This is not a traditional review of Gary Taubes’ Why We Get Fat, though by the end I’ll definitely encourage you to get the book.
It’s not a review for a couple of reasons. First, as Taubes acknowledges, WWGF is the simplified, consumer-friendly version of his Good Calories, Bad Calories. I summarized and commented on the basic points of his argument a little over a year ago, and while I have a couple of concerns about the book (more later), I don’t think my review of WWGF would add much to what I’ve already written.
But if you’d like to read a review, here are a few:
- Supportive – Steve Parker, Tom Naughton, Barbara Berkeley, John Durant
- Critical – Yoni Freedhoff, Harriet Hall, Debra Sapp-Yarwood
But the other reason that it’s not a review is that I’d rather take the opportunity to specifically discuss a couple of the main points of Taubes’ theories in a broader context than a typical book review.
Carbs & physics
Many folks who don’t buy Taubes’ arguments get hung up on thermodynamics and, in my opinion, often misstate Taubes’ point. Rather than go into details here, I’ll just link you to Feinman’s “A calorie is a calorie” violates the second law of thermodynamics — and leave never-ending arguments about carbs and metabolic advantages to those who seem to enjoy them.
Speaking of arguments, it’s a bit frustrating to me that the tone of the conversation is starting to look a lot like partisan bickering in politics.
I realize that we’re all passionate about this, and yes, there’s a lot at stake, but I’m with Monica Reinagel who recently tweeted:
As a committed myth-buster, I understand skepticism. But it can be exercised without snarkiness, hostility, and disrespect.
One reason this is important is that, just as in politics, there’s probably considerable room for finding compromise between the “calories in/calories out” & low-carb crowds. I thought this comment said it well:
The main thrust of the new ideas is that the right dietary composition helps you cut down on calories, whereas the wrong composition does the opposite. Discipline + reduced temptation is more successful than just discipline, and less calories is not a fully separate concept from proper composition.
Carbs & insulin … chicken or egg?
In a recent email interview with Tom Naughton, Taubes wrote:
As I discuss in GCBC, it’s quite likely that sugar — by which I mean a roughly 50-50 mixture of glucose and fructose — is the trigger that first sets off insulin resistance and then the vicious cycle from eating all carbs that leads to obesity, diabetes, etc. And these populations — Southeast Asians, in particular; I’m not really familiar with the Kitavan story — ate excruciatingly little sugar. This, to me, is a primary piece of evidence arguing that sugar may be the necessary trigger. That would explain why when the Asians come to the U.S., they do start succumbing to these metabolic disorders. They start eating more sugar.
Another possible explanation is that the carbs these populations consumed, until very recently, were low glycemic index carbs — not highly refined rice and wheat. There are many variables that could explain it, which is one of the reasons observational evidence like this is so potentially confusing.
Seeing this spelled out this way, though, just creates more questions for me. Is fructose/sugar just a trigger? Or is the fundamental problem insulin resistance which carbs exacerbate? Or is there something else, less well understood, that “breaks” appetite regulation in some folks?
Whatever it is, it’s conceivable that excess dietary carbs might be an issue (fuel for obesity) and that removing them might be useful — at least for some. But if (generic) carbs aren’t actually the source of the problem, then perhaps they’re not the best (or perhaps only) target for the solution.
Insulin sensitivity & carbs
I’ve heard Taubes is working with Robert Lustig on a book about sugar and fructose [update 1/28: turns out they aren’t doing a book after all], and I know that Lustig attributes fructose metabolism in the liver as one of the “cornerstones” of the obesity epidemic.
In fact, in the Naughton interview, Taubes adds:
So it is quite possible — and laboratory work backs this up — that sugar causes the initial insulin resistance because of the effect of the fructose on the liver. So if we never had sugar, we’d be able to eat the other carbs with relative impunity. But being possible doesn’t mean it’s true. I suspect it is, but I’m not sure exactly how this can be tested.
[Sidebar: Lustig addresses carbs and weight in a recent podcast with Jimmy Moore (starting at 4:35):
I think a low-carb diet has a lot of things going for it. My question is whether or not it is necessary for the majority of the population. … To be honest with you, most people can’t stay on a low-carb diet, and that’s what the data shows, [that] people pretty much get tired of it after about six months. …
[That said] there are a lot of physicians who think this is all garbage. They think a calorie is a calorie and it doesn’t matter, and therefore it’s eat less, exercise more and if you don’t lose weight it’s your own fault. I could not be further on the opposite side of that.
Later in the interview, Lustig suggests that the main point of disagreement between he and Taubes is on fiber; Lustig thinks it plays an important role, Taubes less so.]
In another Jimmy Moore podcast, Kurt Harris talked about his disagreement with Taubes (starting at 43:55) (emphasis mine):
If I’ve deviated from being a complete Taubesian, it’s on insulin. … I started out thinking, after reading Good Calories, Bad Calories, and, like a lot of people still think, that the connection was carbohydrates chronically high, you need high insulin to handle the carbs, and [that] the high blood sugar is causing half of the bad things and other half is being caused by the insulin itself. That is backwards in my view.
The reason people have chronically high insulin is because their insulin sensitivity is abnormal. [Abnormal insulin sensitivity] is caused by an abnormal inflammatory state, which may be related to consumption of specific types of carbohydrates, but in my view, no longer do I think of that as being related to the macronutrient ratio of carbs.
Paul Jaminet concurs (emphasis mine):
This brings me to a point of difference with Gary Taubes. Although glucose is toxic in high doses, the body has an extensive machinery for disposing of excess glucose. As we discussed in our last post, all tissues of the body participate in glucose disposal. Dietary glucose is not likely to do much damage unless the body’s glucose-disposal machinery has been damaged by other toxins first.
