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 ?


  1. Paul, I’m not sure I’m following your reasoning in comment above.

    Rice cakes* aren’t an equally tasty substitute for biscotti. It’s just that I can pass up the biscotti because my body no longer hungers for them.

    Am I making any sense?

    *My son-in-laws describes rice cakes as tasting like cardboard that’s gone bad. 😉

  2. “Micronutrient deficiencies will increase appetite, regardless of energy balance.”

    I have heard this claim made in several contexts, but have never seen a reference to any evidence of this or an explanation of the mechanism by which this could occur.

    A quick googling reveals that some micronutrient deficiencies (such as zinc: can *decrease* appetite.

    Can somebody point me to a reference that supports this claim?

  3. Paul I’m always reading through your reactions to comments very carefully, a great additional source of info and ideas.

    Two questions

    After trying it for 6 months or so I reluctantly reduced the 60%-70% fat in my diet and increased safe carbs. So this intrigues me:

    “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.”

    How does it follow from the fact that x has a selective advantage (for reproductive survival potential) that x has an advantage for health-span? I don’t think it does. Think IGF1 and cancer for example, etc.


    You say: “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.”

    Indeed. It seems to me that reward theorists like Kessler and so far Stephan also fail to consistently distinguish between food reward in various senses. Minimally we would need a consistent distinction between the sense of palatability/ gratification/ satisfaction on one side and food reward in the sense of making you want more (of the same food/ of calorie dense food…)–often cooccuring but very different concepts.

    Once the distinction is properly made, it might become clear that reward theorists talk about reward in the sense of making you want more. In other words they talk about food addiction, –like you seem to do also to a large extent. Am I wrong in thinking that the approaches viewed through this lens are much more similar than they might appear at first sight and that the concept of ‘addictive foods/ pathways to food addiction–with obesity as one of the side effects’ unites them?

  4. So, it seems that the root cause is still not known. There’s ‘chronic elevated insulin/resistance’, there’s ‘food reward’, there’s ‘leptin/resistance’, and what I’m reading is that people are saying: Well only AFTER the metabolism is damaged do the above mentioned mechanisms give problems and/or rise in obesity.

    We’ve got a long way to go in understanding food and nutrition on how it’s related to bio-chemical processes/mechanisms in the body.

    I don’t have any alternative theories, but I would say that each individual should look at their own unique situation and assess what type of food they should eat that best suits them. (Wow, sorry to take the ‘sitting on the fence’ route).

    Regardless of what caused these metabolic derangements, once established either through auto-immunity, developed over a life-time, or infection, THEN I truly believe that one should highly consider the elimination of AT LEAST sugars and wheat…(but I say they need more than that such as that found in most low-carb way of eating).

    p.s. Don’t forget the importance of exercise for stress management etc.

  5. Stumbled across this today…

    Pregnant woman in Northern California have the highest bromide toxicity…

    While it’s probable that the human body needs a fairly small amount of Iodine…. for the modern human it is clearly theraputic to have more with the bromide toxicity. I was always a little skeptical of that idea as an argument for Iodine but it looks like it’s quite legitimate!

  6. Hello Paul. Why does everyone get so worked up?! Arguing why and how a toxic/frankenfood diet is harmful seems counterproductive. To me they are pieces of a very complicated puzzle and there is no smoking gun. Food reward is valuable to humans but harmful only when presented with a fake food and highly toxic diet. Macronutrients are seemingly unimportant with respect to dietary ratios except when in the absence of sufficient amounts of activity or what some call “exercise”. Weight gain has a lot to do with simple caloric balance/total energy expenditure. Harkening back to what you mentioned, when non-nutritive/toxic calories are eaten, the body/brain remains wanting and malnourished. Thus, extra calories are taken in in an attempt to satisfy the body/brain’s requirements for “optimal” functioning. Mix a sedentary life into all this (in and of itself independently harmful) and it is no wonder that syndrome X starts to rear its’ ugly head. Also, there are many hormones involved in metabolic signaling, not just insulin and leptin. It would seem that toxic foods are toxic foods because they bypass the body/brain’s normal signalling pathways or even worse, harm them.

