Sunday, December 9, 2012

Challenging Nutrition Dogma: Is it really all about calories?

Along with cholesterol, there may not be a more misunderstood nutrition concept than fat. Is it bad? Is it good? What kinds are good? What's the difference between triglycerides and fatty acids? Why do I hear so much about omega-3s? Why do people say saturated fat is bad?

I recently finished reading Good Calories, Bad Calories: Fats, Carbs, and the Controversial Science of Diet and Health, by science writer Gary Taubes. More so than many other nutrition books out there, Good Calories, Bad Calories puts into perspective current nutritional guidance with what the evidence shows - and I mean all the evidence. The book is several years old (published in 2007), and Taubes has since written another book on similar issues called Why We Get Fat (which is much more accessible for the less technical audience), but for anyone truly interested in nutrition, food policy, and health, this is a must-read.

Coming from a science writer, I expected a fairly thorough presentation of the research. At the same time, though, journalists and the media don't necessarily have the best record when it comes to accurately and objectively writing about health and medical studies (but that's an issue for another article). But, taking one look at the 44 pages of notes and the book's 66-page bibliography, there's an immediate appreciation for the full picture Taubes attempts to paint.
The essential thesis of the book is that "obesity is caused by a defect in the regulation of fat metabolism." In other words, "obesity is a disorder of fat accumulation NOT a disorder of overeating."

To better understand what this exactly means, lets consider several important points.

First, Taubes argues that energy expenditure and energy intake are independent variables. This essentially turns the classic "calories in/calories out" paradigm on its head, which assumes energy intake and expenditure are dependent. In the classic "caloric balance" model, the assumption is that energy change (or fat accumulation), and therefore obesity, is the result of (or dependent upon) overeating (energy intake) or physical inactivity (energy expenditure). 

Taking a little detour back to physics, energy is neither created nor destroyed. So, the change in energy (or change in fat mass) is the difference in energy consumed and energy expended. But, this equation says nothing of causality. Is fat accumulation caused by increased food intake, or does increased fat accumulation cause increased food intake?

This is a good time to introduce a major piece to this entire puzzle -- hormones. In the book, Taubes gives a very illustrative example about why hormones play such an important role in fat metabolism. Think about growing children. The energy balance is obviously positive, which is why children grow. But, children aren't growing more because they eat more. Instead, the causality is reversed, and children eat more because they are growing. "They require the excess calories to satisfy the requirements of growth; the result is positive energy balance. The growth is induced by hormones and, in particular, growth hormone."

One could think of a similar example with pregnant women. Weight gain during pregnancy is the result of hormonal changes. "This hormonal drive induces hunger and lethargy as a result. In the context of evolution, these expanded fat stores would assure the availability of the necessary calories to nurse the infants after birth and assure the viability of the offspring." In essence, fat metabolism, including the distribution of fat, is a hormonal issue. And its these hormonal changes that influence energy consumption.

In terms of fat metabolism, there may not be a more important hormone than insulin. Insulin is produced in the pancreas, and is said to be the "principal regulator of fat metabolism," which has been known since the 1960's. How does it work? Essentially, if fatty acids are to be mobilized from inside fat cells (and burned as fuel), insulin levels must be low (Quick distinction on terminology: fat is stored as triglycerides - the reason being triglycerides are three fatty acid molecules held together with a glycerol making it too big to cross the cell membrane. Fatty acids are burned as fuel. Fat enters/exits the cell as fatty acids, a smaller molecule). Conversely, when insulin levels are high, fatty acids are shuttled into fat cells and stored rather than burned as fuel. This happens when glucose (when burned as the primary source of fuel) produces something called glycerol phosphate, which assembles fatty acids into triglycerides in fat cells. (A good overview can be seen in this series of video clips.)

Basically, the accumulation of fat in fat cells is regulated by the availability of glycerol phosphate, and the production of glycerol phosphate is directly related to the amount of glucose available. Conversely, "when blood sugar levels decrease, fatty-acid levels rise," and therefore become the predominantly energy source. As Taubes puts it, "the one fundamental requirement to increase the flow of fatty acids out of adipose tissue...and so decrease the amount of fat in our fat tissue, is to lower the concentration of insulin the bloodstream."

Taubes recounts early experiments on insulin from the 1920's (just after insulin was discovered) that demonstrated the role of insulin as a "fattening hormone." These studies showed that "when insulin was injected into diabetic dogs in the laboratory, or diabetic human patients in the clinic, they put on weight and body fat. As early as 1923, clinicians were reporting that they had successfully used insulin to fatten chronically underweight children...and to increase their appetite in the process."

Now what causes high levels of insulin? In short, carbohydrates (insulin is also released when eating protein, but a much smaller amount), and most commonly refined carbohydrates and sugar (fructose has a particularly unique effect, which Dr. Robert Lustig discusses in great detail in this now popular lecture 'Sugar: The Bitter Truth'). "The more carbohydrate flooding the circulation after a meal, the more will be converted to triglycerides and stored as fat for future use."

Taubes goes into a bunch of other related issues, such as issues of hunger, satiety, diabetes, and the like (all of which are extremely interesting and thoroughly researched), but here are two basic take-aways:

All calories are NOT created equal. One hundred calories of bread has a distinct physiological and hormonal response compared to 100 calories of salmon. And it's this hormonal response - principally the high levels of insulin - that drives fat metabolism, not necessarily the number of calories.

Fat isn't a bad thing. Two quick examples: Fat is fundamental to the many cells that make up our body. Without fat, there would be no cell membrane to maintain the cell's integrity. Second, without fat, nerve cells would not have something called myelin, which is essential for cell signalling (or how our nervous system communicates, or 'tells' our body to do certain things). This article on fat consumption in children and depression reinforces the close link between fat and cognitive functioning. 


Nutrition science isn't clear-cut. It's littered with studies that claim "associations" and "links," but few point to causality. More so than anything, Taubes reminds us of this in his book. Just because obesity may be associated with something, doesn't mean that it is caused by it. It is this short-coming by which much of current nutrition and dietary guidelines are based. And if for no other reason, this book is worth the read because it firmly puts into context current dogma, and underscores the need for rigorous science to better inform nutrition policy, guidelines, and the general public's understanding of the issue.

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