Insulin, leptin, & the liver
Of course, many low-carb dieters will tell you that they find going low-carb a terrific way to lose weight. I’ve done ketogenic diets in the past, and I was quite pleased with the success I had with weight loss, the energy I had on the diet (thank you ketones), and the lack of hunger and cravings I had.
That said, like the folks Dr. Lustig mentioned, I’ve not (yet?) found that I can maintain low-carb dieting for a long period of time. Back when I did these diets, I had the not-atypical problem that many low-carbers have … I wanted to eat the foods I missed.
I also was (am?) concerned about the long-term implications of very low carb. Yes, I realize that carbs aren’t “essential” in the way that amino acids or some fatty acids are. I also think the ancestral paleo/primal folks are likely correct that the conventional carbohydrate-based diet may not be ideal given human evolution. Finally, I think the role carbs may play in inflammation and endogenous gylcation make them a worthy target for moderation at the very least.
But … if high dietary carbs and insulin response aren’t the primary villain, then what is? I’m becoming increasingly intrigued by the idea of hepatic injury and its role in obesity and metabolic syndrome.
Chris Masterjohn describes one possible connection between liver damage and obesity in his response for the insulin bad-rap post (emphasis mine):
These numbers are pretty similar to what Zelman reported in 1952 (6). Zelman wrote long before the obesity epidemic emerged and it took him 18 months, a full year and a half, to find 20 obese people who weren’t alcoholics. He reported that about half of these people were glucose intolerant, meaning that when they were given a load of glucose, their insulin couldn’t work fast enough to prevent an abnormal spike in blood sugar.
Zelman’s finding was similar to what had already been reported in larger groups. His new contribution was to show that upon liver biopsy, all patient but one — a full 95% — showed signs of at least mild to moderate liver damage. The longer the people had been obese, the more damaged their liver was. Long before the discovery of leptin, a hormone that acts on the hypothalamus, Zelman hypothesized that damage to the hypothalamus caused obesity and cravings for nutrient-poor sweets and fats, that the consumption of too much sugar and fat without sufficient choline, protein, and other nutrients led to liver damage, and he cited another researcher’s suggestion that liver damage led to glucose intolerance.
Why would liver damage lead to glucose intolerance? The liver not only contributes to clearance of glucose from blood, but, more importantly, the liver produces glucose from protein in a process called gluconeogenesis. Ordinarily, the liver stops making glucose in response to insulin. However, if liver damage prevents this response, the liver will keep making glucose even when we don’t need any more of it. More glucose in the blood will cause the pancreas to make more insulin, but the insulin will fail to stop the liver from making more glucose, and a vicious circle will ensue. With increasing levels of glucose and insulin in the blood, many other tissues such as skeletal muscle and fat may deliberately stop responding to insulin themselves in order to prevent glucose overload in their own cells.
Masterjohn suspects that insulin resistance leads to leptin resistance, and it is this leptin resistance that is tied to overconsumption of calories because the brain no longer responds to signals to stop eating. If so, this again suggests that the response should be towards reducing insulin resistance and/or leptin resistance … and that if avoiding dietary carbs doesn’t do this effectively, then it is not an adequate solution.
Back to Taubes
I have two other concerns with Taubes’ arguments in WWGF. One is slightly pedantic: his views on toxic environments.
Of more importance is the concern that WWGF doesn’t reflect more recent research done on other possible (likely?) agents of obesity, such as leptin, linoleic acid, and possible appetite moderators like serotonin, dopamine, or opiod peptides to name a few. [Sidebar: I recently became practically giddy reading New Directions in Understanding Obesity (PPT) and speculating about the effect of excess dietary omega 6s on appetite via the ECS … the same system that is related to marijuana and the munchies. More about this in a later post!]
I don’t fault Taubes for not including discussions of these in WWGF. However, after reading some of his comments since his book launch, I do wonder if he’s grown so invested in his theory that he’s doing what he accuses the calories in/out folks of doing: neglecting evidence that doesn’t fit with the theory.
I do think that reducing carbs helps most people lose weight, though I also agree with Barbara Berkeley that it generally isn’t necessary to do the very low-carb Atkins induction diet that Taubes includes in the appendix of WWGF … and I agree with Jenny that if low-carb doesn’t work, it’s a sign to look elsewhere.
[Sidebar: What I really think is that people would be best off following a diet based on avoiding problematic foodstuffs like grains, fructose/sugar, and vegetable oils. See Kurt Harris, Loren Cordain, Mark Sisson, or my current fave, Paul Jaminet. I also think that HIIT exercise or similar will wind up being essential to changes in diet — not to burn calories per se but to help restore glucose/insulin/leptin/whatever sensitivity.]
All of that said, if you’re still with me (whew!), I certainly encourage picking up Why We Get Fat and reading it for yourself.
Why? For one, most of the people who are either promoting or criticizing the book are biased (like I am). If you’ve only ever heard the calories in vs calories out story, you should read Why We Get Fat, since it will certainly give you another perspective on why so many Americans may be fat.
But even if Taubes is flat wrong re his hypothesis, I still think he deserves credit. Consider the apocryphal story of the man searching under the streetlight:
A cop walking his beat comes across a man on his knees, searching for something under a streetlight:
Cop: “What are you doing?”
Man: “Looking for my car keys.”
Cop: “Did you lose your keys in the street?”
Man: “No, I lost them in those bushes over there.”
Cop: “Why are you looking here if you lost your keys in the bushes?”
Man: “Because the light is better under the streetlight.”
Whether or not Gary Taubes has the story exactly right, I think he’s helping us to search in the right place. For that, I think he deserves props.
Update, 3/2: Darya Pino has a balanced review that’s a nice complement to mine.