    In all this, I didn’t hear mention the combination of PUFA, cortisol, and the adrenal system. To me, these may be major players that override all of the above (excluding wheat and all its devilish schemes to enslave humans worldwide). PUFAs seem to make all the havoc possible and their presence in human tissues must be limited. I still remember your post regarding saturated fat’s protective benefit with alcohol consumption (a known liver toxin). Now, if fructose shares similar metabolic pathways with alcohol, it would seem that saturated fats would offer similar protection with fructose consumption. Now, no one espouses excess alcohol consumption and the same can be said of fructose. However, if the PUFAs have been taken out of the diet, then modest alcohol and fructose consumption (fruits, some juices, and some added sugar to coffee/tea) would seem to be harmless. The reason I bring up cortisol and adrenalin is because both can be related to elevated insulin and both are obviously involved in the stress response (due to infectious burden, malnutrition, hypoglycemia, psycho-social stress, environmental, etc.). When faced with these daily stressors the PUFAs would be a detriment to all aspects of defending the brain/body from said stressors as they disrupt many vital hormonal signalling pathways, damage lipoproteins, make us more sensitive to sunlight, accelerate glycation, and less resistant to social stress. Lastly, simple sugars have a lower insulin response than do simple starches. So, if insulin is a major culprit in obesity, then this part of it does not make sense.

    Send me your thoughts please. I know my rant is a bit much but had to get it out.

  7. Twitted by Viellektric - pingback on August 12, 2011 at 3:11 pm
  8. Hi erp,

    Clearly we have to work up a tasty PHD biscotti.

    Hi Mitch,

    It’s an under-researched area, but there are fragments of evidence. I’ll have to keep it as a blog post topic.

    Hi donat,

    The primary determinants of the ability to reproduce are (a) can the organism survive? and (b) is the organism fit and healthy enough to outcompete rivals for mates? Both require success acquiring food which depends on health. So evolutionary strongly selects for good health.

    I think it’s a safe bet that if high-carb breast milk could make us as healthy as high-fat breast milk, some species would have a high-carb breast milk. I’m not aware of one.

    Re food reward, yes, I think there will be a synthesis between food reward theory and my own view. Note that food reward is primarily about what is happening in the brain, while my theory is primarily about external factors that cause obesity, and what happens in the body. So there’s not an obvious conflict.

    Mila, thanks.

    Hi Bill, thanks for that link. It’s a good reminder that environmental bromine may be widespread – another reason to supplement iodine.

  9. Hi Gabe,

    I’m not worked up. Just enjoying the discussion, putting my two cents in and hoping to learn something.

    I pretty much agree with your first paragraph.

    PUFA is very important in obesity, and there are multiple pathways by which it matters, one of which may be via adrenal hormones and function. I don’t talk much about adrenals because it is one aspect of the larger disease. Once you get into mechanisms within the body things can get complicated fast. Adrenal hormone levels can have diagnostic value, but since they have to be measured over 24 h because of the strong diurnal rhythm they’re not used much. I don’t know much about how to treat adrenal conditions.

    Fructose does share similar pathways to alcohol, and saturated fats to protect against fructose toxicity.

    Best, Paul

  10. Fascinating post and comments….

    Paul, not trying to stir things up or deviate from the GT/SG topic, but it seems like Gedgaudas’ views are somewhat different from the PHD re: carbs, especially starches. Do you think the research supports one more than the other, or is this more of a n=1, find what works for you, Richard Nikoley kind of thing? Maybe it’s different from one person to the next? Maybe one day there will be a DNA test that will inform people what their optimal macro ranges are?

  11. Paul
    regarding toxicity and gut disfunction, what are your views on mercury reduction in body?
    Some of the systems popularly promoted seem to be incredibly involved, not too mention, expensive.

  12. Hi Joyful,

    I think biology is similar for everyone, with diseases/infections being the largest source of individual “terrain” that affects which diet is optimal.

    Nora Gedgaudas is very focused on the mind – she has a clinical practice – and ketogenic diets work great for most neurological conditions. Remember, we live in a high-carb world and the 2% of people who have trouble running their brains on glucose will almost all have some kind of neurological/brain disorders that can benefit from or be cured by a ketogenic diet. So she is strongly oriented toward ketosis, fat, very low carbs.

