jan 20, 2011) and Wheat and Obesity: More from the China Study (Sep 4, 2010) for more.
  • Infections have also been linked to obesity. I’ve blogged about how adenovirus infections of adipose cells promote obesity (Obesity: Often An Infectious Disease, Sep 22, 2010), but another very important pathway is from gut infections to obesity. Briefly, gut pathogens release fat-soluble toxins which can enter systemic circulation, and also modulate immune function. Toxins from pathogens have been shown to induce metabolic syndrome in the liver, promoting obesity. Via the immune system, gut flora can promote obesity. I’ve briefly mentioned one pathway (in Thoughts on Obesity Inspired by Stephan, Jun 2, 2011): gut immune modulation in the gut has been shown to determine whether adipose tissue macrophages are in a pro-inflammatory or anti-inflammatory state. A pro-inflammatory state promotes obesity. Research into the many ways gut flora influence obesity is in early stages, but it’s clearly important.

Due to the diversity of factors which conspire to cause obesity, it is a rather heterogeneous disease. Its unifying character is that some combination of causal factors induces “metabolic damage,” such as leptin resistance, in a variety of organs, including the brain. Metabolic damage can affect both appetite regulation and energy homeostasis.

I’ve discussed Stephan’s views and food reward theory (Thoughts on Obesity Inspired by Stephan, Jun 2, 2011). Food reward theory offers a plausible explanation for many aspects of obesity. I agree that food reward is an important factor in obesity, but consider it one among several factors, and believe that different factors may dominate in different people. Also, it seems likely to me that food reward becomes a dominant factor in obesity only after some form of metabolic damage from malnutrition, toxins, or infections begins to affect the brain’s regulatory systems. In a healthy person a highly palatable diet might have little effect on weight for quite some time. Nor am I convinced that low food reward diets are necessarily the best approach for long term weight loss or for the health of the obese, though I do believe they are great for short-term weight loss.

Distinguishing my view from Stephan’s is difficult because the obesity-inducing diets used in animal studies are generally both toxic and malnourishing and highly palatable. The “cafeteria diet” of Cheetos and such – rich in wheat, sugar, and vegetable oil – is an example.

I haven’t previously blogged about Gary’s views, but I consider very low carb dieting to be an imperfect solution for good health generally. (NB: Low-carb, which I endorse, is for me 400-600 carb calories, very low-carb, which I deprecate, is <200 calories.) Ketogenic diets may be beneficial in some cases of obesity, but I believe they should still include some starchy carbohydrates.

The Exchange

Stephan has transcribed the Q&A between Gary and himself and offers revised answers. I’ll insert my thoughts:

GT: How does your food reward hypothesis hypothesis explain a culture in which mothers are obese and their children are starving?  Are the mothers eating Snickers bars and not sharing them with their children?

SG: The food reward/palatability hypothesis of obesity is not mine, it’s a hypothesis that originated in the 1970s, perhaps earlier, and is a major subject of ongoing obesity research.  I don’t expect it to explain every instance of obesity.  Obesity involves multiple factors, an important one of which is food reward and palatability.  That being said, you have to examine a culture’s food habits in some detail, both before and after a change in obesity prevalence, to determine if reward/palatability may have played a role.  I don’t know enough about that specific culture to judge whether food reward would have played a role there.

PJ: Famines occur in impoverished societies with disrupted social institutions. People in these cultures are driven to eat the cheapest calories, which are the toxic grains such as wheat. They also tend to be malnourished, especially during famines. Malnutrition and toxic foods can create the disease of obesity, especially in a suitable infectious disease context.  Once the disease of obesity is induced, periods of caloric availability lead to weight gain which may be defended during subsequent famines. This explains maternal obesity persisting during a period of food scarcity. The slenderness of their children is a result of the disease process not having had enough time to work. It may take decades for malnutrition and food toxicity to induce obesity in the child.

So the element of long-acting causal factors and history eliminates the apparent conflict between an obese mother and a starving slender child.

Because food reward could induce obesity in the mother prior to the famine which is defended later, and food reward may act differently in growing children, food reward theory may be able to explain the situation. But Stephan prudently allows for the possibility that other causes of obesity besides food reward may be at work.

GT: The Pima indians were obese in 1902, following 20-30 years of famine.  How would your theory explain this?

