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

    • Nice referee work, Chris. What’s the study where the mouse receiving chocolate pudding gets obese unlike the ones getting strawberry or vanilla flavors? Dairy, wheat, chocolate, fructose(glut5 expressed in the brain), salt(chloride influences insomnia in that paper Cordain references) and probably many more, can be addictive. And through intestinal damage and autoimmunity it can be damaging. Add to that lifestyle and genetic susceptibility and there you have it.

      Any chance for a post on gluten et al cross-reactivity or intestinal parasites before the year is done? 😀

  1. I am a female and in January 2011, at the age of 59, I had a brainstem artery infarct. My right side was affected. Closing my stay in the hospital the neurologist reported to me that my blood sugar was normal, my cholesterol was within normal range, blood pressure and heart rate were fine. He said the stroke was genetic and I was one of maybe 1-2% of people who have had that type of stroke who could be having a conversation or alive.
    He said, “In spite of the fact that all your tests are normal, I advise that you get a lap.-banding to lose the weight because we all know that your weight could cause other life-threatening problems.”
    I weighed 294 at the time. It is now Sept 2011 and I have worked on losing weight down to 269lbs. Since I have come home my blood tests show that I have hypo-thyroidism. I am now taking 125mcg Synthroid. I have suspected for a long time that Family Practice Physicians knew very little about weight loss since most of my life, from the age of about 26 and at the weight of 125 lbs. my primary care physicians have suggested that I lose weight, never saying how or why. I have developed a philosophy: ” I have dieted my way to 294 lbs.” I hope that on a low carb, diet, taking 2 TBS of coconut oil each morning and staying away from as many highly processed foods as possible, I’ll be successful. I truly hope your methods and philosophy leads to breakthroughs in helping others who suffer because of overweight.

  2. One other comment. Have you considered the idea that it’s not just genetics that explains the different responses to processed food et al, but that it may be the level of exposure? I’m thinking of Gladwell’s discussion of cigarette smoking and “chippers” in The Tipping Point.

    • I don’t doubt that level of exposure is a factor, but the evidence for genetic predisposition is overwhelming.

  3. Great post Chris… love you’re posts/podcast always! This one is especially great as it encompasses the path/mentality that “paleo” folks should always strive for. Becoming close-minded on the subject is what got us into this mess.

    I’m currently 202 lbs, down from 279 lbs… at 5 foot 9″ theres still a fair way to go but I’m feeling amazingly since going “paleo”… that being said I’m incorporating more sweet potatoes/starchy veg into my diet as of late, especially when accompanied with increased intense activity. 🙂 Last year I could not have hoped to have felt this good.

    Keep up the great writing etc.

  4. Great post. The only time I’ve ever lost significant weight was on low-cal/low-fat diets, but of course gained it all back and damaged my metabolism in the process. Moved on to WAP guidelines diet and continued to gain weight. Changed to low-carb primal diet – lost some weight, but acquired new digestive issues, and then stalled weight loss. Currently on Perfect Health Diet. I’ve grown weary of dogmatic folks who think that their way is the only way for everyone. Thanks for looking at people as individuals.

    • Just curious. What kind of digestive problems did you develop on Primal LC diet? Were they resolved on Perfect Health Diet?

  5. Over weigh or any of the other chronic conditions were thought to be genetically linked. Work by microbiologists, with the help of electron microscopes and results from the many genome projects show that the “genic link” is really a bacterial link. There are more genes of historic bacteria in our bodies then actual human genes. These complex historic bacteria works by infecting our existing cells in many different ways and then slowly reproduce to give us a wide spectrum of chronic diseases including being overweight, diabetes, heart disease and muscular dystrophy to name a few. So, personal theories are not particularly of value when the science behind these problems is now understood. Don’t take my word for this take a look at the many sites that explain it. You could start your search with the Marshal Protocol to see how we could turn our current disease management system into a health care system.

    • Hi Ambrose.

      I liked what you were saying — until I got to the part about historic bacteria giving us a wide spectrum of chronic diseases. Except for major parasites, it seems to me more likely that the historic critters you mention would have set up housekeeping without much damaging us, their hosts. Isn’t that how our guts and other body systems survived and evolved to begin with?