    That’s fine, but as I said in my AHS review, there are people who will have mental health problems on a ketogenic diet due to protozoal infections like Toxoplasma. So I prefer keeping a general approach, matching macronutrients to our body’s needs as a base case, and then tweaking it as necessary to help the body fight infections and/or overcome other kinds of dysfunction.

    The other source of interpersonal variability is in the gut structure and the gut flora. So maybe we’ll have gut imaging and stool tests to personalize our diets.

    Best, Paul

  13. Hi Jay,

    Well, mercury is bad and best gotten rid of, but aside from EDTA chelation which has some risks I’m not aware of treatment options.

    Dr BG is writing a book (with her sister) on chelation therapy. Should be out late this year.

  14. Still trying to figure out what really helps one lose weight,be healthy,have energy and have lab results that are normal.

    Taubes-All he eats is protein. That works for him. It didn’t for me. It also is boring and he even mentioned when he started the diet he passed out on numerous occasions!

    Not a good sign. Broth to fix the problem? Not. Potassium. No way for me. I am not obese. I want to lose the 3 lbs that need to come off but also need a healthy diet!!!!I suffer from chronic fatigue and need energy! I gain weight easily! I do stay active and excerise..

    Sisoon–OMG!! Grass fed meat, organic veggies,sprinting etc,etc,etc…Now he has his own specific antioxidants and protein shakes…Are u kidding? BTW-If u eat like him (MArk Sisoon)you can get an awesome sun tan and do it without getting brown spots and wrinkles. Ok–tell my Dermatologist that and really who can afford the things he recommends?

    Moore Jimmy- LaVida Low Carb-Started out great..He promotes a low Carb,high fat and moderate protein. He advertised recently for Julians low carb. bread. Net carbs?? Is that healthy? I thought he lost weight on high fat,moderate protein and low carbohydrate? These faux breads are definitely not safe starches.
    Things change when you get famous.

    Primal Mind.Primal Body-Sorry, cannot spell her name. Good book. She is Primal. Everything organic.Grass fed animal protein etc.
    ( High fat,Mod. Protein,Low Carb.(from vegetables and berries, organic)Make sure butter and yogurt etc is organic from grass fed animals… She claims it is not expensive!!
    Are u kidding? Look what grass fed meats and organic veggies cost. MAYBE I am missing something?

    Jaminet-Good book. Love the variety. Love the fact that I do believe everyone needs to have some glucose to feel energetic and and look forward to their reward meal.Supplements are necessary for most of us and they have done their research which for most of us has proved beneficial.

    If u do IF (intermittent fasting) then u must consume fat. (coconut oil througout the day)
    How can I eat 400 calories of safe starch a day and lose weight?)..Not happening for me.

    That’s hard. It is very hard for obese individuals and woman in menopause.
    The authors (Jaminet) have admitted that it is not a weight loss book. It is a diet for people with health problems.
    I have admittedly some problems but I also need to eat and maintain or lose weight on this diet..The authors tell us to cut fat (to lose weight).Isn’t fat the basis of good health? Tallow,coconut,home made lard,butter.
    Shou-Ching,the Thai super market loves me because I am such a good customer!! I love all of the products that make your diet so special!

    Now, it’s time to eat. So if I limit the oil or fat..What am I eating to make me satiated,happy and see the scale move???
    (You said to limit fat if u want to lose weight)You also said to eat beef,lamb for the Omegas’s.These are more beneficial.
    I eat fatty fish once a week.So, if I want to feel satiated I need to eat more starches. I tried eating more protein it doesnt’t fill me up.

    I am not a dessert person but need to feel full after a meal.

    I do love both of you for giving us wonderful insight on healthy nutrition.

    I want to lose the few pounds,feel healthy and have normal labs when seeing my MD. Is that possible?

    Thanks for all of the great research!
    I still believe that Asians have a higher metabolic activity to process safe starches.
    If we look at all of the Asian cultures, as long as they stayed on their ancestral diets they remained slim.The ate small amounts of meat,lots of starches and veggies and limited desserts.

    Maybe I am missing something.

    Judy C.