SG: The Pima were first contacted in 1539 by the Spanish, who apparently found them to be lean and healthy.  At the time, they were eating a high-carbohydrate, low-fat diet based on corn, beans, starchy squash, and a modest amount of gathered animal and plant foods from the forest and rivers in the area.  In 1869, the Gila river went dry for the first time, and 1886 was the last year water flowed onto their land, due to upstream river diversion by settlers.  They suffered famine, and were rescued by government rations consisting of white flour, sugar, lard, canned meats, salt and other canned and processed goods.  They subsequently became obese.  Their diet consisted mostly of bread cooked in lard, sweetened beverages and canned goods, and they also suddenly had salt.  I don’t see why that’s incompatible with the food reward hypothesis.  It is, however, difficult to reconcile with the carbohydrate hypothesis.

PJ: The Pima Indian story seems compatible with both Stephan’s and my views, since they ate a nourishing, low-toxicity, low-food reward diet when they were lean but a malnourishing, toxic, high-food reward diet when they became obese. It seems incompatible with Gary’s ideas, since the Pima ate a high-carb diet at all times. Thus it’s a bit surprising Gary is so fond of the Pima story. It weakens, not helps, his case.

GT: There are two possible hypotheses here.  The alternative hypothesis is that sugar and refined carbohydrate consumption changes the regulation of fat tissue, leading to obesity.  The studies you cited in which people lost weight by consuming bland liquid diets would have been low in sugar as well.  “We need an observation that can refute one of the two hypotheses”.

SG: The bland liquid diet in Hashim et al. that caused massive weight loss is called “Nutrament”.  It is 50% carbohydrate, 30% fat and 20% protein.  The primary three sources of carbohydrate in this formulation are lactose (from milk), sucrose (table sugar) and corn syrup.  The bland liquid used in the study by Cabanac et al. (Renutryl), which also caused weight loss, was high in refined glucose and sucrose.  I find this rather difficult to reconcile with the idea that sugar and refined carbohydrate are inherently obesogenic.

PJ:  It’s unclear to me what Gary’s “alternative hypothesis” is. Why are refined carbohydrates different from unrefined carbohydrates? Both may raise blood glucose and insulin levels similarly. If toxic plant foods are the problem, then he should say toxins rather than carbohydrates are the problem. If it’s the macronutrient that’s the problem, why does refining matter?

Stephan scores a point against both Gary and me here, but especially against Gary, since the liquid diets are fairly high in carbs. As there was some sucrose and polyunsaturated fat, this was not a non-toxic diet, and I don’t know if adequately micronutrients were provided – probably not – but on its face the food reward theory seems to work best in explaining this experiment.

GT: “How was it bland then?”

SG: The diet was a liquid formulation that (judging by the ingredients) probably tastes like powdered milk.  The subjects were drinking that for 100% of their calories.  That fits any reasonable definition of a low reward/palatability diet, regardless of the sugar.

GT: What about the Mexican-Americans in Star county, Texas, who were obese despite the fact that there was only one restaurant in the whole town?

SG: Again, you have to examine a culture’s food habits in some detail, both before and after a change in obesity prevalence, to determine if reward/palatability may have played a role.  I don’t know enough about that specific culture to judge whether food reward would have played a role there.

GT: How can we differentiate between altered palatability and altered carbohydrate intake as important factors in the rising obesity prevalence of industrializing nations?

SG: Increased carbohydrate intake is a particularly poor explanation for obesity in industrializing populations, as the majority of them (for example, most of Asia and Africa) are going from a diet very high in carbohydrate, to one that is lower in carbohydrate and higher in fat.  There are also a smaller number of cultures that developed obesity as they went from high-fat to higher carbohydrate, industrialized food.  Therefore, the ideas that carbohydrate or fat are inherently fattening don’t appear consistent with the evidence as a whole.  An alternative explanation whereby both fat and carbohydrate, as well as other factors, are important for reward/palatability, an excess of which contributes to obesity, fits the evidence better.

PJ: It seems to be easiest to induce obesity with a roughly equal mix of carbs and fat; both low-carb and low-fat diets tend to be less obesogenic. This result is compatible with Stephan’s views because carb and fat together are more rewarding than either alone, and with my views because carb-fat combinations can be highly toxic – for instance, a fructose-PUFA combination is more toxic than either alone; or carbs feed gut pathogens while fats carry their toxins into the body.

It is unclear how Gary would explain the evidence from both animal studies and human populations that obesity becomes more likely as high-carb diets shift toward more fat.

Of Glass Houses

Stephan is a model of scholarly virtue, so Gary’s challenge at the end of his talk was a shock. I thought Stephan’s original reply – “Thank you for the advice” – was perfect, but Stephan revises it:

GT: “I would just recommend in the future you should pay attention to populations that might refute your hypothesis rather than just presenting populations that support.  That’s always key in science.”

