Obesity Debate: Cause/Effect, Genetics & Robot Clones | Chris Kresser

Reframing the Obesity Debate: Cause/Effect, Genetics & Robot Clones


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The more damaged you are, the more carbohydrate restriction is likely to benefit you long term.
– Peter @Hyperlipid

I don’t think there are too many people out there familiar with the mechanisms of diabetes and insulin resistance that would disagree with that statement.

But just because a low-carb diet causes fat loss in this population, that doesn’t mean that carbs caused the fat gain or damaged metabolism in the first place.

I wrote about this in a previous article, There is No Single Cause of (or Treatment or) Obesity, but based on some of the comments and discussion I’ve been seeing online recently, I think it bears repeating: in order to properly frame this debate, it’s essential to separate the causes and treatment of obesity and diabesity. If we don’t do this, we might as well not even have a debate at all because we won’t be talking about the same thing.

We know without a doubt that statins lower cholesterol. But does that mean high cholesterol is caused by a statin deficiency? If you break your arm, your doctor will probably put a cast on to help it heal. Does that mean we should all wear casts on our arms to make sure they don’t break?

Metabolically Damaged vs. Healthy: Apples & Oranges

Another important distinction that should be made – but often isn’t – is the difference between how people that are metabolically healthy and metabolically damaged respond to food. Of course excess carbohydrates are more likely to cause problems in someone with leptin and insulin resistance and impaired glucose tolerance. But it doesn’t follow that the same will be true in someone without metabolic problems.

People without gall bladders don’t digest fat very well. Does that mean fat causes indigestion? I have patients with iron overload due to a genetic condition called hemachromatosis. They need to limit their red meat intake because of this. Does this mean we should all avoid red meat to prevent iron overload?

We’re not robot clones. We have different genes, lifestyles, gut flora, immune fitness and exposures to toxins, stress and infections, as well as different emotional and psychological relationships with food. All of these factors play a role in weight regulation.

This explains why two people can react to the same diet in entirely different ways. And it also explains why it’s so ridiculous to extrapolate something that you experience personally to everyone else. (If I read another comment from someone saying that a low-carb diet worked for them, so the insulin-carb theory must be correct, I’m going to lose it. And it takes a lot to make me lose it!)

My Unified Theory of Obesity

For what it’s worth, here’s my “unified theory” on what causes obesity.

Modern lifestyle + genetic predisposition = obesity.

It really is that simple.

Modern lifestyle includes processed, refined and highly rewarding and palatable foods, excess fructose, unprepared grains (especially flour), industrial seed oils, environmental toxins, sedentary behavior, stress, infections and dysregulated gut flora.

But the modern lifestyle doesn’t cause obesity in all people. I’m sure we all know someone who eats a horrible diet, doesn’t exercise, is under tons of stress and lives a shockingly unhealthy lifestyle – but doesn’t gain a single pound.

That’s where genetics come in.

Human Evolution Didn’t Stop in the Paleolithic

A commonly held belief in the Paleo-sphere (I held it myself, until fairly recently) is that our genes haven’t changed much since the Paleolithic era. But recent evidence suggests a much more rapid pace of genetic change in humans than was previously estimated.

The birth of agriculture introduced significant selection pressure, and thus mutation, because humans were not well-adapted to this new way of life. And the evolutionary response to agricultural diet differs because different peoples adopted agriculture at different times and in different places.

Agriculture began in the Middle East 10,000 years ago, but it was never adopted by Aboriginal Australians. Might we expect the descendants of people from these two regions to have different responses when exposed to agricultural diets?

Absolutely. Researchers in Iceland have discovered a gene that regulates blood sugar tolerance. (I discussed the role of genetics in obesity and diabetes in a previous article, Are You At Risk For Diabetes and Obesity?) And we know that Aboriginal Australians have a 4 times greater risk of developing adult-onset diabetes than Australians of European descent.

Lactase persistence is another example. During Paleolithic times, humans stopped producing lactase (the enzyme required to digest lactose, the sugar in milk) shortly after weaning. There was no need for it, since Paleo people didn’t raise cattle or drink milk. Skeletal remains from northern Europeans 8,000 – 9,000 years ago confirm that there was no lactose tolerance at that time.

However, skeletal remains from northern Europeans living in the Bronze Age 3,000 years ago show roughly 25% of adults produced lactase. And today, in certain Scandanavian countries, more than 95% of adults are now lactose tolerant. 1

All of these genetic changes happened within the last 8,000 years, after the advent of agriculture.

The Hand You Were Dealt: Life Isn’t Always Fair

What this means is that some of us are likely better adapted to the modern lifestyle, while others are more susceptible to being harmed by it. Those are very likely the ones that become obese when exposed to a western diet.

But as far as I can tell, they didn’t get obese by eating natural, whole-food carbohydrates. I’ve yet to see a population that got fat eating sweet potatoes, fruit and white rice – without any exposure to modern food. If anyone knows of such a population, please let me know.

Does It Even Matter What Causes Obesity? I Just Want to Lose Weight!

Some might argue that this discussion is irrelevant, since once someone become obese it’s clear their metabolism is damaged. There are two main problems with that argument.