  15. In my own personal experience, I lost lots of weight and stayed lean switching from a crap diet to a conventional wisdom healthy diet (whole grains, low fat) and daily exercise. A typical day of 1.5 C of oats, 1/2 banana, peanut butter, 1 C skim milk; chicken & brown rice stir fry; yogurt & apple with some almonds; lean protein, veggies. I ate some whole wheat bread, but preferred less processed. I find it very difficult to add weight eating more whole grains and protein – they are very filling to me. Definitely less toxins than the crappy diet, but more toxins than PHD.

    I lost more weight moving to VLC and only veggies for carbs, but not enough energy and generally not feeling as good. I think I was too lean. I appreciate the PHD minimum starchy carb recommendation.

    On PHD, I weigh more than I do on the CW healthy diet, but not over-weight. PHD is a more toxin free diet. PHD is less carbs, less protein, much higher fat than CW healthy diet. I suspect I simply eat more calories on PHD as it’s generally less satiating for me compared to CW healthy diet (PHD safe carbs less filling than whole grains; less protein is less filling) and fat calories add up so easily and while fat can be filling it seems food bulk is more filling for me.

    This is from a weight perspective. I “feel good” on both CW and PHD diets. I don’t think Mark Sisson leanness means healthy. For me, the theory is a PHD-like diet is most nutritious and healthy.


  16. Paul writes: fat gain in caloric surplus tends to be more weakly opposed by brain regulatory circuits than muscle loss during caloric deficit.

    Paul, I think I understand this, but if you have time, could you say it one more time in an illustrative manner?

    Thank you.

  17. Hi Judy,

    Yes, I think it’s possible to lose weight, feel great, and have great health markers. Have you read our “Weight Loss Version” post?

    If simple well-nourished calorie restriction is not working with the last few pounds, then I would like at gut dysbiosis creating abdominal inflammation, which causes the adipose cells to retain extra fat. Antifungals, probiotics, polysaccharide digesting enzymes, fermented vegetables are all good things to try.

    Hi Mark,

    Thanks for sharing. I think your experience on high-carb illustrates some of Stephan’s points, very high carb and low fat diets can be as good for weight loss as low carb high fat.

    Hi Michelle,

    Actually I hate to generalize about this because there are so many factors that come into play, and assertions like this have a lot of “other things being equal” caveats, but basically, if you intentionally try to gain weight by over-eating, it will be hard to force the undesired food down but your body will allow some weight gain without making you miserable; whereas if you intentionally try to lose weight by starvation, you’ll be miserable and hungry. So, to overgeneralize incautiously, weight is more strongly defended against loss than gain.

  18. Okay, that was helpful, thank you.

    Chiming in with others, this is a terrific thoughtful post. I’m grateful for your contributions, and I’m learning a lot, which is always rewarding!

  19. Paul,

    Great review and counter points! From my experience, I have been shocked that unlike all previous diets for the first time in my adult life I consistently, not just choose, but desire the PHD foods over the crap foods. I feel full and more satisfied as well as crave PHD tastes. Even my craving for a pizza with its wheat crust has reduced greatly after the first 3 months on PHD. On past gov’t pyramid diet, vegetarian acid/alkaline diet, and even a strict paleo diet, they seem to require a herculian will power to choose to eat “healthy”. I had to definitely choose the less food reward. I came accept this was just the way it is in life…until PHD. I definitely believe that if a diet does not at least match a person’s perceived food reward for the healthy compared with the bad foods, then that diet will fail long term after the short term will power wears out.

    To Judy,

    Just wanted to say that you definitely can lose weight on the PHD! I don’t understand the Jaminets conceding PHD is not a weight loss book. Their section on weight loss is the best advice I’ve found in years of reading diet info. I went from 250 to now 182 in 6 months! It seems to me you need to get more clear exactly what PHD recommends for weight loss. You seemed confused in your description of PHD weight loss. 400 cals? I now eat 600 calories a day of safe starches and continued to lose weight at 2 lbs a week. Remember, total calories is king and the PHD foods will satisfy at a lower calorie intake like no other. Also, you can add lemon in your water throughout the day.

