Pontzer’s Burn and Metabolic Rate Mechanisms

I just finished reading Herman Pontzer’s book Burn.  It’s good, I recommend it! I don’t agree with everything, though. Pontzer is the metabolic researcher who went to Africa to study the metabolic rates of Hadza hunter gatherers.  To his surprise he discovered that hunter gatherers burn the same number of calories per day as  sedentary office workers despite the fact that they spend their days walking and doing hard work like climbing trees to collect honey and digging up tubers with wooden sticks.

The idea that people who have a very active lifestyle burn more calories than other people simply seems to be incorrect, as counter-intuitive as that sounds.  The body compensates.  Pontzer calls this the constrained energy model.  He supports this with the research of his colleagues, citing studies of the Shuar of Ecuador and a study of black women living in Illinois versus a more active population of women in Nigeria.  

He concludes:  people who work harder don’t necessarily burn more calories. On this I agree.

This is a brave conclusion. I’ve now read a lot of metabolic research papers.  The metabolic research field is oddly obsessed with movement.  Researchers will follow people around for days on end marking down the amount of time spent walking, cooking, hoeing a row of corn, sleeping, etc.  They use metabolic machines to calculate the exact amount of energy all of these activities require.  It is difficult to swim against the current of your own field.

Pontzer also cites a large body of evidence that starting an exercise regimen won’t increase your caloric burn as much as you think.  He cites a study from the Netherlands where people who had never exercised before were trained to run a marathon over a period of a year.  By the end they were running 25 miles per week.  Pontzer says this amount of running plus the additional muscle mass should have increased daily burn by 390 calories, but in fact it only increased burn by 120 calories.  So if you train to run a marathon, you can eat an extra one of those little 100 calorie snack packs a day and a handful of peanuts. I’m guessing that’s not the return on investment you were hoping for.

Basal Metabolic Rate

In fact, your total caloric burn seems to be tied quite closely to your Basal Metabolic Rate (BMR, this is very similar to the Resting Metabolic Rate – RMR – which I’ll use interchangeably).  BMR is tested in the morning after an overnight fast. The subject lies on a couch or bed in a reclined position while breathing into an apparatus that measures Oxygen consumed and carbon dioxide exhaled.  From this we can measure BMR.   For most people most of the time your total calories burned will be 1.5-2 times your BMR.

Pontzer is very clear that you cannot increase your BMR.  Nor does he think you can change your total calories out without training like an Olympic athlete, who can increase their caloric burn to around 2.5 times BMR.

He DOES think you can permanently lower your BMR through prolonged caloric restriction, however.  He cites Kevin Hall’s research of contestants on The Biggest Loser TV show, where obese people reduce their caloric consumption by half while training inttensely.  Even 6 years after the show ended, Hall found that the contestants had a lower BMR than expected.  

Then he talks about Ancel Keys 1945 starvation experiment where Keys fed conscious objectors half of their daily caloric needs for 6 months.  Upon refeeding Pontzer says, “As their weight came back their bodies called off the alarm.  Unlike the Biggest Loser contestants, their BMRs returned to normal”.

What’s The Difference?

I found that to be the single most interesting line in the book.  For some reason, the metabolism of Biggest Loser contestants was permanently damaged through caloric restriction but the metabolisms of the men in Keys’ study  were not!  Pontzer is completely incurious about this.  He just states it as fact and moves on.

Surely something is different about the two groups.  Perhaps the difference is because one group was obese at the start of the study and the other group was not.  Perhaps there was a dietary change between 1945 and  2016 such as the rapid increase in polyunsaturated fat in the US diet that was responsible for the change.  Perhaps both are in play.

Pontzer also acknowledges that there are wide variations between BMRs both between and within populations.  He cites the Tsimane farmer-foragers of Bolivia, stating, “Tsimane adults have elevated BMR because of their high levels of parasitic and bacterial infection”.  He states it as a certainty, although in his peer-reviewed  paper​1​ there is more room for interpretation.

“Tsimane RMR is 18 to 47% (women) and 22 to 40% (men) higher than expected using six standard prediction equations.  … An adult diagnosed with helminths and marked WBC elevation (additional 3.0 3 106 cell/lL) can expect to have excess RMR of 143 to 168 kcals/day, depending on the prediction equation used. This amount reflects increases of 10 to 12% and 11 to 15% above predicted mean RMR in men and women, respectively  …  Despite the size and number of significant effects, our best-fit models explain only 9 to 19% of the variance in excess RMR”.