First, not all obese people have deranged metabolisms. Research over the past several years has defined a subset of “metabolically healthy obese” (MHO) people with normal fasting glucose, triglycerides, insulin sensitivity and other markers. I wrote about this in my article Not All Fat People Get Diabetes, and Not All Diabetics Are Fat.

Second, separating the cause and treatment of obesity is necessary to prevent confusion. Something I see all the time in my practice and in the blogosphere is normal or even underweight people following zero- or very-low-carb diets. Why? Because they’ve absorbed the notion that “carbs are bad” from the “carbs-insulin-fat gain” theory, and they avoid them in a misguided attempt to promote health. While this may work for some people, it doesn’t for many others. I know because they end up coming to me with complaints like low energy, hair loss, bad breath, constipation and more.

Food Reward vs. the Carbohydrate Hypothesis: Setting the Ground Rules

I’d like to see a discussion of obesity that acknowledges the difference between cause and effect, considers the varying impact of food on the metabolically healthy and unhealthy, and recognizes the role of genetics in weight regulation.

Unfortunately, these important distinctions seem to be missing from the current debate – which, in my mind, makes it far less compelling.

  1. Cochran, G. Harpending, H. The 10,000 year explosion – how civilization accelerated human evolution. Basic Books. 2009. pp. 77


Join the conversation

  1. Yes, some native populations don’t have western disease on a high carb diet, but are they sedentary and do they eat as much processed carbs and sugar as most Americans? I don’t know what the main mechanisms are, but I think that, for people who low carb diets do work for after being obese (likely not all obese people, but maybe a majority?), those same people probably wouldn’t have gotten obese in the first place on a low carb diet. So, in a sense, you could say the carbs made them fat, or at least, were a necessary condition for them to develop obesity. Maybe sugar/processed carbs also need to be combined with a sedentary lifestyle to really get serious obesity problems?

    I’ve yet to see one of the “LC diets work but carbs aren’t the cause of obesity” people acknowledge that carbs (mainly sugar and processed carbs) are a necessary condition for obesity in at least a subset of the population, though the mechanism may be much more complicated than insulin, including maybe modern wheat’s weirdness, leptin and brain stuff, food reward, psychology, addiction, social situations, sedentary lifestyle, stress etc. But, if you look around your family and see lots of obesity and you think you are also headed down that path, you might want to try a low carb diet to prevent obesity. If it doesn’t work for all that makes perfect sense, everyone is different I agree. Maybe there is an less rigid way for these people to avoid obesity, but if you all agree low carb works for some people, then those same people should also be able to prevent obesity with LC.

    As for me, I’ll see how it goes in the future as I’ve only been on paleo for a few months. I’m not obese and never have been, but I’m surrounded by obesity in my family and I gained weight very easily when I was a carbolic, having to run a lot to maintain my weight. So far it’s easy to maintain my weight on paleo even though my exercising has dropped significantly. I would much rather eat low carb paleo than to eat bland foods that are recommended by the food rewards people. Yuck! Even if the bland foods worked faster to decrease my food intake and thus lower my weight, I’d rather have my yummy paleo food thank you very much.

    • Stephanie,

      I have said that carbohydrates are a trigger for obesity in those that are genetically (or epigenetically) susceptible. In fact that is essentially the crux of my argument: if you are leptin sensitive, macronutrient ratios are irrelevant. If you’re leptin resistant, they matter. There are exceptions, but that’s the way it does seem to me at this point.

  2. As a lay person trying to address her own obesity I found my way here and other sites about a year ago. I stepped away for awhile a few months ago and this is the first article I’ve read (and I follow a handfu of sites) on the subject of nutrition and health.

    Reading this article (and especially the comments) reminded me why I took a hiatus. I start questioning all that I’ve learned and this causes me to go a little nuts thinking that my approaches may need to change, yet again. But then I have to remind myself that it’s easy to get into the ones and zeros of the subject and get overwhelmed. I don’t need to have a background in biochemistry to figure out what to eat. (I don’t remember my grandparents even using the words “protein” or “carbohydrates” – they just knew good nutrition came from food you made yourself).

    I think Michael Pollan has it right when he says you can eat anything – as long as you prepare it yourself from whole foods. Most of us (myself included) are fat because we’ve been eating crap – fast food, highly processed and it’s become a staple of our diets (and who really knows what food scientists are really putting into most of this stuff and what it’s doing to our brains). And I would bet money that if we all were eating whole foods, we wouldn’t have the obesity probelm we have – carbs included.

    • Lisa, I couldn’t agree with you more on all counts. My struggle is not so much weight as autoimmune issues. For the last year I have stumbled from raw to high raw to vegan back to raw and now looking at a moderate approach eating whole foods and avoiding grains/gluten. I’m not terribly heavy on the meat, but I’m ready to try anything wholesome and unprocessed. My sister in law jokingly sent me an article on the newest “label” in eating disorders…Orthorexia. And though she sent it as a joke it made me realize how crazy it is to work so hard at something that should come naturally!
      I am going to let my body be my guide and get back to eating real slow food. An advantage to becoming so sensitive to all that I eat is knowing my body will quickly react and guide me.