  6. Very interesting Chris.

    What about the genetics of our microbiota?

    Quoting from article: http://www.npr.org/templates/story/story.php?storyId=125675700
    “When people in Japan began eating seaweed with their rice and fish, they also ingested some bacteria from the ocean. And as these ocean bacteria passed through the intestine, they exchanged bits of genetic code with the gut bacteria.

    Bacteria actually do this sort of gene transfer all the time. It provides them with a sort of evolutionary overdrive, Hehemann says.

    “This can happen really quickly,” he says. So a bacterium that can’t digest nori one day, can the next.

    This sort of digestive evolution has probably helped humans adapt to lots of new environments and lots of new foods.”

    I’m guessing genetics, whether they are human or bacterial are why I see conflicting information from patients regarding what foods they can and can’t tolerate despite having the same digestive condition, like Crohn’s. Some swear by white rice, while I can’t eat it well. I did some experiments on myself. I ate white rice and have a difficult time tolerating it. But I can eat white and whole wheat bread without any gastro intestinal problems. They even seem to improve my stool quality, to my surprise. I gained weight like crazy though and my acne flared up a bit.

    • Reid: I completely agree. That’s what I was referring to when I mentioned “dysregulated gut flora” in the article.

  7. Thank you for an interesting article. I have been listening to your other pod casts and enjoyed Dr Jaminet’s pod cast. I was thinking that it may be that it is the other way round. For virus and bacteria etc to live on they must co habit with us. So do you think that along with poor diet and other environmental stresses that it is us the host that is being tested for suitability? I don’t were I am going with this but it s just a weird thought!

    • My hypothesis is that aspects of the modern lifestyle (altered gut flora, insufficient dietary fiber, poor omega-6:3 balance, psychological stress, insufficient sleep, micronutrient deficiency, and physical inactivity – to name a few) cause inflammatory signaling in the hypothalamus, which causes leptin resistance and increased body fat. Also, disruptions in the hedonic regulation of food intake caused by excessive consumption of palatable food can trigger neuroadaptive responses in brain reward circuitries similar to drugs of abuse. Put these together – along with genetic predisposition – and you get obesity.

      • With all of these potential variables, don’t you think we’d see greater incidence of obesity? Most of the people I know are stressed, eat poorly, don’t sleep enough or well, lack enough exercise, eat highly palatable foods…

      • In this comment reply you mention sleep, but you left unnatural sleep patterns out of the main article under your description of modern lifestyle. Perhaps an edit is in order?

        • Regarding the term ‘obese’ though, don’t you think it tens to give us all a somewhat inaccurate picture of the situation? The media present a certain image of obesity that we have all become accustomed to, and so when we think of 20% of the population being ‘obese’ we think of these people waddling about something like 50+ pounds to lose. But this is actually not what an obese person is like. Obesity is defined as being more that 10% above the top of idea weight range. So a 5′ 5″ woman who weighed 168 pounds would be something like 18 pounds overweight and yet termed obese. Yes, she would be overweight, but she wouldn’t be in anything like the extreme condition we picture. In fact what we are accustomed to thinking of as ‘obese’ would be termed ‘seriously obese’ or even ‘morbidly obese’. So, while the situation where 20% of the population is obese is obviously not ideal, it’s also not quite as ghastly and extreme as our mental images might lead us to think

  8. “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…. I’ve yet to see a population that got fat eating sweet potatoes, fruit and white rice – without any exposure to modern food.”

    Time and time again, we’ve heard of non-Western cultures raise of heart disease, obesity, and diabetes coinciding with an increased adoption of the Western diet. That doesn’t mean they are also adopting a Western lifestyle, or a change in “environmental toxins, sedentary behavior, stress, infections and dysregulated gut flora.”

    And couldn’t we also suggest that “sedentary behavior, stress, infections and dysregulated gut flora” are to some degree a RESULT of poor diet that also do eventually contribute in a vicious cycle?

