Calories-in, Calories-Out (CICO) must die.

This post is a reaction from reading Adele Hite’s brilliant and hilarious post on a talk by Walter Willett: Walter Willett is the Chair of Nutrition at the Harvard School of Public Health, and is recognized as a leader in the field of nutritional epidemiology.

Please go read Adele’s post. It’s a short read. Then come back to read the rest of this post.

I know it’s “just rats”, but I had 8 rats that had become obese on a refined foods (REF) diet over a 9 month period (well, they became obese in two weeks, and maintained it over the rest of the 9 months).

I then put them into cages with access to a running wheel for 5 weeks. And I switched half of the rats to a healthy control (CON) diet.

What happened?

The rats on the REF diet continued to increase in weight while the rats on the CON diet lost weight.

Weight in running wheels

Okay, that’s expected. Eat a healthy diet and lose weight.

According to Willett’s argument, the CON rats should have lost weight because they exercised more and ate less. Likewise, the rats that stayed on the REF diet should have ate more than before being placed in the running-wheel cage, and should not have exercised much at all. This is classic CICO.

Okay, let’s take a look, first at amount of food consumed:

Food consumption in running wheels

Doh! BOTH groups of rats consumed less food after being placed in the running-wheel cages. Even the rats continuing to eat the REF diet and gain more weight over the 5-week period consumed LESS food than before being placed in the running wheel cages!

The same story emerges when we plot energy consumption per rat by diet condition:

Mean Energy consumed in running wheels

Well, obviously the fat rats on the REF diet must have been stupendously lazy and not run in the wheels at all, otherwise how could they lose weight while eating less? On the other hand, the rats switched to the CON diet both ate less and exercised a lot more in order to lose their weight. Right?

Mean distance ran in running wheels

Oops! The rats switched to the healthy CON diet actually ran less distance per week than did the rats that stayed on the REF diet!

Holy balances and scales Batman! What gives?

Perhaps CICO and its adherents (WW and the good folks at the Harvard School of Public Health) are wrong?

Oh wait, but these are just rats. This scenario would NEVER occur in humans…

Diet Research Insanity

A new study was just published on the health effects of a low-carb/high-fat (LCHF) diet in mice.

It has been getting a lot of media attention with headlines touting things like

“New study says Paleo diet ‘unhealthy and fattening’ angering ardent devotees”.

The above was from the Telegraph:

Given that a LCHF paleo style diet (PSD, more primal due to inclusion of dairy products), I was skeptical, so I downloaded the paper and supplementary table.

Turns out I had a right to be skeptical.

Exhibit A: From the methods section: “The carbohydrate content of the LCHFD was exclusively derived from simple sugar (sucrose: 106 g kg−1)”

Doh! what a major flaw in this study! A healthy LCHF PSD like the one I and many of my friends and colleagues follow minimizes natural or added sugars, especially from refined sources like sucrose, and the relatively small portion of carbohydrates we DO include in our diets are from whole-food sources and tend to be of the complex starch variety, such as tubers, plantains, root vegetables (beets, carrots, etc.), and some fruit (in moderation). That is, we follow a WHOLE FOODS diet from ingredients that receive relatively low amounts of processing.

The diet used by the researchers was made of very highly processed ingredients. I’ve published evidence in a wild-type rat model showing that it is the degree of processing, irrespective of macronutrient ratio, that seems to be heavily implicated in health outcomes, including cognitive function:

Here’s the supplementary table showing the actual ingredients they used in their study:

The ingredients were mostly derived from highly processed sources. For example, the protein comes completely from casein, which has been shown to make mice highly susceptible to aflatoxin-induced cancer: Hat tip to Chris Masterjohn for his detailed analysis of this literature.

Exhibit B: the mice used in the study were genetically modified to develop obesity. This is the topic of a whole other blog post, but it is often the case that mice that have been genetically modified to mimic a disease or disease process found in humans, turn out not to be a good model for the mechanism of the disease in humans.

Exhibit C: perhaps even wild-type mice would be a bad model for studying the health effects of a diet for humans because they are adapted to quite a different dietary niche than are humans. A great argument for this has been made by my friend and colleague Richard Feinman:

They summarize in their abstract: “In sum, the response of mice to a carbohydrate-free diet was greater weight gain and metabolic disruptions in distinction to the response in humans where low carbohydrate diets cause greater weight loss than isocaloric controls. The results suggest that rodent models of obesity may be most valuable in the understanding of how metabolic mechanisms can work in ways different from the effect in humans.”

This statement matches my own observation in the effect of a LCHF PSD in myself and others (though not everyone, which is an important point that we should not discount individualized approaches to diet and health).

Of course the news stories everywhere are claiming “Paleo diet shown to be harmful!”.


Professor Aaron P. Blaisdell