Pontzer et al., “High resting metabolic rate among Amazonian forager-horticulturalists experiencing high pathogen burden

I have argued on this blog that pure starch eating cultures have very saturated body fat and this gives them a high metabolic rate when food is plentiful. The largest study on obese caucasians found an average BMR of 28.6 kcal/kg of fat free mass (FFM) amongst men​2​.  The Biggest Loser contestants had a BMR of 27.1 kcal/kg FFM 6 years after the contest, although they had a quite respectable 34.5 at the beginning​3​.  The Harris-Benedict equation, developed in the US in 1919 predicts “normal” BMR to be 30-31 kcal/kg FFM by my calculation.  Male rice farmers in Korea were reported to have a BMR of 36.3 kcal/kg of FFM in the off-harvest season​4​.  Male Lao rice farmers were reported to have a BMR of 39.9 kcal/kg FFM.  Thai male rice farmers, averaging 46 years of age, had a BMR of 37.8 kcal/kg FFM at harvest season​5​.  Their wives (same age) registered an eye-popping 40.8 kcal/kg FFM.  By comparison, the Tsimane men who Pontzer says have an elevated BMR due to pathogen burden have a BMR of 38.0 kcal/kg FFM.  In this context, the Tsimane BMR are not exceptional, they are normal for a starch eating culture.  

The Thailand study also includes a dietary analysis.  The macros that produced the female BMR of 40.8 kcal/kg FFM was 84% carbohydrate (as rice), 11% protein and 5% fat.  This is what I mean when I say “starch eating cultures”.

This can be seen globally.  Female Mossi farmers growing sorghum and millet in Upper Volta (West Africa) were found to have a resting metabolic rate of 41.3 kcal/kg FFM.  This paper has its problems – RMR was not measured first thing in the morning and it’s unclear if any of the women were lactating – but it is still another piece of evidence that metabolic rate isn’t set in stone.

Conversely, there are studies that show quite low metabolic rates, all the way down to 23.9 kcal/kg FFM among male farmers in Tanzania​6​.  I suspect metabolic rates that low are due to long term food shortage, but that data is not presented.

PopulationBMR (kcal/kg Fat Free Mass)
Male Farmer Tanzania23.9
Obese White Males28.6
Biggest Loser Contestant Before34.5
Biggest Loser Contestant 6 Years After27.1
Harris-Benedict Equation Prediction30-31
Male Tsimane farmer-forager38.0
Male Korean Rice Farmer36.3
Lao Male Rice Farmer39.9
Female Thai Rice Farmer Pre-harvest32.4
Female Thai Rice Farmer Harvest40.8
There are huge differences in metabolic rates between groups and within individuals that cannot all be chalked up to inflammation.

Mechanisms Matter

Given the massive variation in BMR measured around the world, I would expect more curiosity from Pontzer about the mechanisms that control BMR.  Instead his position seems to be that your BMR is your BMR and there is nothing you can do about it, not even exercise will help.  To suggest that BMR can be changed only opens the door to hucksters and charlatans.  

Yet in addition to seeing variations in BMR between cultures and individuals there are also large differences WITHIN individuals.  The BMR in the Biggest loser competition varied from 34.6 kcal/kg FFM before the contest to 27.1 kcal/kg FFM 6 years after.  The female Thai rice farmers BMR varied from 32.4 kcal/kg FFM in the pre-harvest season to 40.8 during harvest season.  If the Biggest Loser contestants had a BMR of 40.8 kcal/kg FFM and a typical total energy expenditure of 1.7 times that, they’d burn 4900 calories a day, which Pontzer argues is at the top end of how much the human digestive system can absorb in a day.  What causes the variation?  Why did the metabolic rates of the conscientious objectors bounce back in the Keys study but not in the Biggest Loser contestants?

I am fat and I’m a molecular biologist, so I think about the mechanisms of obesity.  I know that mice lacking SCD1 have very saturated fat, extraordinarily high metabolic rates, are protected from obesity and have a high ratio of NAD+/NADH.  I presume that the mechanism by which saturated fat regenerates NAD+ is by generating mitochondrial ROS, of which glutathione is oxidized in the process of scavenging.  Oxidized gluathione is recycled by glutathione reductase which generates NADP+, which the mitochondrial enzyme NNT uses to regenerate NAD+.

The NAD+ allows the citric acid cycle to continue spinning and activates the sirtuins to keep our mitochondrial enzymes deacetylated.  In other words, NAD+ keeps our metabolisms humming. Knowing this, my prediction was that I would find the highest metabolic rates in the world in rice eating cultures, and I did.  Rice is incredibly low in fat (and therefore PUFA)  and it is easily stored so that rice-growing cultures don’t have as much of a metabolism depressing  “hunger season” as some other farming cultures.  Eating mostly (almost entirely based on the macros given in the Thai study) white rice will make your fat very saturated, just like the SCD1 deficient mice.