      I have tried to explain to my daughter, raising her kids, that it isn’t really that I’m a total freak about foods and what to avoid. It is the fact that, among other things, the food industry has corrupted all the “governing” agencies that were in place to protect consumers. Instead they are involved in cover ups, and sheer blatant greed in their “You scratch my back I’ll scratch yours” “wink wink” policies. We were duped by the food industry into trusting advice that was not based on good science but pure greed and self serving propaganda. We now have a couple generations of young people who have grown up with chemically altered, genetically modified “food”, and the deception runs very deep. After preaching all these years about every fad that came along, ie unfermented soy and vegetable oils, and against eggs, butter, animals and animal products, I’ve done an about face and now try and convince her of the benefits of Grandmother’s cooking. She’s a bit leery but gradually making changes.

  3. “I’ve read it. Please be specific about how I’ve been generalizing. Remember that Gary’s position is founded in biochemistry and the information has been around for decades. Guyenet’s position is basically cals in/out. It’s as if he is dismissing what we’ve known about fat regulation for almost a century. Why I wonder. None of what Stephan said refutes the carbohydrate hypothesis. Give me one example.” – Fred

    You are coming off as very arrogant and insulting to anybody who dares disagrees. Wow. I am how can anybody in their right mind possibly question your position that is the only one based on “biochemistry.” Dr. Guyenet must be a real idiot! He does not a lick of biochemistry from the past 100 years! “Give you one example.” So ignore and write off his entire article dismissively and then demand “one example” when the article explains multiple reasonings and studies arguing against. What arrogance!

    “Try it. Find out your maintenance level of cals as best as you can figure it. For the next year eat 80% of your cals from carbs. See what happens. I guarantee you you will get fatter and feel like crap.”

    Yeah, your probably correct that no human could possibly live on 80% carbs AND be healthy and especially not for a lifetime. Oh and a whole culture doing that now your taliking crazy…Oh wait,,,,you mean eat like the Kitavans!

    • It is probably best to just ignore Fred. On Chris Masterjohn’s recent blog post speaking out against dietary dogmatism, Fred showed up and started claiming that there was nothing wrong with low-carb dogmatism because the low-carbers are right. No point arguing with some who advocates low-carb dogmatism.

    • “You are coming off as very arrogant and insulting to anybody who dares disagrees.”

      Why? Because I am stating some facts? Why would you read into my comments in such a way? It seems as if you are taking my statements personally for some reason. I’m not attempting to insult anyone.

      “Wow. I am how can anybody in their right mind possibly question your position that is the only one based on “biochemistry.” Dr. Guyenet must be a real idiot!”

      No, Dr. Guyenet is really bright and has some good thoughts and ideas. But he’s wrong about insulin.

      “He does not a lick of biochemistry from the past 100 years! “Give you one example.” So ignore and write off his entire article dismissively and then demand “one example” when the article explains multiple reasonings and studies arguing against. What arrogance!”

      I never dismissed his entire blog post. Why are you acting in such away? My feeling is that Stephan is fishing around for things that might disprove the role of insulin in fat regulation – which is ok – but I don’t think his blog post achieves this goal. I think his blog post in the end is just another cals in/out rules the day.

      “Yeah, your probably correct that no human could possibly live on 80% carbs AND be healthy and especially not for a lifetime. Oh and a whole culture doing that now your taliking crazy…Oh wait,,,,you mean eat like the Kitavans!”

      Here we go with the Kitavans again…oy vey. I’m not going to get into this one right now. And it’s beside the real point which I have allowed myself to stray from which is why we become obese.

      • Fred,

        “Why? Because I am stating some facts?” Your only stating your opinion so far.

        “Why would you read into my comments in such a way? It seems as if you are taking my statements personally for some reason. I’m not attempting to insult anyone.” Not personal at all, just insulting to the intelligence of anybody reading your comments who knows even a fraction of the issues involved.

        “But he’s wrong about insulin.” Just stating opinion again. Where’s the facts?

        “I never dismissed his entire blog post.” You didn’t?…”Guyenet’s position is basically cals in/out. It’s as if he is dismissing what we’ve known about fat regulation for almost a century. Why I wonder. None of what Stephan said refutes the carbohydrate hypothesis.”

        His ideas are so simple and stupid right? And “none of what Stephen said refutes” certainly does not “dismiss” his “entire” position? …rrriiiggghhhhtttt.

        Yes the Kitavans. So let’s see here, if someone eats 80% and overweight and then eats 80% carbs to lose weight, then by lowering total calories they have changed to a “low-carb” diet? Is that really your reasoning? Because a person would still be eating 1,500-2,000 calories of carbs or 300+ grams. That’s not low carb is it? The asian cultures that stay slim on high % of diet as carbs must all be on low carb diets after all? Of course, how stupid of me and the experts like Stephen. And then there’s Weston Price’s groups like Swiss, Scots, and some of the other primitive groups were healthy, long lived, and high carb, but your saying they’re actually low carb like high sourdough rye for the Swiss…rrriiiigggghhhhhtttttt.