    Lastly, thanks Paul for mentioning Dr BG’s chelation book coming out this year. I’ll look for it since my dad has used chelation a lot for his heart disease and seems to have had success using it.

  20. Hi Jay,

    Thanks, great comment!

    As I’ve argued in the past, I think food reward evolved to teach us how to be healthy, and the best strategy to lose weight is to make one’s self as healthy as possible. That means following natural food reward impulses, not a bland low food reward diet. It also means I do believe our diet — which we did optimize for health — is also the optimal weight loss diet.

    So I’m not conceding that we’re not a weight loss diet! I just don’t know how to prove it except via empirical evidence from people like you and erp. I need to start collecting these anecdotes on a web page.

    Best, Paul

  21. Paul, I am with you re food reward and evolution. I like this quote* re food reward gone awry: “People overeat Doritos because those foods are designed to trick the body’s beautiful ability to be able to self-regulate. When you eat primarily health-supporting foods you will recover those protective mechanisms.”

    To me, Stephan’s prescription is likely to be about as successful as either a strict LC or LF diet: initially lots of weight loss, but then struggles with longer-term compliance. At the risk of being a broken record, I think Yoni Freedhoff is spot on: it’s about living the life you love, not the one you’ll tolerate!


  22. Paul, what are your thoughts about anorexia? Do you believe many of the same mechanisms are at play—that is, malnourishment, food toxins, infections—disrupting the brain’s feedback loops (appetite, energy expenditure, fat regulation).

  23. What an EXCELLENT blog this is.

    This is among the first blogs I have seen to admit obesity and human physiology are both hellishly complex, with the unknowns being far greater than the knowns.

    Genuine science admits to uncertainty and vast unknowns.

    No one has a complete understanding of the mechanisms behind obesity or coronary artery disease. That would require a complete understanding of human cellular metabolism.

    You are much like Urgelt, my friend and mentor.

    Take care,


  24. Hi Judy,

    Losing those last few pounds are the toughest. One common cause for weight loss stall is prolonged calorie deficit where metabolism slows down too much to burn fat.

    Have you considered calorie cycling? … eating at a calorie surplus some days and calorie deficit other days, with more days at a deficit to lose fat weight. The idea is the calorie surplus days will rev up the metabolism to burn fat. Some randomness keeps the body guessing and continually adjusting.

    Resistance exercise can also help to boost metabolism.


  25. I think obesity is not bad for health if cause is food reward from non toxic food item. Because I think it will not cause visceral fat accumulation. Do you have any thought on that.
    I don’t know if any wide reliable study is done in this regard; Do you know any such study?

  26. I’d be glad to offer testimony confirming that PHD is a weight-loss diet. My own loss isn’t dramatic, about 15 lbs. in the past year.

    My primary health problem is sleep apnea, which I’ve had for many years/decades. It has led to high blood pressure and weight gain. It is not caused by my weight but rather sleep apnea caused me to gain weight. I’ve been thoroughly tested and know the reasons for the apnea and am recovering primarily by using a cpap breathing machine at night.

    PHD got my attention because it was primarily about good health. I started following it a year ago and can say that it has significantly improved my health. In addition, I also began to lose weight, a welcome side benefit.

    I follow the basic diet recommendations and take all the supplements.

    I get enthusiastic about PHD and tell my friends about it, but the most frequent response I’d get was that it may be great, but it means home cooking everything. I’d counter that home cooking isn’t hard. So finally I set up a small website that shows how I’ve done my own interpretation of a PHD meal plan and the home cooking that make it possible to do it during the week, working 50-hour weeks and making 2 or 3 meals a day for me and my spouse. I call it “10 minute meal.” It might be of use to others:

  27. Hi Vizeet,

    I am not sure that weight gain caused by food reward will be entirely isolated away from the organs and non-inflammatory. So I wouldn’t totally agree. But I think there will not be a dramatic weight gain without some kind of toxicity. So as a practical matter I agree.

    You can find more of my thoughts on food reward theory here:

    Hi Gary,

    Thanks for the testimony! Always great to hear success stories.

    10 Minute Meal is a great resource, I’ve added a link to the “Open Thread for Recipes” post (it was already in the blogroll.