SG: People who live in glass houses shouldn’t throw stones.

Presumably Stephan is challenging Gary to address some of the populations who seem to refute his hypothesis: Asian populations that have become more obese while dropping carbs from 75% to 50% of diet, or the Pima who remained lean on a high-carb diet for centuries.

In other words, to seek a theory that can explain all phenomena, as a scientist should.

In general, I find Gary’s work rhetorically artful but not very helpful to scientific progress. He often neglects to consider the full implications of his own evidence. This is especially true when he ventures into molecular and cellular biology.

For instance, he uses genetic lipodystrophies to illustrate that fat storage can be a disease of molecular biology, rather than excess food consumption. Now, the mutations in these lipodystrophies are generally not in insulin, the insulin receptor, or even centrally located on insulin pathways. So the lipodystrophies show that other molecules besides insulin can be responsible for fat storage (or negative regulation of fat storage), and may be relevant to obesity.

But when he looks into which molecules might be responsible for obesity, he offers only one candidate: insulin.

More startling is his neglect of perhaps the single most important molecule in obesity, leptin. Stephan writes:

[H]e sent me a manuscript for his book Why We Get Fat and asked for my advice prior to its publication.  I explained to him that he needed to use the word “leptin” in the book, particularly when discussing animal models of obesity that are obese because of defects in leptin signaling (ob/ob mice and Zucker rats, for example).

This is just like his use of lipodystrophies: mice get obese due to mutations in leptin, but he doesn’t discuss the role of leptin, preferring to keep the spotlight on insulin.

I don’t want to sound harsh because I think Gary is on the side of the angels. He has done very beneficial work refuting saturated-fat-phobia and encouraging low-carb diets, which improve the health of nearly all westerners who adopt them (although the reason is probably reduced toxicity from wheat and sugar, rather than reduced carbohydrate calories).

But I think he would do well to be more generous to others. I was excited when he began blogging, but disappointed by his first post:

conventional wisdom … almost incomprehensibly naïve and wrong-headed … nonsensical notion … I’ve been consistently amazed at the ability of researchers … to accept some of the rote ideas … without seemingly giving it any conscious thought whatsoever, or without wanting to ask the kinds of questions that a reasonably smart junior high school student should ask if given the opportunity…. I don’t understand this failure of intellect … nonsensical explanations … he falls short, as he’s working outside his area of expertise … we’re being fed nonsense … we will typically pass that nonsense along … If the experts had ever been open to a little skeptical thinking from others or had they been appropriately skeptical themselves … What’s been needed (and still is) was for someone (a reasonably smart 14-year-old would suffice) to ask the obvious questions and then insist on intelligent answers.

I find such talk ungenerous; and ironic, because in places in that very post Gary’s own reasoning is unsound.

Biology is complex, none of us have all the answers, and a lifetime is too short to acquire all the answers. Since we have no choice but to live in glass houses, we should all be humble, and refrain from casting stones.

Leave a comment ?

108 Comments.

  1. Great post, Paul. Thanks for adding your perspective.

  2. Thank you for taking the time of writing this post, I appreciate your point of view!

    Paul, you seem very level-headed. May I ask if you perfrom some form of meditation?

  3. I’m going to post the same thing I did on Stephan’s blog:

    Perhaps everyone should go back to first principles:

    …the mobilization of fat from adipose tissue is inhibited by numerous stimuli. The most significant inhibition is that exerted upon adenylate cyclase by insulin. When an individual is in the well fed state, insulin released from the pancreas prevents the inappropriate mobilization of stored fat. Instead, any excess fat and carbohydrate are incorporated into the triacylglycerol pool within adipose tissue.

    I would hope the above quote is not controversial. Go back to understanding what causes insulin resistance and chronically elevated levels of insulin.

    Paul, your ideas about malnutrition, toxins, and infections could easily explain why we become insulin resistant. The fundamental scientific fact remains that insulin regulates fatty acid metabolism. If this is indeed controversial, then take it on with the medical biochemistry people. Arguing about it over the blogosphere isn’t advancing science.

  4. Hi Ben,

    My only meditation is upon how far behind I am in my work.

    Hi js,

    All true, and yet insulin is not the only molecule that regulates metabolism, fat storage, and fat release. Nor is insulin resistance the only pathology in obesity.

    If it were simple, obesity would have been licked long ago.

