Layne Norton Discusses the Stephan Guyenet vs. Gary Taubes Debate (a Debate on Joe Rogan’s Podcast)

157 minutes to listen the Stephan Guyenet vs. Gary Taubes debate on Joe Rogan’s podcast is a bit much for me right now. If you want to see the video of the whole podcast yourself, here it is:

However, I did read Layne Norton’s review of the debate, shown at the top. Let me engage with the scientific issues Layne raises. I want to be clear that I am not in this post defending or attacking anything that Stephan Guyenet or Gary Taubes said or didn’t say in the podcast itself. I’ll only be talking about my own views and Layne’s views as he expressed them in his review.

Evidence on the Effect of Insulin on Calories Out. The biggest criticism I have of what Layne says is that he repeatedly acts as if the energy balance or “calories in/calories out” identity were a theory. It only becomes a theory once you specify what determines calories in and calories out. On what determines calories in “in the wild” of people’s actual lives, the metabolic ward studies that Layne refers to repeatedly are uninformative, because they carefully control the amount of calories people consume. On what determines calories out, metabolic ward studies can provide some evidence on purely metabolic effects, Layne doesn’t address the study I discuss in “Framingham State Food Study: Lowcarb Diets Make Us Burn More Calories.” The other effect on calories out is how energetic one feels and therefore how much activity one does. Metabolic ward studies are also not great at showing these effects to the extent that not many activities are available while confined in the metabolic ward. And these studies might often try to standardize the activities of subjects in the studies.

One clue to a problem with the studies that Layne cites is this passage:

He would also likely point out that there was a small increase in energy expenditure on the ketogenic diet (that was near the detection limits of the equipment analyzing it). This difference in energy expenditure was transient during the first week of the ketogenic diet and didn’t last past that and didn’t produce meaningful differences in fat loss. This small increase in initial energy expenditure may likely be from the adaptation period of moving to use ketones & fats for fuels vs. carbohydrate. After that initial adaptation to ketones & fats, the small difference in energy expenditure disappears. In fact, it appears that when calories are equated, fat restriction may produce greater loss of body fat than carb restriction by a small amount. 

Since any signal from each subject combined with a large enough sample can overcome any amount of uncorrelated noise, “near the detection limit” is a hint that a study is underpowered statistically. Nothing should be called “small” simply on the basis of having a low level of statistical significance in a small sample. And nothing should be called “small” if it could possibly cause, say, the pound a year weight gain of many American adults that is a description of much of the rise in obesity.

The fact that obesity comes on as slowly as it does for many people means that metaphors about fat being locked in cells (which I have used myself—see “How Low Insulin Opens a Way to Escape Dieting Hell”) when insulin levels are high must be taken as an indicator of direction, not as absolute statements. Layne makes the point I am making nicely in the following passage:

Now we have 2 central themes of the CIM with extremely strong evidence to the contrary. Let’s examine this notion that insulin is a magical fat storing hormone. Gary focuses on short term effects of insulin after a meal on fat storage (particularly around 2:09:35). Yes, insulin drives free fatty acids into cells, but assuming this is the cause of obesity takes a very simplistic view of adipose cell metabolism. Fat is constantly being stored into adipose and released from adipose. It is the net synthesis of fat minus the breakdown of fat in adipose that will determine fat balance and net fat loss or gain (I’m simplifying the model here but it’s accurate for our purposes).

Insulin doesn’t have to inhibit the release of fat from fat cells completely to be an important enough obstacle to fat burning to have a long-run effect. And if insulin levels, while not completely stopping fat burning, inhibit fat burning enough to lead in the long-run to weight gain, it could usefully be called a magical fat storing hormone.

How the Carbohydrate-Insulin Model Works. Let me now turn to what I find Layne’s most interesting paragraph. It’s first sentence is:

Hopefully, you’re convinced that part of the CIM [Carbohydrate-Insulin Model] is not plausible (calories don’t matter only carbs), but we can also rebuke other aspects of it.