When you’re interested in biological  mechanisms, it is easy to come up with testable hypotheses.  Here’s one: within a given population, BMR should be correlated with the lactate/pyruvate ratio in the blood.  Blood lactate and pyruvate are easy and cheap to test and give an indirect indication of NAD+/NADH ratio.​7​

When you’re not interested in them I suspect it is easy to get caught in a loop of measuring activity levels and white blood cells and immune markers forever and winding up at “our best-fit models explain only 9 to 19% of the variance in excess RMR”.

ASIDE:  If you grew up eating oils, switching to an all-rice diet will probably not work the same for you as it does in Thailand.

  1. 1.
    Gurven MD, Trumble BC, Stieglitz J, et al. High resting metabolic rate among Amazonian forager-horticulturalists experiencing high pathogen burden. Am J Phys Anthropol. Published online July 4, 2016:414-425. doi:10.1002/ajpa.23040
  2. 2.
    Lazzer S, Bedogni G, Lafortuna CL, et al. Relationship Between Basal Metabolic Rate, Gender, Age, and Body Composition in 8,780 White Obese Subjects. Obesity. Published online January 2010:71-78. doi:10.1038/oby.2009.162
  3. 3.
    Fothergill E, Guo J, Howard L, et al. Persistent metabolic adaptation 6 years after “The Biggest Loser” competition. Obesity. Published online May 2, 2016:1612-1619. doi:10.1002/oby.21538
  4. 4.
    Kim EK, Yeon SE, Lee SH, Choe JS. Comparison of total energy expenditure between the farming season and off farming season and accuracy assessment of estimated energy requirement prediction equation of Korean farmers. Nutr Res Pract. Published online 2015:71. doi:10.4162/nrp.2015.9.1.71
  5. 5.
    Murayama N, Ohtsuka R. Seasonal fluctuation in energy balance among farmers in Northeast Thailand: The lack of response of energy intake to the change of energy expenditure. Eur J Clin Nutr. Published online January 1999:39-49. doi:10.1038/sj.ejcn.1600675
  6. 6.
  7. 7.
    Istfan N, Hasson B, Apovian C, et al. Acute carbohydrate overfeeding: a redox model of insulin action and its impact on metabolic dysfunction in humans. American Journal of Physiology-Endocrinology and Metabolism. Published online November 1, 2021:E636-E651. doi:10.1152/ajpendo.00094.2021

17 thoughts on “Pontzer’s Burn and Metabolic Rate Mechanisms”

  1. “When you’re not interested in them I suspect it is easy to get caught in a loop of measuring activity levels and white blood cells and immune markers forever and winding up at “our best-fit models explain only 9 to 19% of the variance in excess RMR”.”

    Ouch, or should I say…burn?

    Anyway, the difference between the Minnesota Starvation Experiment participants (or long term POWs and concentration camp victims) and modern “eat less, move more” calorie restriction dieters seems quite stark to me. The former became skin and bones emaciated, while the latter often become more skinny-fat with both reduced lean mass and stubborn fat plus significant rebound weight gain. I have wondered why this should be the case, and the framework laid out here seems to be one of the most credible attempts at resolving these conflicts. There may also be an element of protein restriction and amino acid profiles which is definitely pushing into Peat territory.

  2. Always a good day when you post, Brad.

    The problem you focus on a lot is losing calories to adipocytes. There are 2 ways we can compensate for this: eating more to feed the other cells, or simply downregulating metabolism. Probably both. Most people get lost in the downstream effects of those 2 things.

    I’ve had the same experience of making mechanistic theories. Everything else seems so lame in comparison. On that topic, I had an “aha moment” the other day. PUFA lowers LDL and SFA raises it. Everybody talks about what it means for heart disease. But we know by Protons/ROS that PUFA makes adipocytes insulin sesntitive. So PUFA lowers blood lipids *specifically* by stuffing it in adipocytes. That seems like an important thing to understand! The downstream effects of that are obesity or diabetes or both (depending on # of fat cells and ability to make more). Once adipocytes are sufficiently overstuffed you get actual pathologically raised lipoprotein levels, extra vulnerable to oxidation owing to their high PUFA content. So, CVD, diabetes, and obesity all belong in the same discussion and can be connected by mechanisms rather than medical correlation. You don’t even need to cite amorphus “inflammation!”

    I’ve been making a lot of posts/comments on r/SaturatedFat on mechistic theories. You would like them. I’m u/10dencies. Mostly recently I postulated that mercury accumulation could explain bad reactions to ALA. I’d love to chat with you directly some time.

  3. A rice diet *might* work. Dr Kempner created a rice diet in 1939 to treat hypertension and found that it helped with weight loss, T2DM and a few other diseases. There are a few contemporary high starch, low protein, no/low fat diets that claim to have multiple benefits (McDougal, Esselstyn etc). The irony here is that the body will convert some of that starch to saturated fat if it needs to. Then there is The Potato Hack, eating nothing but potatoes. I think the guy did it for a year. The problem is that these are mind-numbingly boring. Kempner used a riding drop to “encourage” his patients to keep to the diet (they were locked up in a hospital). It could be that being low fat means low PUFA. A high starch + SFA might work. Oh wait, that’s kinda like TCD isn’t it?

