due to the destruction of the LH. They hypothesized that if a rat’s setpoint was reduced, the rat’s body would try to maintain the lowered setpoint and resist weight loss or gain.
In fact, that’s just what happened. When the rats with the LH lesions were force-fed to gain weight to their previous levels, their metabolic rate increased substantially so they burned more calories. 12 In other words, restoring their old weight caused their body to use mechanisms to get them back to their new setpoint weight. Conversely, reducing their weight from the lower levels they were already maintaining caused a sharp decline in their metabolic rate so they could conserve calories and return to their setpoint. Fat or thin, it didn’t matter: All rats returned to their setpoints.
The scientists concluded that the LH must not be the only hunger center, because if it were, the rats wouldn’t have regained their drive to eat. Instead, they suggested, the LH must work in concert with other areas of the brain to regulate hunger and determine setpoint. Further research determined they were right.
From Rats to Humans
All this information simply underscores what scientists had already suspected: We have a setpoint and our setpoints can be manipulated.
Even as desperate as many people are to lose weight, sticking an electric probe in your brain and damaging parts of it is going a little too far. That’s why scientists are now hard at work figuring out how to change the signals that go to and from your brain to turn down signals to the LH and turn up the signals to the VMH via drugs or lifestyle changes rather than surgery.
In fact, as you’ll see in chapter 4, there are even specific compounds in foods that can alter these messages, partially accounting for raised or lowered setpoints.
Still skeptical? Well, consider this study in humans.
Researchers pulled together 100 volunteers who had effortlessly maintained a stable weight for six months, an indication they were within their setpoint range. 17 The volunteers agreed to live in a special hospital ward where their food intake and activity levels were carefully monitored and manipulated.
First they had to gain weight until they weighed 10 percent more than their original weight. Then they had to lose weight until they tipped the scales at 10 percent less than they originally weighed. Whether they started out fat, thin, or somewhere between, the results were consistent: When the volunteers ate so much that they gained an extra 10 percent of their body weight, their metabolism increased by 15 percent. Their bodies were clearly trying to drive their weight back down! And when they ate so little that their weight fell to 10 percent below their starting point, their metabolisms slowed by 15 percent.
Now, how can you possibly doubt the existence of your own setpoint?
Identifying Your Setpoint
Your setpoint is:
• The weight you maintain when you listen and respond to your body’s signals of hunger and fullness.
• The weight you maintain when you don’t fixate on your weight or food habits.
• The weight you keep returning to between diets.
Leptin . . . Your Fat Meter
Now you understand the role the hypothalamus plays in maintaining fat homeostasis, or your own setpoint. But just how does the hypothalamus learn what’s going on in the weight department? After all, it’s not like it forces you to weigh yourself every day.
To answer this question, scientists turned to a strain of mice, called ob/ob mice, with a genetic mutation that kept them fat, eating too much, exercising too little, and burning calories very slowly. If you put them in cages with other mice living under the same environmental conditions (all had the same opportunities for eating and exercise), the ob/ob mice stayed fat while the others stayed slender.
To find out why, a scientist sewed an ob/ob mouse to a “normal” mouse (an