        Now, I eat low-carb on the Perfect Health Diet, but let’s not say low carb is the end all be all for the human diet. Kresser and the rest are simply pointing out there is more going on, which is supported by so many people’s experiences like ill effects even from a low carb diet.

        And remember, Taubes has clearly been scrutinized by the blog world where his stated position is that any and all carbs increase insulin and cause obesity and health problems. His nuance of refined carbs and fructose being worse is not the full position he has stated and must defend. If insulin is the boogie man then he also needs to address protein’s insulin effect.

        Yes I have read GC,BC and the other one, red book Fat something.

        You can not be taken serious when you so easily dismiss a PhD’s article directly destroying the carb-insulin is the all-cause answer. Try taking one point from his article and the cited source and try refuting it. Even an amateur like me can respond to any article and say that it was not convincing and dismiss it out of hand without explaining a single counterpoint and just generalizing my opinion.

  4. the genetic factor is the key here in most cases…specifically those that are manifest with pathological issues such as metabolic syndrome, etc…
    most obese people are probably more familiar with a non-reward, unpalatable diet than their thin or regular weight peers. why isn’t this discussed? there seems to be a stereotype of fat donut and ice cream glutton at play here in the comments.

  5. Very valid point, didn’t mean to suggest that behavior is non-biological! Merely that it is an emergent phenomena that may involve many different inputs including macro-nutrients, other nutrients and other sensory ones. My overarching point is that it may not be very fruitful (another unintentional pun) to try to isolate food reward from carb consumption as an underlying cause as they may reinforce each other in very complex ways.

    • Agreed. I also suspect our categorization of macronutrients is too broad. Sweet potatoes and bread are both “carbs”, but I suspect have significantly different metabolic endpoints when regularly consumed.

      I see red flags waving around a statement like “increase of availability of highly palatable food as a major cause of obesity”, because it doesn’t really say anything about cause and effect. The usual usage of “excessively palatable” is a food that causes obesity, i.e. one for which the emergent behavior is to eat in excess of the body’s ability to regulate energy balance. And not surprisingly, one of the emergent behaviors for highly palatable food is going to be to make as much of it as possible. The relevant question is what causes the underlying metabolic regulation (which includes palatability/food reward) to fail and bring about this situation?

      • Your characterization seems correct to us; just like financial markets and other highly interconnected systems, ’cause and effect’ is not really the right picture. This is why the battlelines between ‘food reward’ and ‘low carb’ seem artificial to us as they could be quite intangled.

        On regulation you are definitely hitting on the right question, but it isn’t so obvious to us that something has to discretely ‘fail’ or whether there is a range of regulation effectiveness across the population and by moving into a new regime of food consumption we are seeing that variation in the form of the ‘obesity epidemic’. Alternatively one could hypothesize that on an individual level regulation is only effective within some range of inputs. When the frequency of exogenous shocks to consumption (of something) crosses some tipping point, the market feedback effect of making more highly palatable food leads to a systemic effect.

  6. Great post! We referenced it and made some comments in a blog post on our site:

    Obviously people have been thinking hard about these issues for a long time but given how scattered the understanding of the underlying biological processes are and the lack of any complete simulation of how they work together, trying to prove anything about the causal properties of one macro observation (carb consumption) whiles excluding another (food reward response) seems futile. And in addition, the obesity epidemic itself is a hazy and broad characterization…

    • Krista – What’s your point? and what do you mean that the understanding is “scattered?” You cannot become obese unless your diet is high in carbohydrate UNLESS you have some sort of hormonal disorder like pituitary gigantism or Hashimoto Thyroiditis.

      Have any of you read GC, BC or Protein Power or a half dozen other books on the subject?

      As I said in an earlier post, show me an obese population that does NOT derive most of their calories from carbohydrates?

      • I certainly have read all of those books. Let me try to clarify the point, and will probably expand upon it in a blog post.

        Our own observations and read of the literature strongly support the hypotheses that:
        1. drastically reducing carbs, especially wheat and sugar leads to weight loss
        2. wheat and sugar have severe adverse health consequences

        That said, obesity as a macro phenomena (no pun intended) seems obviously a result of behavioral and biological factors. If food reward factors contributes significantly to high carb intake, then it seems reasonable to see the increase of availability of highly palatable food as a major cause of obesity.

        Fred, you say “you cannot become obese unless your diet is high in carbohydrate…” This may be perfectly true but with the caveat that “high” may need to be defined individually based on their genetics, history, and level of food addition (people who are following an on-average low carb diet who occasionally binge may do more damage to themselves than people on a higher average carb diet– negative convexity!!).

        • What behavioral factors are not biological?

          Food reward is learned. Palatability is dynamic, and changes in the context of overall metabolic regulation: try eating 20 pieces of bacon. The key question is what gets broken in the communication about energy requirements (or that of other nutrients), palatability, and ultimately the resultant behavior.

    • I’ve read it. Please be specific about how I’ve been generalizing. Remember that Gary’s position is founded in biochemistry and the information has been around for decades. Guyenet’s position is basically cals in/out. It’s as if he is dismissing what we’ve known about fat regulation for almost a century. Why I wonder. None of what Stephan said refutes the carbohydrate hypothesis. Give me one example.