    Best, Paul

  5. I just viewed Dr Lustig’s talk at AHS, and he seems to have proven in some of his trials that insulin is indeed the overriding factor in energy storage and usage, in conjunction with a host of other molecules.

  6. I should have said, he seems to think he has proven…

  7. Paul,

    I have just received a script for 50mgs of Diflucan from my derm for my mild seborrheric dermatitis based upon this study:

    http://www.ncbi.nlm.nih.gov/pubmed/16918053

    She would not, however, prescribe me the cholestyramine. I plan on starting the Diflucan next week and I am about to order a massive tub of Chlorella. I am also planning to up my intake of NAC from 1200mg once daily to twice daily, Curcumin for liver, and lower my carbs just to get the necessary 150 grams of glucose. I got some Kolorex as well to add in there. I also plan on taking 4-6 tablespoons of Coconut oil a day and making sure I consume plenty of helpful plant foods.

    Am I possibly doing too much? Is my plan sound? I plan on going to a sauna frequently to sweat out as many toxins as I can, as well as begin a topical lotion with Borage Oil to heal the skin barrier as the fungus is killed off.

    My theory is, my folliculitis had a fungal component. The bacteria were not the problem, but the vast shedding of skin cells due to the damaged barrier and fungal overgrowth/immune response would cause any topical left on the skin to cause a massive clogging reaction, leading to the folliculitis. This is why when I cease all topicals, the folliculitis disappears but the skin flakes consistently, even when oily. Sweat also seems to sometimes make things worse.

    The Diflucan should eliminate the fungus on the skin, and the Borage moisturizer should repair the skin barrier… so even when the Diflucan is done, the skin should be able to protect itself with continued use of the moisturizer. I will wait to make sure much of the flaking is gone till I try the moisturizer. I am also considering topical VCO.

    The borage study I found is here

    http://www.ncbi.nlm.nih.gov/pubmed/20579590

    Not sure if my science is 100% sound here, but I am hoping this works. I plan on continuing the Kolorex for a bit, and working further on gut health with possibly some raw milk yogurt… kefir seem to make the dermatitis on my scalp much worse and I am attriubuting this to the yeast content, which yogurt is free of.

  8. Forgot to add that I am also up to 1 Iodoral daily without any of the acne side effects I had last summer when I attempted it! Have been on 1 pill for little over a month.

  9. Paul,

    It’s not about being the only pathology; it’s about the significant one(s). 80/20 rule: work on the first order effects first. Getting side tracked by higher order effects and edge cases seem like academic exercises.

    To be fair, I’m not accusing you of being side tracked, though. I appreciate your time in responding to me. 🙂

  10. Hi Bill,

    Your primary care doctor will probably be happy to prescribe the cholestyramine, he can justify it for lowering cholesterol. The dermatologist is reluctant because it’s not normally prescribed by derms.

    I’m not sure you want so much coconut oil, 2 tbsp coconut oil and some olive oil might be better. Olive oil polyphenols are antifungal.

    You have an interesting theory and I hope it works! Let me know. Also, great to hear about the iodine. Early on it triggers acne but in the long run it is therapeutic I think.

    Best, Paul

  11. Paul, you bring a refreshing perspective to the obesity puzzle.

    My suspicion is that, even for those who remove toxins and add appropriate nutrients, gut pathogens lurk, and thus people like myself find it difficult to lose those last 20 pounds. My hunch is that these pathogens are somewhat unique, due to long-term feeding on high amounts of fructose, wheat, and other neolithic foods. The immune system isn’t quite sure how to handle these guys.

    Although food-reward approaches ‘hack’ at the signaling between the gut and the brain, I don’t think they address the root cause. Or maybe it’s that I hope my long-term solution doesn’t include eating endless amounts of cold boiled potatoes.

    I am so looking forward to your posts on how to remove the obesity-promoting infections.

  12. Thanks, Paul. You already know where I stand. Both Stephan’s and Gary’s observations are not explained entirely, or even mostly by their mechanisms. Too much anticipated food being caused by consistent dopamine spikes and insulin resistance being caused by carbohydrate are not naming the underlying cause but that which exacerbates the underlying cause, that cause is probably what you have suggested, a body that doesn’t work to counter-regulate its functions properly, caused by inflammation, malnutrition, and however food toxins and infections tie into those or act in their own right.

    I will continue to advocate the approach that gets people on a path to the healthy and sustainable lifestyles that they should have been living all.

  13. Third sentence should read “too much anticipated food reward…”

    Last sentence should end in “along” 😛

    I just got back from the blood donor clinic and haven’t eaten yet. Time to get on that.

