Update: For the past two weeks, I have been discussing the changes in the way scientists have felt about cardiovascular fitness over the past two decades. The major changes involved a modified suggestion to "accumulate 30 minutes or more of moderate-intensity physical activity over the course of most days of the week," and to add some type of strength training to your activity program.
This week I would like to discuss the changes in the way science approaches obesity and weight control. When I first became interested in this topic, there was little room for new ideas; if you were fat, it was because you ate too much. I was taught, and in turn taught students, that weight control was simply a matter of energy balance. If you ate more calories than you used, you got fat; if you ate fewer calories, you would get thin. Since it took so much effort to use calories with exercise, dieting was the preferred approach.Over the years, we have seen literally hundreds of different diet plans, and diet centers have made millions of dollars helping people control the amount of food they eat. Physicians, fearing for their overweight patients' health, came up with the very low-calorie diet plans, diets where patients eat from 500 to 700 calories a day, and supplemented the diets with vitamins and minerals to avoid nutritional deficiencies. Little was said about exercise. The success rate for all of these approaches was abysmal, to say the least.
In the early 1980s, two colleagues and I reviewed the literature on weight control and found evidence suggesting a body weight "set point" or "thermostat." These ideas were ridiculed by some members of the scientific community because no feedback mechanism had been elucidated to exert control over the fat cells or feed information back to the hypothalmus regarding the amount of fat. However, thinking in terms of a weight control, thermostat control helped explain some of the early studies that seemed to contradict the energy balance equation approach.
For example, an early study by Sims used prisoners who volunteered to gain weight. For 200 days they ate heroically but found it difficult to gain and maintain the weight gain, no matter how much they ate. Following the experimental period, weight loss came readily to most of the men, as if their bodies were happy to return to some set-point weight. Other studies showed major differences in weight loss among subjects, even though all ate the same amount of food and did the same amount of exercise.
Based on the studies we read, we wrote the book "How to Lower Your Fat Thermostat," which suggested changing the diet to include more fruits, vegetables and grains as opposed to restricting the number of calories, and beginning and maintaining a cardiovascular-type exercise program using the major muscle groups to reset the fat thermostat and use energy.
Since that time, there have been many studies showing the role genetics plays in weight loss and gain, and several obese genes have been found and named. And, researchers have found a protein messenger, called leptin, that signals the appetite centers about the amount of fat in the fat cells. Obese rats injected with leptin get thin. Obese people have not responded as well to the protein messenger and may have a problem with the receptor site in the brain so that the protein cannot perform its signaling function.
In the future, there will be new treatments and drugs to help control obesity; but for the present, I still like the approach used in the "Fat Thermostat" book, which suggests a healthy lifestyle as the basis for a weight control program.