  7. When I lived on low-fat/low-cal diets, they were mostly full of carbs and sugars. I ate a LOT of processed, fake food, and literally starved myself.

    If I input that diet into fit day, it was a VERY HIGH carb diet, around 65-70% carbs. I lost a lot of weight. But I also got very sick, gained it all back and then some, and of course I still have lingering health issues.

    So I don’t think one can necessarily state that low-cal, low-fat diets are ALWAYS lower carb and lower sugar. Mine certainly was not. Of course, now that I know about nutrition, I would NEVER advocate that type of diet for anyone on the planet, unless they don’t mind metabolic syndrome, insulin resistance, chronic arthritis pain, etc.

    • What I meant was, people who adopt a low calorie diet (especially in studies), to lose weight always eat less carbs than they did before.

      and Chris is suggesting in this blog post that some people might actually do better on a high carb, low fat diet. My position is that is not possible – not if you’re human. While we do have some genetic differences, we are virtually identical to one another. We all breathe the same air. We all drink the same water.

      You lost weight because you were eating very little food. the issue of weight loss is different than weight gain and specifically becoming obese.

      There are no calorie receptors in the human body. Dr. Jeff Volek states it perfectly “You are what your body does with what you eat.”

      Food gets complicated because so many people have damaged systems due mainly (IMHO) to intestinal permeability caused by eating too many grains and their antinutrients. Though Chris points out that some people have adapted to lactose over several thousand years of suffering through it, I certainly don’t want to be part of that evolutionary experiment by eating grains until my great, great, great, great grandchildren can eat wheat without suffering any health issues.

      You can’t point to a population that eats a lot of wheat and seem not to suffer from any intestinal maladies and then say “See we are all different. Wheat is good for some people and not for others.” Wheat is not good for anyone – ever. Yes an absolute statement that is not wrong or short sighted in any way. Some “foods” are bad for every human but some humans don’t suffer as much because the damage is not great enough to show symptoms. But the damage is being done.

  8. rg – I never said you said that. My feeling is that you are purposefully not wanting to understand. 2000 calories a day for a really fat person is a starvation diet. He was starving – do you really not see the difference? Do you really not understand the basics of how the human body stores fat?

    • I get it. I’ve read GCBC and WWGF in their entirety.

      Honestly, I don’t know how much he ate, so probably not a good example. I was just throwing out 10 cups as a caloric example.

      • This reminds me of the 100 bananas a day guy, Durian Rider (sp?).

        He eats just fruit, but he’s an endurance athlete so his caloric needs are extremely high. By the time you eat 4000 calories worth of bananas you actually get enough protein and most amino acids – someone ran a fitday analysis of his diet and if you can burn that many calories and use up that many carbs -and you’re not already metabolically damaged – you can be relatively healthy eating just fruit. There’s probably a little luck in his genes also.

  9. Hi Chris –

    This is an interesting blog Chris but I have to say I’m not sure what you are trying to say exactly. Are you trying to say that obesity is NOT a result of too many carbohydrates in the diet or or that obesity can result even if someone’s diet is low in carbohydrates?

    You said: “But as far as I can tell, they didn’t get obese by eating natural, whole-food carbohydrates. I’ve yet to see a population that got fat eating sweet potatoes, fruit and white rice – without any exposure to modern food. If anyone knows of such a population, please let me know.”

    I’ll toss one back at you – show me an obese population that does NOT derive a large portion of their calories from carbohydrates.

    It doesn’t matter that there are some populations out there that eat a good deal of plant matter and are not obese. That is totally beside the point. There are people who smoke and don’t get lung cancer but smoking causes lung cancer. Not in everyone, but it does cause cancer.

    We all are well aware that there are many factors that contribute to obesity like thyroid issues.

    As for leptin, leptin resistance is seen in people with insulin resistance or who have a very low fat, high carbohydrate diet. You generally won’t find leptin resistance in lean people who eat mostly animal matter and some plant matter only. And what is the part of the “cure” for leptin resistance if one has it? A low carb/sugar diet.

    “I’d like to see a discussion of obesity that acknowledges the difference between cause and effect, considers the varying impact of food on the metabolically healthy and unhealthy, and recognizes the role of genetics in weight regulation. Unfortunately, these important distinctions seem to be missing from the current debate – which, in my mind, makes it far less compelling.”

    This is discussed all the time Chris – but the fact is regardless of your genetics, if you are obese, you are probably eating a lot of carbs – usually refined carbs but a lot carbs nonetheless. You will never find an obese person who eats mostly fatty animal matter, some plants and no grain products, whose total carb intake is under 200 grams. No one is saying you can’t gain fat eating too much meat – but you can’t become obese.

    Since you’ve been helping obese people for some time now, have you ever suggested to a single obese client that they adopt a high carb (of course real carbs), low fat diet?

    • I think the point is that while everyone seems to agree carbs may have a major role, it is difficult to tell what that role may be with so many confounders.

      • We know for a fact that insulin plays THE major regulatory role in fat gain. Insulin is the big kahuna of fat regulation. Every biochem texts says so. The confounding factors are always there. Everyone who has cancer sneezes. But sneezing is not a confounding factor for cancer.