  14. Great post.

  15. Hi Paul

    I really enjoy reading your perspective, including your conclusion that we don’t have all the answers. I have found most people’s perspectives to be over simplified by their intense focus on one particular aspect of the overall complex issue of obesity.

  16. Paul, have you considered that food reward, combined with social influence (peer influence, marketing, what your parents now consider “food”) could be what sets people on a course for obesity as an initial cause?

    Then, when a tipping point of adipose tissue is reached, fat mass takes over, like a tumor and Gary’s ideas (hormonal disregulation) become dominant?

  17. Richard, I’d add the internal environment to that list around food reward – I became obese when I got depressed at 17yrs old and started eating for the dopamine hit. I’m sure that’s the time that tipped me into metabolic derangement – I was fit and healthy before that, but something fundamental changed and now it’s 30 years later and I’m still deranged (in so many ways, lol). Overeating, sugar, depression and increasing obesity became my ‘perfect storm’.

  18. Hi Kirk,

    Perhaps someday I’ll do a post “Infections: A Dominant Factor in Obesity.”

    Stabby, missed you at AHS. Next year in LA!

    Hi Jacquie,

    The more you know, the less you think you know.

    Hi Richard,

    It was great meeting you and Bea last week!

    I think that’s a good description of how it usually gets started:
    1. Food reward and peer pressure get people eating crap food.
    2. They’re poisoned and malnourished by the crap food.
    3. … Metabolic damage …
    4. Fat tissue starts growing, appetite cravings start, activity diminishes …

    But here’s the thing, I think they could make equally addictive, high reward foods out of non-toxic ingredients. Rice and glucose and butter/coconut oil snacks instead of wheat and fructose and vegetable oil. And I think the obesity outcome would be totally different.

    So I wouldn’t blame the food reward for the obesity, but the toxins.

  19. Erik La Gattuta

    Hi Paul: great post; I’m fascinated by the exchange of ideas precipitated by Stephen’s talk.

    In your book you mention that converting glucose to fat (as happens above 600 cal/ day if I recall correctly) is more stressful on the body than eating the fat directly. Presumably this is true even if the glucose comes from healthy starches.

    Is it possible that this conversion stress (on the liver?) could lead to metabolic damage, and ultimately obesity? Rather than, as GT proposes, simple post-meal insulin spikes; since it seems there is little evidence that this normal function is capable of deranging metabolism on its own.

    In other words, excess glucose–even from white rice or potatoes– becomes a toxin, as you point out in your application of the marginal benefit curve to nutrients.

    If you agree here, could you say more about how the conversion of glucose to fat stresses the metabolism?

  20. I was all ready to go to LA but the airport security wouldn’t let me on the plane. They said I had to ride in a kennel like a dog! The nerve. Maybe next year I can disguise myself as a baby.

    Such a good conversation here. I agree with your chain of events for why people start eating so much to begin with, they can’t get it out of their heads, and it is clearly biological. Cultural explanations for behavior too often try to exonerate themselves from having to explain why the culture is like that in the first place. There has to be a reason why people can’t stop thinking about food and can’t stop eating, and we can find a lot of instances of high availability and high palatability that don’t result in gorging. Classical France, for example. It is dubious that twinkies are more rewarding than traditional French cuisine, you’d have to abandon the normal definition of reward.

  21. Jacquie:

    Yea, I’d consider that part of the social/cultural axis. We face modern pressures that exceed or are too different from our evolution in small groups where you only account for 30-60 other individuals and have a real ability to influence the direction of the whole group.

    Far from a voting booth, or a public school with 1000+ students.

    This is great, and fancy meeting you too, Paul, and your wife. I’ll be recording a podcast about this controversy and a few others with Angelo of This Week in Paleo on Saturday. So all of this helps in my preparation.

  22. Great post Paul.
    I’m not completely sold on Gary’s or Stephan’s hypothesis either. I think you offer great additional insight which may explain why some of the cultures don’t fit any of these hypotheses.
    Thank you!

  23. Hi Erik,

    I don’t think glucose can cause obesity – not easily. The body’s ability to dispose of glucose is vast – almost every cell in the body can do it, and does when blood glucose becomes elevated. And blood glucose isn’t known to cause any metabolic damage until at least 140 – 160 mg/dl. Unless you have metabolic syndrome you won’t go over that.

    So I think you have to get metabolic syndrome first by other means, then glucose becomes a possible factor in obesity/diabetes.