    It does seem like the need for home cooking will be the sticking point for a lot of people. Hopefully food companies will be coming out with more PHD-compatible products and it will get easier. But once you get in the habit, cooking isn’t that hard, as you’ve shown.

    Best, Paul

  28. The PHD Food Plate | Perfect Health Diet - pingback on August 14, 2011 at 5:19 pm
  29. Hi,

    for most people i talk with, the sticking pointing seems “give up (or at least) minimize wheat”

    either they really don’t know what to eat anymore, or they’d insist that “surely there’s some wheat that is healthful!”
    (i.e. whole wheat) or “surely there is enough individual variation, i have had no problem with gluten….”

    i’d usually stop @ that point. (not wanting to be a food police)…


  30. Paul, I am also of the opinion that weight gain just by food reward is not easy. But some cultures did gain weight for short period (Like during festive season). And so I think without adding inflammatory food weight gain is still possible even in short duration.

    If you eat just at home chances are you are eating food that have similar basic flavor and similar environment and will not change your diet dramatically, but if you eat food at different peoples home at ceremonies chances are environment and food flavor may impact your diet and increase your weight.

    I do think food reward (alone) is not dominant factor in obesity but it is still an important factor and not necessarily always have association with inflammation.

    I know some animals like wild boar have large amount of subcutaneous fat. My thinking is in that line.
    So my question is — Is this possible in humans?

  31. Hi Vizeet,

    There are shared pathways between animals and humans, eg for hibernation and fat storage, which seem to be much less active in humans but nevertheless exist.

    It may be that part of the pathology of obesity is activating these more strongly.

    It’s an interesting question.

  32. PJ said: “If simple well-nourished calorie restriction is not working with the last few pounds, then I would like at gut dysbiosis creating abdominal inflammation, which causes the adipose cells to retain extra fat. Antifungals, probiotics, polysaccharide digesting enzymes, fermented vegetables are all good things to try.”

    THIS. I’ve never felt that the insulin hypothesis explained ( or fully explained) my weight gain. I did go low carb, but also completely gluten-free at the same time, as I discovered that I am celiac and also sensitive to soy. I gained all my weight eating a vegetarian diet that contained a ton of whole grains and soy (and veg oils).

    Always had gut problems, even as a child, and the weight gain in my late teens was accompanied by inflammation – when I first started losing weight, I looked as if I’d shed 20lbs, when I’d in fact only shed about 5lbs on the scale. Took me 2 years to lose about 30lbs, and my gut was still distended.

    In trying to shed the last 5-10lbs, I found that carbs etc don’t matter – the state of my gut does. I still have a sensitive gut (certain vegetables set me off, for example) and am working on treating it (probiotics, fermented foods, enzymes etc). When I am having gut problems, I immediately start gaining weight, 10+ lbs or so…. even on homemade, whole, low carb foods. I’ve long suspected that gut issues can prevent fat loss irrespective of macronutrient composition of the diet, so it’s refreshing to hear someone state just that.

    THANK YOU. Looking forward to reading more of your work.

  33. Thank you for this very interesting blog.

    What I find lacking from most internet discussions about nutrition and, particularly, about causes of obesity, is the lack of attention given to the dire effects of many prescribed medications. I myself gained a great deal of excess weight as a consequence of taking HRT, and much later discovered that sodium and water retention had caused this, and cause similar harm to other unfortunate people who gain weight when taking prescribed steroids.

    I was invariably given inappropriate, ineffective advice by the medics I consulted about what to do about the weight gain – advice usually accompanied by sneers and insults.

    There is certainly a widespread ignorance among doctors et al that the most effective way to prevent or to reduce excessive weight gain from steroids (and antidepressants, antipsychotics, some anti-epileptic/anticonvulsant drugs, etc) is to avoid salt and salty food as rigorously as possible. I lost 51 pounds by doing this, and a friend lost 70 pounds in a year by following my advice about seriously cutting down on sodium.

  34. Found interesting paper:

    Diet and the evolution of human amylase gene copy number variation

    Looks like individual ability to use CHO as a food differs on genetic level a lot and that might explain why some people don’t have problems with higher CHO and vice-versa.