        I have been helping people lose fat for a decade using LC eating plans. When followed, it has worked every single time and many times amazingly so. It is not possible for it not to work unless some other issue is at play that NO diet of any kind would help. And there is not a single obese person on this Earth that would fare better on a low fat, high carb diet even if the carbs were all yams, rice and vegetables. Not a one.

        • Plenty of people have lost weight on the low-fat, higher-carb diets. While I am not a fan of Ornish, Oz, and the like, they have no doubt had success. Denise Minger points out that what they also excluded from their diets was similar to “Paleo” eaters: sugars, refined carbs, industrial oils.

          • This just reminded me of a friend’s brothers who was a VERY overweight teen. The boy was FAT. And by the time he got to college, was upset about it. Some time went by when I moved to another state for grad school, but came back to visit, and hung out with these guys. Guess what? That fat boy had become a skinny man. How did he do it? He ate nothing but dry, white rice. One cup alone is 44 carbs. He ate many cups a day. He is now in his 30s, and still remains a skinny man. A pure carb diet.

            • First of all that is not all he ate or he’d have died. He may have said that’s all he ate, but that’s not possible. And even if he did, he also lost a lot of lean mass. Not a healthy way to lose fat either. Very low calorie diets will of course result in weight loss. Again, totally beside the point.

              • Nope, that is all he ate. At the time, his family was pretty angry with him when they found that out. I don’t doubt he lost a lot of muscle mass, but he lost most of his fat. Didn’t say it was healthy or a good idea. Just an example of a 100% carb diet that resulted in dramatic weight loss.

                And while yes, it was most likely lower calorie than his previous way of eating, it still contradicts that eat carbs, get fat theory. He replaced meals of fats, protein and carbs for 100% carb.

                • No it does not. He was LOSING tissue – not gaining. No one can gain fat eating a bowl of rice or two only. No one can become obese unless they are eating significant carbs. Not possible.

                • I never said he was eating “a bowl of rice or two”. He was eating A LOT of rice per day. Many, many bowls, which certainly produced enough glucose and calories. Ten cups of rice alone is 2000 calories.

          • But these same people have also greatly reduced their total carb/calorie intake. So compared to what they were eating before, they inadvertently adopted a LC diet.

    • Fred, these are excellent points. I think there needs to be a clear definition of what we mean. I think it is important to consider the data and the metrics used. If you have read Moneyball, it’s sort of like that in the sense we have data, it gives us a general sense, but there be more powerful data, or data that we are not considering. That being said, low carb seems right, but the questions in my mind, and I think Chris’, are how low? Which carbs? How do we verify that? And why is that so?

      • When I was a kid Jupiter had 9 moons. Now it has 63. But it always had moons.

        We will never discover that insulin and thus total carb intake is NOT a factor in obesity just like we will never discover that Jupiter has no moons.

        No one is saying that we should not continue researching the subject. But to be certain that total carb intake affects insulin production and that insulin is main fat regulating hormone is not a limiting factor in obesity. It is not being shortsighted to say so.

        Sure – in a few years we might discover all kinds of new hormones like we did leptin in 1994. And as you know, leptin is made in the fat cell. So being fat causes leptin resistance – it does not cause it.

    • Fred, Thank you for making some points that have been troubling me in all this debate.

      I agree with Chris when he says to show him a population that got obese off of potatoes and rice and that it’s impossible. But that’s not what the American public is eating, now is it? If that’s what we were eating, we wouldn’t be having these discussions.

      I feel like Taubes’s message has gotten watered down and all we’re focusing on at this point is whether his insulin theory is correct. And he admits in his books that it’s a theory without solid, incontrovertible evidence. So why the attacks? We’re all working toward a greater understanding of how this all works, and there are many seats to be had at that table.

      What I’m still confused about with regards to food reward is this: every example I’ve seen of a “palatable” food is a carb. Chips, candy, etc. But there are many other factors to these foods that can be causing problems: vegetable oils, sugar, grains, etc. I have no trouble accepting food reward as a valid component of this, but it is not the entire answer. If someone eats chips and eats more than they planned to and gets hungry a little later and eats more chips, sure, food reward could be playing a role. But I don’t understand why insulin doesn’t also have a role in this. When people’s hunger cues go out of whack, we’re talking about metabolic derangement (in whatever stage), and at that point, the whole issue is multifactorial.

      Why aren’t these theories compatible rather than in conflict?

      • I should add that I don’t think Taubes is talking about sweet potatoes or rice when he says “carb”. I feel like he’s mainly guilty of oversimplification, which is fine by me if it gets people thinking about what they should be eating instead.

        • Actually he is. In a recent interview he complained about half the new My Plate being composed of vegetables and fruits because some vegetables like potatoes are starchy and high glycemic index. In interviews he usually gets more strident about carbs in general.

          The problem his theory has in this regard is that insulin metrics do not explain the difference between refined carbs vs unrefined carbs or Western diet vs ancestral diet. Rice is higher Glycemic Index and higher Insulin Index than pasta (refined wheat) or breakfast cereal. Potatoes have a very high Insulin Index (up in candy bar territory, higher than bread, breakfast cereal, and pasta).

