Low Carb?

As part of a new series, I wanted to mention an article, book, and dietary phenomenon which seems to explain the sharp rise in obesity over the last 30 years. First, the article, titled “What if It’s All Been a Big Fat Lie” is by Gary Taubes and was first published in the NY Times Magazine in 2002. What Taubes does is question the oft-repeated dogma that a low-fat diet is generally the cure for obesity. In general, he states that not only has this government-sponsored diet not only failed to reduce obesity, but the (related) carbohydrate-based food pyramid has placed the country’s dietary focus around precisely the food that will make them the fattest.

While I had long been suspicious of the low-carb craze lead Dr Robert Atkins, Taubes convincingly uses well thought-out scientific reasoning to make the case that carbohydrate-based diets may be the cause of the nation’s obesity epidemic. After extensive research he turned the article into a book, Good Calories Bad Calories, which was published in 2007 (which I was impressed with) and more recently has published another called Why We Get Fat.

While the science gets complicated very quickly, there are a couple of key points as to how elevated carbohydrate intake contributes to obesity. A key role is played by insulin, which is a hormone central to regulating carbohydrate and fat metabolism in the body; without it cells can’t absorb glucose. This hormone is produced in the islets of Langerhans (sounds like a spooky vacation spot) in the pancreas. Tuabes explains why it’s so key to these type of diets and to obesity in general.

The primary role of insulin is to regulate blood-sugar levels. After you eat carbohydrates, they will be broken down into their component sugar molecules and transported into the bloodstream. Your pancreas then secretes insulin, which shunts the blood sugar into muscles and the liver as fuel for the next few hours. This is why carbohydrates have a significant impact on insulin and fat does not.

But insulin also regulates fat metabolism. We cannot store body fat without it. Think of insulin as a switch. When it's on, in the few hours after eating, you burn carbohydrates for energy and store excess calories as fat. When it's off, after the insulin has been depleted, you burn fat as fuel. So when insulin levels are low, you will burn your own fat, but not when they're high.

So, basically, carbohydrates lead to elevated blood sugar which leads to an insulin response, which leads to your body burning any sugar molecules in your blood and not depending on your fat stores. After sustained exposure to insulin, cells eventually become less sensitive to it (i.e., resistant), and thus an increased amount is needed to move the sugar molecules “into the muscles and liver as fuel.” A positive feedback loop ensues as higher levels of insulin make it even more difficult to burn fat, cells are desensitized further, and obesity soon results (cause the fat stores are rarely relied on). Compounding the problem is the fact that the muscle and fat tissue of obese people is naturally less sensitive to insulin, for largely unknown reasons.

Admittedly, there is something of a chicken or the egg thing going on, in that researchers aren’t totally positive whether obesity causes insulin resistance or if insulin resistance causes obesity. It makes sense, however, and research (and Taubes’ book) appears to show, that cells that are constantly bombarded by insulin (because of a high intake of certain types of food) would, over time, become less sensitive to it. Wikipedia explains:

As elevated blood glucose levels are the primary stimulus for insulin secretion and production, habitually excessive carbohydrate intake is another likely contributor [to insulin resistance]. This serves as a major motivation behind the low-carb family of diets.

And whether the resistance comes from a sedentary lifestyle, diet, or genetics, the result appears quite simple (again, from wikipedia):

Once established, insulin resistance would result in increased circulating levels of insulin. Since insulin is the primary hormonal signal for energy storage into fat cells, which tend to retain their sensitivity in the face of hepatic and skeletal muscle resistance, [insulin resistance] stimulates the formation of new fatty tissue and accelerates weight gain.

So maybe those people avoiding bread (whom we called weirdos) were on to something? Soon we’ll look at the effects of carbs and insulin on satiety and we'll explain something called ketosis. Watch this space.