  35. Thanks, majkinetor. Of course evolution of digestive capabilities doesn’t imply differences in bodily nutrient needs, only differences in food availability.

  36. It might imply differences in bodily nutrient needs too.
    For example, loss of Vitamin C creating gene accompanied rise of specific protective elements in the body, for instance type of GLUT receptors in RBCs as much as its somatin switch that regulates preference for glucose or C, and that is not present in any species not having dysfunctional gene. So, the body did need it, but it “learned” to survive without it. Depending on time elapsed, adaptations are expected.

    So, we need to ask 2 questions:
    – Have we adapted to specific nutrient or its absence ?
    – If so, is the adaptation good enough to support long and healthy life ?

    For instance, the basis of genetic hypoascorbia hypothesis is that second question has negative answer, and it looks like first one has positive answer [or we would all be dead from scurvy].

    Now, that leads us to interesting parallel – if we think we might adapted to the absence of C which almost any other living form on Earth uses in large quantities (including microworld to some extent), that means that we could adapt to varying amount of carbohydrates [since they are so similar],no matter how much body needs it at the specific moment in its genetic history.

    We also have problems related to digestion, since this is the part where problems will be first encountered. If subpopulation, lets say, adapted to low CHO, then more CHO might lead to bunch of more or less stealth problems, from indigestion over hyperinsulinemia to microbiota rebalancing (which, now we know, release some neurotransmitters on its own and thus influence not only physical health but behavior apart from their ability to use or create nutrients we need). The same could be said for the opposite direction.

  37. BTW, here is full paper.

  38. One thing that these debates never calculate–how many calories did the Pima take in pre and post the introduction of wheat? Because I’ve been on an authentic Japanese diet, and tracked the calories, and found myself eating around 1000 calories a day (my mother is Japanese). But when I go on a diet that is still mostly whole foods and vegetables, but substitute pasta, bread and rice, the caloric intake increases dramatically.

    I would bet you that pre and post the introduction of flour, the Pima’s caloric intake varied dramatically and are not equal.

  39. Hi Marie,

    It’s a great point. I wish I could find studies relating wheat consumption to calorie intake. I believe you are right, wheat does promote calorie intake, but I’m not aware of validation in Pubmed.

  40. I have been trying to figure out how to email this question directly, since I’m not sure where it fits…and I’ve been scanning your site to see if I can find it addressed-so far I haven’t;
    I started eating very low carb in April of this year and have lost 24 lbs; better yet, I’ve completely “cured” my 35 +/- year history of carb bingeing, complusive eating and bulimia! However, after reading your book I though it made good sense to add in some safe starches, only problem is, even at only 100 calories of yam, or potato or rice, my appetite sky-rockets and I am back to having trouble controlling how much I eat & wanting to snack…any suggestions?

  41. Paul, I ran across this blog entry while trying to read more about Guyenet in response to Gary’s latest post, where he once again criticises the food-reward/palatibility theory. You know I like your work, but I just don’t understand why it just can’t be as simple as processed foods are responsible for the hormonal derangement that create toxins, malnutrition, and screw up your brain and body? You are taking a food out of nature by processing it, and your body get totally out of whack. I know that it doesn’t sound scientific, but really so what? I don’t really care if the tail wags the dog as long as the dog does what its supposed to. I, of course, am a Plastic Surgeon, and there is not this high level of science in what we do. If your screw up a rhinoplsty or it looks good, we ALL know. It is very pragmatic, and we don’t always necessarily care how you got there. But I realize that is my bias…

  42. Hi Kimji,

    That pattern suggests some kind of issue with glucose regulation, often related to a small bowel infection.

    You might want to get a glucose meter and examine how your blood glucose responds to a small potato with butter, and also whether your fasting glucose is normal. This will help with diagnosis.

    If you do well on very low carb then eat that way, but use the time to try to heal your bowel. See our bowel disease series for some ideas. Sauerkraut, kimchi, yogurt; digestive enzymes; traditional herbs and spices; antimicrobial oils are all helpful for promoting good gut flora.

    Hi Srdjan,

    I think it’s clear that processed foods are a major factor, but why that is needs elucidation. Is it their omega-6 and fructose and wheat content? Toxins introduced in processing? Also, they are probably not the only factor, since some people eat them and stay thin. So we have to find the other factors too.