There are two ideas here. It would be silly if the Carbohydrate-Insulin Model said that “calories don’t matter.” Calories are part of the causal pathway, the point of the Carbohydrate-Insulin model is that—even focusing on biology apart from psychology—calories are not the beginning of the causal pathway. As I interpret it, the Carbohydrate-Insulin Model emphasizes that—especially for those of us who aren’t in metabolic wards—calories are endogenous; therefore one should focus on the hormonal forces that drive calories in and calories out, rather than immediately jumping to trying to directly control calories in and calories out, as many people attempt to do.

Calories do matter, but the weight-loss strategy most people in our culture follow when they fixate on calories is usually a failure. Focus on eating low on the insulin index and on when you eat and calories in/calories out is likely to move in a direction that leads to weight loss without your directly thinking about calories. (See “Forget Calorie Counting; It's the Insulin Index, Stupid” and “Stop Counting Calories; It's the Clock that Counts.”) Once you have moved to low-insulin-index eating and a short eating window each day, you might want to experiment with thinking about the number of calories you are eating, but thinking about how much you eat should definitely come only third after thinking about what you eat and when you eat.

The reason to focus first on what you eat and when you eat and only then on how much you eat is that your body has decent mechanisms for controlling how much you eat at a sitting when you are eating healthy things, and how much you eat at a sitting puts a reasonable limit on how much you eat overall if you aren’t eating all the time.

Does Insulin Lock Fat in Fat Cells? The remainder of Layne’s most interesting paragraph is:

The idea that insulin traps free fatty acids in cells making the other tissues feel like they are “starving” has also been demonstrated to be incorrect. If this was correct, we would expect to see depleted levels of free fatty acids in blood during fasting in insulin resistant people. But we don’t. Obese people release MORE fatty acids from adipose, not less.

This is not a good argument on Layne’s part. As soon as one recognizes that even fairly high insulin levels do not completely lock fat in fat cells (even though insulin has an effect in that direction), it becomes obvious that number and size of fat cells is a factor in how much fat gets out into the bloodstream as well as insulin levels. So one should compare blood levels of fatty acids during fasting of people who have the same weight and amount of body fat but different levels of insulin to see the extent to which insulin goes in the direction of locking fat in fat cells.

Does Locking Fat in Fat Cells Leave the Rest of the Body Feeling Starved? But wait, Layne has an argument that even if fat is locked in fat cells, that doesn’t lead to hunger that causes one to eat more:

Hold on though, I’m not done crushing the CIM. Remember that one of the core themes of the CIM is that insulin causes fat to be trapped in fat cells and thus we can’t burn it and it’s not accessible to the other tissues of the body so we end up overeating because the rest of our tissues are “starving.” This aspect of the CIM has also been tested (indirectly) using a drug called acipimox which inhibits release of fats from adipose tissue. Not only did the subjects taking the drug not get fatter but they also did not increase their caloric consumption relative to the placebo group. [8: Makimura, H., Stanley, T. L, et. al. (2016, March). Metabolic Effects of Long-Term Reduction in Free Fatty Acids With Acipimox in Obesity: A Randomized Trial. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/26691888]

The problem with this argument is that the people in this this Acipimox trial were eating freely, which for most Americans means eating almost all the time. If you are getting plenty of sugar and fats in your bloodstream from food you have just eaten, you don’t need fat from your fat cells in order to keep hunger at bay. It is when trying to lose weight that having plenty of fatty acids in the bloodstream from your fat stores is crucial for not feeling hungry. My prediction is that taking Acipimox would make it more painful to fast and more painful to try to lose weight when using the common strategy of reducing calories while keeping one’s schedule of eating unchanged. It is a very different experiment to see if Acipimox gets in the way of attempts at weight loss than whether it causes weight gain.

