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Eat AND Live

July 16, 2010 | Tags: Featured , Food , Fruit , Health , Vegetables | Post comment

Eat AND Live

 

EAT AND LIVE

Continuing on the theme of quality vs. quantity, there was an interesting article in the WSJ this week titled Eating to Live or Living to Eat?

While the science can be fascinating, my interest is in the persistent and subtle ways we in the U.S. continue to promote certain causalities regarding obesity instead of examining causalities related to diet quality.

From the article: One thing is clear: Obese people react much more hedonistically to sweet, fat-laden food in the pleasure and reward circuits of the brain than healthy-weight people do. Simply seeing pictures of tempting food can light up the pleasure-seeking areas of obese peoples' brains.

Is this really so clear?  Why aren’t we looking at the differences between the ways obese people who eat the standard American, health-depleting diet react to junk food and the ways obese people who eat a health-supporting diet react?   Isn’t it possible the brain is responding the way it is not because of excess adipose tissue but because of the interference created by such toxic foods?

In an interview in Salon when his  excellent book, The End of Overeating came out, Dr. David Kessler, former commissioner of the FDA said:

We don't know which one weighs more heavily, genetics or the environment. But if you look at 2-year-olds, they compensate for their eating. If you give them more calories at lunch, they'll eat fewer calories for the remainder of the day. By the time these kids are 4 and 5, they lose the ability to compensate. Given the exposure to fat, sugar and salt when they're 3, 4 and 5, the reward pathways of the brain take over and hijack the normal body's homeostatic mechanism to regulate itself. It used to be that 3-, 4- and 5-year-olds compensated, and fewer of them compensate today. That kind of change suggests environmental forces, that learning has a profound consequence.

When you think about it, we're conditioning the brains of millions of our kids and that conditioning, that neural circuitry laid down after exposure to highly palatable foods, lasts a lifetime. It has profound consequences not only for the individual but also for public policy.

And a few years before him, Dr. Robert Lustig, of UCSF, published a study in Natural Clinical Practice Endocrinology & Metabolism (Vol. 2, pp. 447-458). In an interview with FoodNavigator.com about his research, Lustig made a similar point as Kessler’s: it’s the food that’s causing the brain to react differently, not the body fat. Here’s an excerpt from the article:

Lustig said that it well established that insulin acts on the brain to encourage eating through two separate mechanisms. First, it blocks the signals that travel from the body's fat stores to the brain by suppressing the effectiveness of the hormone leptin, resulting in increased food intake and decreased activity. Second, insulin promotes the signal that seeks the reward of eating carried by the chemical dopamine, which makes a person want to eat to get the pleasurable dopamine 'rush'.

"Our current Western food environment has become highly 'insulinogenic,' as demonstrated by its increased energy density, high-fat content, high glycaemic index, increased fructose composition, decreased fibre, and decreased dairy content," said Lustig.

"In particular, fructose (too much) and fibre (not enough) appear to be cornerstones of the obesity epidemic through their effects on insulin."

And here’s one more reason we ought to want to see studies comparing people—their health, their brain function, their hormones--by diet quality and not by weight.  From an article in UPI:

It's not just a matter of lack of willpower to stop eating, or of an obesity drug not working, but the body's counterbalancing mechanisms that stops people from losing weight," says Dr. Louis J. Aronne, director of the Comprehensive Weight Control Program at New York Presbyterian Hospital-Weill Cornell Medical Center.

The chemical culprit is called the endocannabinoid -- EC -- system, and when activated, it increases hunger and decreases satiety, driving the desire for tasty food, says Aronne.

"When you eat a high-fat, high-carbohydrate food, it activates the endocannabinoid system, leading you to eat even more," says Aronne. "The endocannabinoid system interacts with other hormones to make you feel hungrier, increases body fat, and drives weight gain."