    Best, Paul

  43. Paul, I think it’s probably a combination of all of those things that you mention, which are all excellent points–no doubt–and it’s quite clear that people can lose weight on a calorie restricted diet that includes only junk food, aka the Twinkie Diet. But this is where the quest for theoretical consistency can be problematic in my view. Let me give you an example from my own life: Do you know a Type I diabetic? Have you been responsible for managing their blood sugars? I hope you don’t, but you should. Managing blood sugar is totally an art, and there is great science on how to do it, but it’s really hard to do in reality. And so, you have to rely often on what works, even if the science says a diabetic can eat any carbohydrate and all carbs are the same. That is perhaps scientifically correct withi the paradigm, but the reality is that processed foods raise blood sugar like crazy in diabetics more than anything except maybe really ripe fruit and you can only do good for managing blood sugars by removing them as much as possible. You can certainly include some, but the more you move on the side of removing processed food, the better you will be. That’s how, in my view, the theoretical can inform the clinical. Are their fat people who never eat processed food? Sure. But ultimately, you have to go with what works. Is the science that suggests that processed carbs are bad, and sugars make you fat good, and better than low-fat process food grain based diet. Sure. We agree on that, so within those confines we develop a system of what works. That’s the clinical pragmatism that I use, and it’s kind of what Gary espouses, though he tries to use hard science to make his point. I personally think he can be a science writer, and espouse what works and that’s okay. He can be judged on that. That’s a main reason why I like your work as well, as it allows for the most possibility for things that work than one size fits all diets. I also have a real problem with Stephan’s comments. They are coy and evasive, in my view. Though they are scientifically correct, and more correct than Gary’s. Yes, I admit that, but if I were a food executive, whose comments and research do you think I would use to sell more food and say it was totally harmless? If you can’t commit that it’s more likely than not that the Pima got fat with processed foods, and the other examples Gary gives, it is scientifically correct and ‘honest.’ But I wouldn’t be surprised that more food and government execs and scientists read Stephan’s blog regularly to find out how to get people to eat their food, and justify that processed carbs do not have any link to diabetes, metabolic derangements, obesity, and the like. This is my perspective from a clinical viewpoint as a doctor. I realize though clearly I am not always scientifically correct within that paradigm. I accept that, but I don’t think what I am saying is totally wrong either.

  44. Hi Srdjan,

    Yes, I agree! You do have to go with what works, and removing processed foods is sufficient for many people.

    I don’t believe that food executives are reading Stephan’s blog, or designing their food based on the research he reports.

    I am not saying that processed carbs don’t have any link to metabolic diseases — they do. But they are not the sole cause. And removing them is not necessarily going to be sufficient to cure obesity or to achieve a normal weight.

  45. I think we basically agree, Paul, and I will not pursue it any further as I feel that in the low-carb community we sometimes make false enemies, as you yourself have been the subject of some rather unkind an unfair sentiments. So, I will not engage in this as I do admire your work as well as Gary’s and Stephan’s very much and I like to continually read what all of you are up to. Perhaps it is a bit conspiratorial of me to think that food execs read Stephan’s blog, but after reading the Omnivore’s dilemma, and examining the money spent on research in the food industry to overcome the fixed stomach problem, I wouldn’t place that outside the realm of possibility, as Stephan’s work could very well be used to get people to eat more than they should. I did spend a lot of time reading Ray Bradbury, Orwell, Aldous Huxley, Robert Heinlein, and Theodore Sturgeon (Kurt Vonnegut) growing up so am I influenced by these visions of a contolling soylent green future.

  46. By the way, Paul, your malnutrition argument is very compelling and worthy of consideration. There is a lot to malnutrition that is not discussed on the blogs. Kwshiorkor and marasmus, etc. Many other things…

  47. Srdjan

    The End of Overeating by former FDA chief Kessler covers the whole topic of how food companies create foods that will get you to keep eating …mostly it comes down to tasting panels and focus groups. Even with already having a good sense of what goes on in the so called “food” industry, reading this was fascinating and,of course, very depressing.

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