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eating and activity levels as well as your metabolic efficiency, the rate at which you burn calories, to get you to regain the weight.
     
    At first the hypothalamus enlists your help. It can initiate the release of particular hormones that influence your appetite and mold your drive to eat, including changing how food tastes and how much it appeals to you. It can also lead you to actually crave higher-fat food if it wants you to get concentrated energy and gain weight. It can even decrease your drive to move, leading to serious couch potato behavior.
     
    These actions are particularly strong if the hypothalamus senses that body fat levels are dropping too far below the setpoint. Under-eating sets you up for brain activity that produces an urge to eat way beyond the ability of food to satisfy your hunger.
     
    Of course, sometimes we’re able to temporarily override the hypothalamus’s efforts to restore homeostasis. For instance, if you’re trying to lose weight, you may be able to consciously overcome feelings of hunger through your own willpower. People on diets manage this—albeit not for long. Or perhaps you don’t want to cancel on your friend, so you make it to the gym despite your feeling of lethargy.
     
    So then your hypothalamus gets more aggressive, affecting systems beyond your conscious control. You may feel cold, a sign your body is trying to conserve energy by sending less blood to the periphery, reducing your metabolic rate. Or you might feel sluggish, another sign that your metabolism has slowed. Conversely, you may feel hot after a big meal because your brain has boosted the metabolic effects of food to help your body burn off the extra calories.
     
    Need some convincing that your body—not you—is really in control? Consider some of the following studies.
     

Of Rats and Setpoints
     
    Some strains of rats have higher weights than others. Observing their growth, scientists determined that genetically heavier strains of rats ate more than thinner rats during adolescence and early adulthood, until they settled into a stable, setpoint weight. Once they reached their setpoint, they ate amounts similar to the thinner rats.
     
    Ordinary adult rats, given unlimited access to food and opportunity for exercise, maintain stable setpoint weights. If food is restricted and then provided again, the rat knows just how much to eat to return to its setpoint weight. Fat, thin, or somewhere in between, it didn’t matter: The rat returned to its setpoint weight once food was accessible again.
     

When a Rat Is Hungry
     
    To examine the role of the hypothalamus in setpoint control, early researchers used two sources of evidence. Both involved placing an electrode directly into the brain of a laboratory rat. The electrode either damaged that section of the brain so it no longer functioned or stimulated that section of the brain to produce more neural activity.
     
    The researchers focused on two sections of the hypothalamus they identified as playing a large role in eating behavior: the lateral hypothalamus (LH) and ventromedial hypothalamus (VMH).
     
    When the LH was damaged and dysfunctional, the rats refused to eat and eventually died. 8 But when the LH was electrically stimulated and turned on, the rats ate, even if they were full, and got fat. 9 This behavior led scientists to conclude that the LH housed the “hunger center.” Turn it on and we want to eat; turn it off and we’re no longer hungry.
     
    In another experiment, the scientists again created lesions in the LH, damaging the appetite center. Although the rats again stopped eating and lost weight, this time the scientists force-fed them to keep them alive. 10 11 Eventually, the rats started eating on their own. At some point their weight stabilized, although at a much lower level than before the lesion. In other words, they now had a lowered setpoint.
     
    In other experiments, scientists examined how the rats expended energy after losing weight