The study claimed benefits of Acipimox. Such benefits are reasonably plausible: if one is eating enough that the fatty acids in the bloodstream from one’s own fat cells wouldn’t (on net) get used, those extra fatty acids are not really helpful and might have some undesirable side effects.

One of my most important contentions is that insulin above a certain level makes it painful to cut back on calories. So it is better to both stick to low-insulin-index foods and to go to the extreme for certain periods of cutting calories back to zero so that insulin levels go low enough that the gates are wide open for fat to come out of the fat cells. When you cut back on calories, you need energy resources from your fat cells to take up the slack, and high insulin levels interfere with that. A few calories of high-insulin-index foods could easily make you quite miserable on a low-calorie diet—much more miserable than you would be eating nothing at all. And far from being miserable, you might not suffer much at all eating nothing if the last things you ate before fasting was food that is low on the insulin index. (Fasting here means drinking water—and maybe unsweetened tea or coffee—but not eating food.)

Exercise. One place where both Layne and I disagree with Gary Taubes is this:

Gary also states in the debate that exercise doesn’t really matter (see 1:42:10). If that was the case, where are all the fat marathon runners who eat high carb diets? Where are all the pro athletes gaining massive amounts of weight on high carb diets?

I said my piece on exercise in last Tuesday’s post: “On Exercise and Weight Loss.” The most relevant point there is that exercise is very valuable for avoiding gaining weight, but much less helpful for losing weight.

Gary Taubes. When I listen to most people, including Gary Taubes, I habitually try to turn what they are saying into the strongest version of the argument that I can come up with. Then I focus on my version of the argument. That makes me value people who have a take on things that provokes useful thoughts. Gary Taubes is one of those people. I can see that he might be frustrating to people who, instead of taking his arguments and improving on them, can only see his arguments as stated. I have yet to meet anyone who is right all the time or anyone who is wrong all the time. But I feel that Gary’s ideas are in a very useful direction—a direction that can be converted into testable science by those whose business it is to turn rough ideas into testable science.

Update, April 9, 2019: Layne Norton and other respond on this Twitter thread.

Layne Norton: good attempt at a rebuttal I guess. But your point about low carb causing greater energy expenditure and that @KevinH_PhD 's may have been underpowered (not based on previous data) ignores the other 30 studies looking at the same thing and actually slightly favoring low fat on EE

Kevin Hall: Our ketogenic diet study was powered to detect a 150 kcal/d effect size for the primary outcome. This was pre-specified in the protocol to be the minimum physiologically important effect on 24hr EE & signed-off by @NuSIorg. The null result led to shifting goalposts by @garytaubes

Sarong Joshi: If the bmj study is correct and LC increases metabolic rate And majority of hunter gatherers for majority of the part were low carbers And if optimum foraging strategy is correct That would just mean LC has least return on investment, evolution would've wiped out low carbers

I should say that, whatever Gary Taubes said, something less than 150 “calories” (technically, the usual calorie is a “kilocalorie”) a day, say 100 calories a day, is still an important effect. (Sarong’s argument is robust to that point.)

Don’t miss my other posts on diet and health:

I. The Basics

II. Sugar as a Slow Poison

III. Anti-Cancer Eating

IV. Eating Tips

V. Calories In/Calories Out

VI. Other Health Issues

VII. Wonkish

VIII. Debates about Particular Foods and about Exercise

IX. Gary Taubes

X. Twitter Discussions

XI. On My Interest in Diet and Health

See the last section of "Five Books That Have Changed My Life" and the podcast "Miles Kimball Explains to Tracy Alloway and Joe Weisenthal Why Losing Weight Is Like Defeating Inflation." If you want to know how I got interested in diet and health and fighting obesity and a little more about my own experience with weight gain and weight loss, see “Diana Kimball: Listening Creates Possibilities” and my post "A Barycentric Autobiography. I defend the ability of economists like me to make a contribution to understanding diet and health in “On the Epistemology of Diet and Health: Miles Refuses to `Stay in His Lane’.”