    As far as high-carb stress, I think it’s much milder than the toxicity that causes obesity. A high-carb diet makes glucose more available to bacteria … exercises glycolytic pathways that help establish the cancer phenotype … and occupies liver resources that might be better used otherwise. But the stress is mild.

    That’s why I don’t object to Stephan’s higher carb consumption much. There’s not much evidence that high-carb is harmful, except the evolutionary evidence with which we open the book. Why do mammalian diets and breast milk consistently deliver high fat rather than high carb? There must be some selective advantage to fat.

    Stabby,

    Offer me a French dinner and I’ll be delighted, offer me Twinkies and … best not to say.

    Richard,

    Sounds like a must-listen.

  24. I wanted to add to my previous comment that in my own n=1 experience, that of the triad of repair, paleo eating, resistance training and IF, I think IF is heads & tails the most powerful.

    More on that later.

  25. Ancestral Health and still tweaking | Rethinking mental health - pingback on August 11, 2011 at 7:04 pm
  26. Paul,
    Thank you for posting this. I’m so enjoying your blogging!
    Sincerely,
    Michelle

  27. Interesting post, Paul.

    I think leptin resistance may be tied to high triglycerides … http://lowcarbage.com/blog/2011/04/07/leptin-resistance/ Many people with high triglycerides get them under 150 by reducing carbohydrates.

    For the carb counters who don’t count calories, Paul’s low carb diet of 400 calories from carbs is 100 grams of carbs (and 600 calories is 150 grams of carbs). At the higher part of that range, its still about half what the average American is said to eat.

    “Very low carb” at 100 calories is below the Atkins induction phase level of about 40 grams, or 160 calories from carbs.

  28. You offered a great insight saying “it seems likely to me that food reward becomes a dominant factor in obesity only after some form of metabolic damage from malnutrition, toxins, or infections begins to affect the brain’s regulatory systems.” It seems obvious maybe, but I think it really helps clear up our understanding of how food reward is affecting body weight and who it might pertain to.

    I do think you are the closest of the 3 so far, but I definitely agree with Stephan (and KGH in the comments over there) and I think your views are more or less the same and definitely not contradiction.

  29. “I think they could make equally addictive, high reward foods out of non-toxic ingredients. Rice and glucose and butter/coconut oil snacks instead of wheat and fructose and vegetable oil. And I think the obesity outcome would be totally different.”

    Interesting Paul… And, actually, similar to previous recommendations I’ve gotten from Mat Lalonde. In one of his seminars, in response to the question “what do I do if I like baking”, he offered this as a solution: use dextrose as a sweetener, coconut oil or butter as a fat, and coconut flour, thus eliminating the toxins both you, Mat, Kurt and others often refer to…

  30. Whenever people talk about simplistic mechanisms behind obesity, I always think of the Obesity System Influence Diagram:

    http://www.shiftn.com/obesity/Full-Map.html

    There’s a lot going on there.

    And it also makes me think of the answer given by Nigel Goldenfeld at Edge.org to the question, “What scientific concept would improve everyone’s cognitive toolkit?” His answer, in short, was that one should realize that complex systems are often best explained by a “web of causality” that cannot be boiled down to one single factor.

  31. Send me your extra Twinkies (or other “crap”), I’ll eat them when I have a few pounds to ‘lose’. Nice read, thanks for posting :-). Cheers–Mark

  32. Thanks for the review and thoughts Paul. When I was a child in the 1950’s, people in the US were eating plenty of what you are calling toxic foods, including lots of wheat, sugar, and crisco, in diets that were very palatable, but very few people were overweight compared to today. That doesn’t seem very consistent with either your theory or Stephan’s. However, perhaps a combination of the two theories makes more sense, with the recent rise of industrial convenience foods made from cheap low-nutrient foods that are made very palatable by additives such as sugar, vegetable oils high in PUFA, salt, and MSG but leave the body wanting more because of nutrient deficiencies. Maybe this is the recipe for obesity. Great for business profits by generating increasing consumption and profits, but bad for health.

    From my own experience in gaining weight, I suspect that MSG also interferes with normal satiety signals to increase over-eating and sugar and salt may also do that to a lesser extent.

    And then there are the paleo Venus idols. How did some paleo people get fat, as apparently at least some did? They were not likely eating much wheat, vegetable oil, or sugar, though they likely did have numerous infection related problems.