          There is something significantly different in Western diet and lifestyle, but it is not “carbs” and according to insulin metrics it is not insulin. If Taubes would have looked at all the cultures of the world eating rice and potatoes, then looked at a table of Insulin Index values, he would have moved on to the real question – “what exactly is different about Western diet and lifestyle?” Where did the broken metabolisms come from?

          And he would have been the father of the ancestral health movement. Instead he is married to the Insulin Hypothesis and going around telling people to be careful of starchy vegetables.

      • They are compatible. In fact, they’re probably inseparable. Food reward is learned, i.e. you eat something and your brain integrates various inputs to decide if it’s good or bad, and how much. For instance, if a particular food makes you violently ill, that likely gets programmed into the secondary taste cortex, and next time you taste that food you will find it “yucky”.

        Insulin and glucose both stimulate positive reinforcement. So “carbs” reinforce food reward, and highly refined (glycemic) carbs probably do so even more. But that still doesn’t answer the question of how metabolic regulation fails. Fats and amino acids are presumably also rewarding, but it’s pretty hard to get fat eating them, since food reward is dynamic and adjusts based on the brain’s perceived requirements. So if you pig out on bacon, it stops tasting good, and probably won’t taste good again until the brain perceives sufficient caloric deficit. I’ll bet the same thing happens for whole food sources of carbohydrate. So while carbs causes insulin release which ups fat storage, the key question is why your brain would still drive you to consume more even though your fat cells are are “full”. If things are working right, you ought to just not be hungry again until that fat is used up.

        Don’t sumo wrestlers get fat on rice?

      • They are compatible. Taubes like others who offer an alternative hypothesis to the cals in/out hypothesis is saying just that – let’s look at an alternate hypothesis. And the hypothesis is the most scientifically supported one thus far as I see it. And Taubes, Eades, etc. all are clear that refined carbs are the main culprit but total carbs matter.

        Try it. Find out your maintenance level of cals as best as you can figure it. For the next year eat 80% of your cals from carbs. See what happens. I guarantee you you will get fatter and feel like crap.

        Guyenet says that no lipid researchers take the insulin hypothesis seriously. Sure they do – many do. it’s an aggressive assertion to make. Why he said this is anyone’s good guess.

        Bacon and bone marrow is far more palatable to me than a bowl of bran flakes I can tell you that!

  10. Sonja, that is a a good point. I think what I was trying to get at is that obesity is not one thing, and you have to have the proper measures to define and categorize it. I tend to think that BMI is insuffcient, and you need to determine is a person metabolically obese. Although blood lipid profiles are goods way of determining this, as are things like CRP, ESR, and other inflammatory markers, I still tend to believe there is a lot more information that we could get, and that data would help people who are think, but metabolically obese vs people who are mildly obese, but metabolically thin. I am not sure those types of tests are 1. feasible: they may require invasive tissue biopsies 2. Fiscally possible: especially in the climate of healthcare now, ie overspending for mediocre results( in regards to chronic illness in particular, although I think acute care can lack too). I agree with Chris in the sense that there is not current unified theory, and there probably won’t be, but I do believe there is a lot more that needs to be understood, and with our current understanding, it is insufficent. Also, with the bad backdrop of healthy whole grains, and low fat diets, it will be hard to move forward in an efficient manner since the dogma of the medical establish tends to not agree…

  11. “What this means is that some of us are likely better adapted to the modern lifestyle, while others are more susceptible to being harmed by it. Those are very likely the ones that become obese when exposed to a western diet. ”

    I don’t think you can say that people that don’t become obese on the modern lifestyle are not being harmed by it (the lifestyle). They might not be obese, but they might have a higher likelihood of getting heart attack, cancer, or other fatal illnesses. Just because a person is thin, doesn’t mean he/she is healthy.

  12. Hi Chris,

    as an Australian who has worked and moved about thru Australian Aboriginal populations, I can attest that diet and lifestyle also play a highly significant role in the ocurrence of diabetes in this population. This disease may occur at a fourfold rate to the rest of the Australian population but I am not convinced that difference can all be accounted for by genetic pre-disposition. For many reasons large numbers of Australian Aboriginal people live in extremely deprived conditions and poverty is an aspect of daily life for large numbers. In many aboriginal settlements fruit and vegetables are not even available to be purchased. Their diet can consist of white flour/tea/sugar/coke/alcohol and what “might” be able to be suplemented by some of the womens hunting and gathering efforts. I think you might be shocked if you were to view the lifestyle of many (not all) Australian Aboriginal people.

  13. Certainly people have a thermostat that helps keep them at their “ideal” or natural weight, whatever that means. Is obesity a disease, or is it the symptom of something else, ie insulin metabolism? That may be part of it. If we say obesity is a symptom, like fever, well then a lot of things can cause it. I think the terminology will need to get more accurate and different types of obesity will be then defined.

  14. chris – bravo! You hit this one dead-on! I appreciate your dedication and your ability to clarify this subject so often discussed and so seldom understood.

