December 22, 2011 Update: It would be more appropriate to say that including the data “greatly diminished” the relationship than that it “demolished” the relationship because the positive relationship still exists. See this excellent analysis by Denise Minger.
If we are going to criticize Keys for cherry picking, it behooves us to root out cherry picking from our own communities as well. This requires constant self-criticism, because bias is human nature, and anyone who isn’t engaged in a devoted battle to overcome their own bias will be its prisoner. I myself cannot claim to always be victorious in this battle, but I do try.
Let’s take a look at these diets.
About seven minutes into a recent interview on sugar and health, Dr. Lustig stated the following:
Those animal studies are very clear in terms of what’s going on. If you wanna do diet-induced obesity, people say you put the rat on a high-fat diet. Garbage. Here’s why. You can’t get a rat to eat a high-fat diet, unless you add 20 percent sucrose to the diet. Basically what you’re doing is you’re giving them cookie dough. But if you give them lard, they won’t eat it. They actually lose weight on that because that’s the Atkins diet for them. It’s not palatable, they don’t like it, and they actually lose weight and their metabolic parameters improve. The only way to get an animal, rat, monkey, or any other animal for that matter, to eat a high-fat diet, is to lace the fat with sucrose. So the question is, which is doing the damage? The fat, or the sucrose in that case? And the answer is, both.
Research Diets marketed the first high-fat diet specifically designed and marketed to induce obesity in laboratory animals, and currently estimates that it ships enough high-fat diet to keep 50,000 mice worldwide on the march toward obesity at this very moment.
Nowadays, their 60% fat diet is most popular. Again, most of the fat comes from lard. The diet contains less than 7% of its calories from sucrose, which translates to about 3% of calories from fructose.
The diet also contains 13% maltodextrin, which is partially digested starch. The maltodextrin used in this diet averages ten glucose units per molecule, so can hardly be called a “sugar.” A “sugar” would contain one or two units per molecule. In any case, maltodextrin does not contain fructose.
As I pointed out in “They Did the Same Thing to the Lab Rats That They Did to Us,” the American Institute of Nutrition (AIN) recommended the inclusion of 13-15% maltodextrin broken down even further than this as well as 10% sucrose in order to reduce the amount of heat damage that would occur during the pelleting process. Thus this diet can hardly be said to be high in maltodextrin and it is pretty low in sugar.
Kirpich IA, Gobesjishvili LN, Bon Homme M, Waigel S, Cave M, Arteel G, Barve SS, McClain CJ, Deaciuc IV. Integrated hepatic transcriptome and proteome analysis of mice with high-fat diet-induced nonalcoholic fatty liver disease. J Nutr Biochem. 2011;22(1):38-45.
We can see the effect of fat if we compare the black and white bars to the patterned bars. Clearly, fat increased adiposity more than sugar in each strain of mouse, but the effects were much more pronounced in the strain of mouse shown on the right. The white bars represent a 58% fat diet that had no sucrose in it whatsoever. This diet clearly increased adiposity, especially in the susceptible strain.
Lest we be afraid the maltodextrin is the culprit, let’s take a look at this study by the same authors:
After 16 weeks, fat increased adiposity in both strains (this time adjusted for body weight). The white bars represent the 58% fat diet that had no sugar. On top of this, none of the diets contained maltodextrin. Clearly high-fat diets can induce obesity in mice even without any sugar.
One interesting study showed that including sucrose instead of starch on a similarly high-fat diet can increase adiposity in rats by 23%. Unfortunately, this study did not include a low-fat control group so we can’t really tell whether the sugar-free, high-fat diet induced obesity. Fortunately, however, the same authors performed a very similar study that compared starch to sucrose on a low-fat diet, which allows us to make a rough comparison:
The red and blue bars represent rats on diets that were 64% fat and 14% protein, with 21% carbohydrate as either starch or sugar. The green and purple bars represent rats on diets that were only 16% fat, 20% protein, and 54% carbohydrate as either starch or fat.
By comparing the blue and red bars, we see that a very high-fat diet produces 23 percent more adiposity in rats when it is accompanied by sucrose instead of starch. The sugar-free, high-fat diet shown in red, however, produced 74% more adiposity than the sugar-free, low-fat diet shown in purple. This would suggest that very high-fat diets produce adiposity in rats even when they do not contain any sugar at all. Or maltodextrin, for that matter.
Am I about to blame fat as the cause of obesity? Not in a million years.
There are a few reasons.
It also means that with the sheer quantity of people using this diet to induce obesity, there is plenty of room for failure to go unpublished.
In any case, fat or fructose may well operate very differently in whole foods than in purified diets. It is overall dietary patterns that produce health or disease, not isolated dietary components. This will relate to the overall nutrient-density of the diet, the diet’s effect on satiety and the metabolic rate, and as Stephan Guyenet’s new series is revealing, the effect of the foods within that diet on the reward centers of the brain. All of these effects are determined by interactions between different components.
As I pointed out in “Reductionism and Holism Go Hand in Hand,” looking at isolated components is important for understanding how things work, but if we don’t re-synthesize the big picture our reductionism is pointless. Blaming fat because of its effect in these purified diets would be an example of “pulling a Campbell.”
There are many different factors that affect the ability of a high-fat diet to induce obesity in rodents and reviewing all of them is a gargantuan task for another day.
In any case, we can see quite clearly that fructose is not required for high-fat diets to induce obesity in rodents. While I do want to help steer our society away from junk foods full of refined sugar and high-fructose corn syrup (and fructose-free white flour!), I don’t think that contriving fictitious myths about the effects of dietary fat on rodents is going to help us uncover the true causes of obesity.
That’s not to say that you can’t produce weight loss if you restrict carbohydrates to less than one percent and protein to less than ten percent. You can, as was done here. Although this is not because the rats won’t eat the diet. But that’s a topic for the next post.