    1. I’ve been doing this for a few months now. A little weight loss but nothing mind-blowing. The starch does tend to give me the same “omg energy!” feeling as stearic acid-enriched low-carb foods used to do. One nice thing is it’s generally cheap, or can be. Main concern I have is getting enough calcium – already working on my vitamin D levels but I suspect high-starch diets can be deficient in calcium if you’re not including a ton of beans or specific high-calcium veggies. Maybe other minerals need bolstering too.

      1. So I’d say this might corroborate Brad’s last thought that – if you have seed oils in your belly – rice diet won’t necessarily produce mind blowing results. But over years, maybe it will, if you stick to it faithfully enough & work to burn off the extra fat by traditional exercise means from time to time.

        1. Total N=1 here:

          Hubby and I have been “aware of” TCD since about Sept. now. Hubby has been diligent on it since then (so, 5+ months) and has totally resolved his hypoglycemia. He can now intermittent fast or whatever perfectly capably in a fairly physical/engaging job just by eating TCD.

          The other week I got a cute mini rice cooker. I discovered Kempner’s rice diet and offhandedly mentioned it to him as a way to maybe lose the Lbs a bit quicker. He’s always game for new things so he was like “sure I like rice I’ll try that” (LOL)

          OMFG. He was dying. He couldn’t even function half a day on rice with zero fat. Had to get fat into him before he passed out. He isn’t at all one to be dramatic – if something works for him and is cheap and easy he is all about it, so this wasn’t him “complaining” or anything.

          Somehow over 5 months of TCD his mitochondria became fat adapted (I guess?) and didn’t know what the heck to do with pure starch. It would have been comical if it wasn’t so sad.

          Took him a day to recover (he gets tremendous hypoglycemia swings and physical internal belly pain on carbs prior to TCD) and he’s good as gold now.

          His breakfast this week has been a bowl of rice with butter. That gets him through 8-10+ hours before he eats dinner in the evening. So just 2-3 T of butter makes all the difference.

          Not sure what to take away from it for anyone not hypoglycemic, but I figured I’d share. 🙂

          1. Wanted to add:

            When first starting TCD he had several weeks of intense swings and pain. He actually was at the point he said he doesn’t think it will work for him.

            He was carrying around butter croissants and bagels with butter & cream cheese in case of emergency. Like, so he wouldn’t pass out on the highway sort of emergency.

            That was all of September pretty well, and since then he’s like a new person. It’s incredible.

            He used to do well comfort wise on keto but his thyroid and adrenals tanked (his body temp is still low and his testosterone is still tanked as we speak, so dealing with that now)

            He never thought he could eat carbs. He thought he would have to choose between hypoglycemia and keto. This has been life changing.

          2. That’s an interesting observation. I never go without a little fat – cream in coffee and usually 1/2 tblsp butter used to saute the veggies I put on my rice. My goal is <=40g fat a day, but not 0g. (I usually exceed that 40g by a bit)

    2. Forgive my ignorance, but how could anyone eat nothing but potatoes (or rice) for a year and not die from malnutrition? B-12, K2, for a start. Not found in pure starch as far as I know. There are very few, if any long term vegans who are healthy, and that’s even when they are eating a wide variety of plants.

      1. I’m not sure about K2, but the theory is B12 comes from bacteria – always does anyway – and traditional starch eaters were not, uh, as “sanitary” as we are nowadays.

        From one of John McDougall’s videos, there is a demarcation here-

        Above-ground starches (grains, etc) need supplemental things – usually vegetables

        Below-ground starches (especially potatoes, sweet potatoes) are theoretically whole nutrient sources. I’m a little skeptical about white potatoes vitamin A content though. Sweet potatoes should be fine.

        McDougall advocates his vegan followers use a B-12 supplement and it’s the only supplement he suggests; he’s passionately anti-supplementation otherwise. As a doctor, he does acknowledge folks with vitamin D levels <20 should have that addressed somehow.

        1. My understanding is the potato diet includes a small amount of butter to provide missing nutrients. A few people have talked about it; I know Nikoley (freetheanimal.com) has a bunch of posts, and Eades (marksdailyapple.com) has a few.

        2. May want to look into Grant Genereux and his claim that vitamin A isn’t even a vitamin but a toxin. Before rejecting out of hand he has a lot of compelling observations including being on an almost zero A diet for 7 years now with nothing but positive health effect. https://ggenereux.blog/

  4. Q came to mind after rereading this post-

    Do you have any blog posts or otherwise research articles associating fasting & calorie restriction with PPAR gamma and/or SCD1?

    Thinking about Ancel Keys experiment vs Biggest Loser here.

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