  33. thanks for the nice post.

    i honestly don’t find Twinkie (or a lot of industrial junk food)
    rewarding even palatable.

    maybe short term, eating bland food recalibrates the palate?

    but i really dread to think that i must eat boiled & unseasoned potato/meat/veg all the time in order to keep healthy & thin.

    regards,

  34. great post paul!

    @Hugh – wow that is a complex diagram that should deter anyone from trying to come up with an overly simplified theory.

    “it seems likely to me that food reward becomes a dominant factor in obesity only after some form of metabolic damage from malnutrition, toxins, or infections begins to affect the brain’s regulatory systems.”

    I disagree with that statement but I think you have it spot on with your later comment –

    “I think that’s a good description of how it usually gets started:
    1. Food reward and peer pressure get people eating crap food.
    2. They’re poisoned and malnourished by the crap food.
    3. … Metabolic damage …
    4. Fat tissue starts growing, appetite cravings start, activity diminishes …

    I think that the food reward concept is necessary to explain why anybody would favour eating nutritionless/poisonous food over nutrient dense healthy food. Imagine there are two plates of food to choose from – one has a plain boiled potato, a shot glass of coconut milk, and an orange; the other has a doughnut. the first plate is reasonable nutritious and the second is virtually devoid of micronutrients and contains many actively harmful ingredients (gluten, fructose, omega6). Many people will choose the doughnut and find it more rewarding as it takes advantage of our inclination to eat foods that are starch dense, fatty, sweet, and also contain exorphins (opiod peptides found in grains) which activate reward centres in the brain. Combining them all into a single food seems to amplify this effect. If the doughnut’s ingredients were presented as a plain slice of dry bread, a shotglass of vegetable oil and a pile of plain sugar then the first plate starts to look a lot more appetising.

    I think it is this manipulating of food to take advantage of human taste preferences to create superstimuli foods that are virtually nutritionless that leads uninformed people to make poor food choices. Regularly consuming these foods then leads to micronutrient deficiencies, metabolic damage, poor gut function, poor immune function etc which is why I think Stephan is justified in calling food reward a “dominant” factor in obesity as it initiates the viscous cycle. In the absence of industrially processed foods, people will generally make healthy food choices.

  35. I should add that I don’t think you can become obese by eating nutrient dense foods combined in deliberately rewarding ways. I like your idea of creating healthy rewarding food that can compete with unhealthy rewarding food. One of the reasons I find it easy not to eat junk food is because I genuinely find my own prepared meals just as rewarding due to deliberately manipulating different food combinations, ingredients and textures to maximise reward value.

  36. Paul,

    I think I still don’t get this food-reward thing. I mean, I read all of Stefan’s blogs regarding and still don’t get it.
    I have to agree with GT’s question on how in these famous bland liquid food studies (which don’t seem to be available online and we just have SG’s report on it) a drink can have 50% of calories from sugars and another one having only sugar-calories and nothing else, be bland?
    After thinking about what about caloric density? How high was the water content? How many calories per 100g of liquid? Was it calorie-dense like a classic coke? Or was it more like that glass of sugar water (just tall glass of water with 2teaspoons sucrose ~35 calories – it tasted sweet and “rewarding” still) I used to drink from time to time as a kid? Or less dense?
    Or with other words:
    What fills you up and satiates you more, a bag of potatoe chips or a big ass steak(matched for calories- check it out!) with a side of green beans?

  37. Hugh, wow … that’s an awesome infographic!

  38. Josh,

    taking of from your last post, I find it easy not to eat unhealthy foods (e.g.potatoe chips) because I stuffed myself with whole healthy foods (e.g.steak+beans+a potatoe if you wish) beforehand! There’s simply no space in my stomacch to even think about more food before I head to bed!

  39. I agree with you Franco. When you’re hungry, you can get cravings for “bad” food. So if you can make sure that, instead, you fill yourself up with healthy choices, the craving goes away. Stay disciplined with the healthy choices and full is full; your stomach doesn’t care how it achieved satiation.

  40. That’s kind of what I was getting at. When you are hungry and crave food, you have to use willpower to avoid “bad” food and choose the “healthy” food. This is an intellectual decision rather than instinctual. No species of animal in their natural environment has a discrepancy between what they instinctually crave and what is actually good for them – they would be weeded out by evolution. Through carefully designed industrialised foods, humans now have this paradox where what they crave is not actually what is good for them, it’s the exact opposite. This leaves two options – either use intellect and willpower to choose the less desirable healthy foods or try and make healthy foods just as desirable as the industrial garbage e.g. cook potato chips at low temps in coconut oil rather than at high temps in oxidised high pufa vegetable oils.