    One would expect that not all people become diabetic or obese because of xyz reason. That is how genetics work. Survival of the most fit. However, modern medicine and an abundance of food resources (whether good or bad) have allowed genetics proliferate that should have not. Just because some people (even a majority) don’t experience certain diseases of civilization does not suggest that there are not very specific underlying causes that are ultimately definable in a non-kitchen-sink theory.

    The focus should be: why do the people who become obese become obese? Not what potentially could make all people obese. It’s a red herring.

    • Robby: I agree to some extent, and that’s certainly true on a large population level, but there is a lot of research implicating environmental toxins in the pathogenesis of obesity. A high burden of environmental toxins tends to go hand in hand with modern, industrial foods, so it’s difficult to separate their effects. But more and more evidence suggests that those effects (of toxins) are significant, so any discussion of the causes of obesity should include it.

  9. Hi Chris I am so very proud of myself as in the last 3 months I have reached my Goal Weight of 140# down from 194#.
    I am just hoping I can keep it there. It took me 3 years to do it. Rosalyn

  10. And I wish there was more discussion in the debate about whether or not metabolic derangement is fixed or reversable. Of course, for the LCers, reducing carbs seems to be the end game. Me, I’m (foolishly?) betting that there’s a path to reversing metsyn. We’ll see what comes of my own little n=1!

  11. Hi Chris. Good job. I agree with you.

    Although I’m aware than australian aborigenes have a higher tendency to T2D, I do not have any reference to back up what you said:

    “Aboriginal Australians have a 4 times greater risk of developing adult-onset diabetes than Australians of European descent.”

    Do you think you could get me that?


    Best wishes


          • Thanks Chris. I’m already checking references on page 233 to see what comes up, since I try to keep an archive with the major references regarding health and disease in traditional populations.

            The other one I’m tracking concerns the vision acuity of Australian aborigenes (apparently under their traditional diet & lifestyle they could see almost as much as an Eagle) and Maori. I learned about this from an Australian physician friend of mine.

  12. This seems correct to me. Theories that attempt to explain human processes are very seldom (if ever) black or white. Yes, food in general is more processed, portions are larger, and snacks are everywhere. But none of that “makes” me obese unless I eat them. I lost a lot of weight eating “paleo” but stopped loosing very quickly. So in my case, there had to be more to it than avoiding foods that more than half the world eats quite successfully. I had to think seriously about how I became obese. Too much of everything is the short answer. That is why the palatability/reward and set point ideas are so interesting. I am working now on cutting fat, portion size, and salt (don’t eat much sugar), to see what happens.

  13. Great post Chris. I know Stephen Guyenet doesn’t seem to think that industrial seed oils play a role in obesity. I would love to hear/read an expanded discussion on this.

  14. A few things that might be added to “modern lifestyle”: (a) less sun exposure; (b) modern drugs allowing individuals (genes) who would have succumbed to TB and other killers to survive childhood (Dr Broda Barnes “New Population”); (c) genetic and other modification of plants (i.e. Dr Davis’ Wheat Belly); and, (d) plentiful supplies of cheap carbohydrates. Also, bad advice from government.

    • i’ve seen this point made before too, in the context that in modern life (non 3rd world contries specifically) we no longer have true selective pressure as we would have had naturally at most points leading up to our modern genotype. simply said factors that would not allow genetically non-fit people to live old enough to reach reproductive age and actually reproduce have been eliminated allowing for undesirable genotypes to continue to be propaged (which with this post would make sense, i.e genetic mal predisposition to cho tolerace, etc.).

      still even when nature loads the gun, it’s people who tend to pull the trigger most often.

  15. i’d like to add another ground rule: when discussing how an individual reacts to carbohydrates(i’m speaking primarily about glucose) it should be specified was to whether that person has a metabolism in a normal range or if they have symptoms of metabolic syndrome.

    • I mentioned that one in the article. It’s under the “metabolically damaged vs. healthy: apples & oranges” heading. I agree completely.

  16. Great read Chris. I agree with you about seeing the discussion revolve around your 3 last points. Especially more about the “role genetics plays in weight regulation”. Thanks!