  15. Chris, thanks for taking time to write and podcast – especially with a new baby!

    So what’s an overweight, celiac, pre-diabetic, post-menopausal female without gallbladder supposed to do? I have yet to figure out what my best course of action is… I am reading the Jaminet’s Perfect Health Diet and am concerned about micronutrients. Following a Paleo type diet, low carb (under 40gr daily) I was sicker last winter than I had ever been. I caught every bug going around.

    Clearly, I still haven’t got things right. But gallbladder removal in the early 70’s came with zero recommendations on what I should do once I was released from the hospital. It’s been a roller coaster ride ever since. Celiac diagnosis 2 years ago.

    I am not that concerned about the weight – I wear a size 10 and should be a 4-6 since I am petite. I want health more than anything. But how to eat is the million dollar question. No one, as far as I can tell, has discussed this issue in the Paleo/ancestral blogoshphere.

  16. Hi Chris

    I love your blog and being that I get a third of my hits from you, I guess I should. I just put up this blog and it takes a very different tack at this whole issue. http://ketosisprone.blogspot.com/2011/07/thinking-about-western-technology-food.html.

    I am very much with the idea that genetics as a big part of the problem. As you know, I’m a Ketosis Prone Type 2 diabetic and this is a widespread form of diabetes in people of color. One of my main themes is that most diabetic research and training comes from western countries and that this research does not apply as well to the the rest of the world due to genetic differences. This latest blog continues this idea but with the thought that now these same metabolic derangements are showing up with far greater frequency in the western world. My point is that the speed at which this is happening seems to preclude behavioral or genetic explanations though certainly those things are involved. It seems to me that something has entered our food supply. You might call it a “toxin”. I simply think that our push for food production has brought in some element which poses a metabolic problem for us on some level and now we are reaping the “whirlwind”.

  17. Interesting timing, I’m just in the middle of a paper about type II diabetes in Australian Aboriginals (I live in Aus.).
    I used to be one of those metabolically healthy obese. I had normal everything, great fasting glucose tolerance, low fasting insulin, low trigs and good HDL. Only trouble was I weighed 250lbs.
    I used a low-carb diet to try to lose weight and it was moderately successful except that when I next had rountine blood work my T3 levels were tanked! T4 was in the upper range TSH very slightly above normal, no thyroid antibodies.
    I’m now on Armour and have managed to lose weight with a Perfect Health Diet style eating plan and a reduction in calories.
    I would really like to get off the Armour now as it seems from the reading I’m doing here and on PHD site that I may not need it if I keep my carbs up?

    • Emma, I am interested in learning about your story. Did you have thyroid problems before you tried low carb? How did you pursue low carb, ie what did you eat in terms of your carbs, grams consumed, etc? Did you excercise, and what did you do? I am interested in finding out more about metabolically healthy people that are obese, and metabolically sick people who are thin. There has to be an explanation, and I think it would be an important thing to know, rather than categorized you as an outlier.

      • Srdjan,
        Thanks for your interest. I first had an abnormal TSH reading after my twins were born (2004) and I was trying Atkins for the first time (approximately 6 months into my very-low-carb journey) but my conventional doctor paid no attention to the lab and didn’t order further tests. Prior to that, I had never had abnormal labs of any kind. I did exercise at that time but only lightly, just daily walking. My carbs were Atkins induction levels of sub-20 net grams. I did Atkins from approximately 5/2004 to 2/2005.
        In 2005 I fell pregnant again and started eating carbs, once my third child was born I decided to lose weight with Weight Watchers during which I followed the Core plan of eating whole grains, legumes, skim dairy and lots of vegetables and fruit. I lost well and my thyroid labs (TSH only tested) were normal from 2005-2009. Exercise again was just daily walking. I then decided to try a low-carb approach (again Atkins style sub-20g carbs) again and lost 50lbs. This was the beginning of 2010, My blood work in mid-2010 shows raised TSH again and this time my doctor decided to do further testing, this was when we discovered the high-normal free-T4 and the low free-T3. I was also symptomatic by this stage, I experienced fatigue, hair loss, dry hair and brittle nails. My doc was a typical GP and looked only at my T4 and decided that giving me Thyroxine would not be a good idea and so sent me home with nothing. I then started to research myself and found Dr Kharrazian and then Dr James Wilson (of adrenal fatigue fame) and then the Paleo world. I found a functional physician who put me on hydrocortisone and Armour and I adopted the Paleo diet. I saw an immediate improvement in my symptoms and after reading and listening to Chris, reading the Perfect Health Diet and playing around with macronutrient ratios, I discovered that I feel better when my starchy carb intake is around the 100g level daily. Now, I want to find a way to get off the Armour and Hydrocortisone and see if I can manage my condition with diet and exercise alone.
        As to why I was metabolically healthy when I was obese, I can’t answer that. I can tell you that my diet has always been mostly whole-foods based, I have always craved and eaten saturated fat-rich foods, unfortunately, I also ate a lot of grain and sugar as well. Whether the saturated fat had any protective factor against metabolic syndrome I don’t know, perhaps by virtue of fat’s GI lowering effects on carbs I managed to avoid too many blood sugar spikes?
        I hope this has answered your questions.