  41. Josh,

    I agree, great exposition.

    I think the key is to shift from crappy foods to nutritious, non-toxic foods. Making the healthy foods tasty is a better strategy than making them low in food reward, in my view and yours.

  42. Josh– right on 😀 I think I will try making those chips w/ coconut oil soon. Trader Joe’s has some Taro or Yucca chips that are almost there. They’re fried in palm oil. I wish they were fried in palm kernel oil, which I think is the better oil of the two. Sweetened lightly with cane sugar. I think this is probably not such a healthy’ish snack after all, now that I think of it 😉 there’s fructose and pufa somewhere in that fried mess. But man oh man, are they good.

  43. Whole Foods has potato chips fried in avocado oil for those experiencing withdrawal. My roomie said they were “okay.” I tasted one and couldn’t tell the difference between them and other chips I’ve had, but I’m no great fan of chips.

    Pam, I agree completely with Paul that when you’re well nourished, you’re never hungry. I’ve been following the PHD/cum supplements coming up on one year next month and can honestly say, I have no cravings and am never hungry.

    When I see one of my former nemises like hazelnut biscotti, while walking the aisles of the grocery store, I need only remember that I have visible ribs now and have moved down from size 16 to size 6, to smile and move on.

    Good luck.

    It took a while, but the trip is well worth it.

  44. Paul

    I am confident we can make food that are non-toxic but as tasty as the industrial crap. More tasty actually!

    I just think Stephans concept of rewarding involves stuff thats not even tasty but which we learn to like, thus affecting the brain like tobacco, alcohol, msg etc.

    It seems to me that many commenters seems to regard the reward theory simply as a flavour thing…

    Btw, how come alcohol is so rarely mentioned when obesity is discussed? I know I can only cut fat if I dont drink for a few weeks. Well, maybe thats just my liver working properly, but judging from the amount of alcohol consumed on average (12liter per year pure alcohol in Europe) it must have an impact? Also because so many people dont drink much at all, there must be a lot of people hovering around 20 liters mer year… or something…

    Anyways, thanks for your excellent blog!

  45. anand srivastava

    Great article Paul. And Josh added something very interesting to the mix.

  46. Josh – I like your example of breaking the donut down to its parts.

    Paul – I am somewhat skeptical though of the approach of replacing extra-tasty “bad” food with extra-tasty “healthy” food. That is the basis of many diet programs like Nutri-systems, Weight Watchers, etc…, though the definition of “healthy” might (or might not) be key.

    I think I see too much the way people balk at the idea of taking away their extra-tasty foods. There does seem to be something akin to addiction going on there.

    Maybe going to blander food for awhile can help “reset” this need for extra-tasty foods and help re-adjust the body to more healthy food reward.

  47. Hi Niclas,

    Well, the food reward concept is confusing. It has historical roots in Pavlovian psychology and thus it unites the general concept of attraction with those of addiction and associations/pattern formation.

    Just look at this thread; we talk about food reward being the initial source of attraction to crap food – here there is no addiction, just taste – but also a factor that makes the obese eat more than non-obese or have hard-to-resist cravings – thus a pathological condition.

    And Stephan does suggest low-flavor meals, eg lacking salt and seasonings, as an extreme weight loss program.

    Thanks for the suggestion to look at alcohol and its roles in health, esp weight regulation. I do think I need to do that. We are supportive of moderate alcohol consumption but we need to go into the pros and cons more deeply, and how they may vary across persons. The absence of an alcohol section is a big defect in our book!

    Shou-Ching and I drink about 2 bottles of wine a week, so 1 bottle per person, 375 ml * 52 per year, or 19.5 liters of wine/yr … so we’re right in your ballpark if your numbers are for total beverage … if they’re really for pure alcohol then I’m shocked how much people are drinking.

    Best, Paul

  48. Hi CPM,

    That’s very possible and that’s what’s exciting about the prospect of food reward theory being thoroughly investigated. It may be very helpful to those who have “addictive”-like alterations to the food reward system.

    There’s no doubt this is true of some people. But is it true of everyone? Erp’s addiction to hazelnut biscotti disappeared as soon as she substituted nourishing, tasty substitutes. Which pattern is more common? And if erp’s experience is the norm, then advising people to give up tasty food may backfire by causing them to stop complying with the diet.

    These questions have to be resolved empirically and I’m looking forward to the issue being tested.

    Best, Paul

  49. maybe gary taubes is wron about carbs - MESO-Rx - pingback on August 12, 2011 at 10:25 am

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