In an Associated Press article dated Tuesday, November 16, Marilynn Marchione reported on a study presented by Suzanne Phelan at a meeting of the North American Association for the Study of Obesity. The study was based on data from the National Weight Control Registry, a registry run by doctors from the University of Colorado in Denver, the University of Pittsburgh, and Brown University (Providence, R.I.). This decade-old registry provides statistics on persons who’ve lost at least 30 pounds of weight and kept it off for a year. The purpose of this ongoing registry is to learn what works and what doesn’t. And what doesn’t — at least in this study — is low-carb dieting.
The 2,700 participants (average age 47) lost an average of 72 pounds. All reported eating approximately 1,400 calories per day. It didn’t seem to matter much how the calories were distributed for the initial weight was loss. What counted was how the weight was kept off. Those who increased fat at the expense of carbohydrates tended to gain back more weight than those who ate more carbohydrates.
Is it too soon to place the stamp “fad” on the low-carb approach to weight control? First let’s revisit the reasoning behind it and see if there’s something we missed.
Maybe food manufacturers shouldn’t rush to beat their plowshares back into swords just yet, and pork rinds may not be a better snack than popcorn after all.
Proponents of low-carb dieting explain it as our nature to live on a low carbohydrate diet, the “diet of our ancestors.” After all, we started cultivating grains only 10,000 years ago — we’ve been eating meat for 2.5 million years. Thus we’ve got the genes and will adapt to this diet, correct? The question is, what is that adaptation?
Long before our ancestors were low-carb-eating hunters and gatherers, they were high-carb eaters dwelling in the African forests. When the forests receded in response to plummeting global temperatures, our fruit-eating ancestors were forced to adapt to the high-protein/low-carb diet offered by the tropical plains. According to J.C. Brand Miller of the University of Sydney, Australia, it was an altered glucose metabolism called insulin resistance, the postulated trigger of Type II diabetes, also known as the result of what was termed the “fat gene” or “thrifty gene."
What is the practical meaning of insulin resistance? It means the liver makes more sugar from protein, the muscles use less glucose for immediate energy and store less glucose as glycogen (our ready energy reserve). We do, however, maximize the storage of excess energy as fat.
Insulin resistance is a survival mechanism that conveys an advantage to the bearer when food, especially carbohydrates, are scarce. It’s what the body does when times are tough — a kind of get-out-of-jail-free card. When food is abundant, especially the more refined carbohydrates, it’s a disadvantage because fat-making machinery has already been built.
Perhaps the people in the study simply couldn’t comply with the rigors of the low-carb diet. On the other hand, maybe their bodies interpreted the persistent use of this extreme diet as “times are tough again, so hang on to the fat.” You see, we aren’t simply low-carb eaters; we are a complex species whose diet is subject to numerous influences and interconnected factors.
The upshot? Maybe food manufacturers shouldn’t rush to beat their plowshares back into swords just yet, and pork rinds may not be a better snack than popcorn after all. Balance, it seems, has precedent and is probably more sophisticated than we suspect.
Dr. Mark Anthony, retired University of Texas at Austin nutrition scientist, is author of Gut Instinct: Diet’s Missing Link. To find out more about the role hunger plays in diet and health, visit www.dietsmissinglink.com
Miller, J.C. Brand and S. Colagiuri. The carnivore connection: dietary carbohdrate in the evolution of NIDDM. Diabetologica (1994) 37:1280-86.
Groop, LC. Insulin resistance: the fundamental trigger of type 2 diabetes. Diabetes, Obesity and Metabolism. (1999) 1(suppl. 1) S1-S7.