Hunger and Satiety
Eating has been much in the news recently. It has been noted that obesity is becoming more common as a new generation of children has been raised on high-fat fast foods, raising concerns about associated diseases of obesity such as heart disease and diabetes. There has also been concern expressed about the opposite condition, fostered by the glamorization of waif-thin women by Hollywood and the fashion industry. Why is it so hard for some overweight folks to loose weight and keep it off, and why do others work so hard at loosing weight that they endanger their health or even literally starve to death? In this paper I describe some of the physiological mechanisms of hunger and satiety and offer some observations about weight control.
Physiological Mechanisms of Hunger and Satiety
Early research on the physiological mechanisms of hunger and satiety focused on that important little structure in the brain that seems to be involved in so many basic drives: the hypothalamus. This research suggested that the hypothalamus contains two distinct "centers," one responsible for hunger and the other for satiety. This hypothesis came to be known as the dual center hypothesis.
We now know that the dual center hypothesis is wrong, but I'm going to describe it and some of its supporting evidence to you anyway, because it provides a nice way to organize early findings and the later evidence which began to weigh against this interpretation.
The Dual Center Hypothesis
Early researchers used two sources of evidence to construct the dual center hypothesis, both involving placing an electrode directly into the brain of a laboratory rat. The electrode could be used to create a lesion, or small area of destruction, around the tip of the electrode. Alternatively, the electrode could be implanted permanently and used to stimulate the region of brain surrounding the electrode tip. Ideally, these two methods should yield complementary data: the same behavior aroused by stimulation should be lost by lesioning. Here are the results which led to the dual center hypothesis:
The model developed from this evidence went like this: hunger signals arising from such factors as lowering of glucose (blood sugar) or an empty stomach would stimulate the LH. The LH would then inhibit activity in the VMH and send a signal to higher areas of the brain, giving rise to feelings of hunger and enhancing the attractiveness of food-related stimuli. The animal would seek out food and consume it. As the stomach filled and nutrients began to enter the bloodstream, hunger signals would diminish and satiety signals would strengthen. When these reached sufficient intensity, they would overcome the weakening inhibition of the VMH by the LH, the VMH would switch on, and this in turn would inhibit any remaining activity in the LH while sending a signal to higher areas in the brain, resulting in feelings of fullness or, if feeding continued beyond this point, positive revulsion of the food. Feeding would cease.
- Lateral Hypothalamus (LH)
- Lesioning: Aphagia (lack of eating). The rat no longer seemed interested in food, would refuse to eat, and would waste away unless force-fed.
- Stimulation: A rat that had just finished consuming a meal, apparently satisfied, would return to the food and resume eating.
Taken together, these two findings suggested to researchers that the lateral hypothalamus functions as a hunger center. That is, when the LH turns on, the individual feels hungry and becomes motivated to seek out and consume food.
- Ventromedial Hypothalamus (VMH)
- Lesioning: Hyperphagia (over-eating). After recovery from the surgery, the rat would begin to eat more than it had before, and rapidly gained weight until it weighed perhaps two to three times its normal weight of around 500 grams (male rat).
- Stimulation: A hungry rat in the midst of a meal would drop the food pellet and ignore the food for a couple of minutes following a brief burst of stimulation of the VMH.
These two pieces of evidence suggested to researchers that the VMH might function as a satiety center. When activated, the satiety center would produce that feeling of having had perhaps too much. More than the mere absence of hunger, this would be a drive to avoid any further consumption of food, even if it continued to taste good.
Evidence Against the Dual Center Hypothesis
The dual center hypothesis seemed to make a lot of sense, but unfortunately, new evidence began to emerge that called it into question:
- Rats with LH lesions that were kept alive by force feedings eventually recovered voluntary eating. If the lateral hypothalamus is the brain's "hunger center," and the hunger center has been destroyed, hunger should not return.
- Although rats given stimulation of the LH began nibbling on food pellets when these were available, the same stimulation seemed to induce other behaviors, depending on the availability of environmental support for those activities. If wood were provided, the rats would gnaw wood. If a running wheel were provided, the rats would run. It began to look as though the stimulation was arousing the animals to general activity rather than inducing a specific state of hunger.
- Those hyperphagic rats with VMH lesions were, according to the dual center hypothesis, in a chronic state of hunger due to the destruction of the satiety center. Yet after a period of overeating and weight gain, the rats would cut back some on their eating and their weights would level off. Force feeding the rats would cause further weight gain, but upon a return to normal eating, the rats would eat less than before until their weights returned to pre-force-feeding levels. Or, if the rats were put on a diet and lost weight, when allowed to feed freely again, they would overeat and regain the lost weight, then cut back and maintain it. This is not a picture of animals in a permanent state of hunger. They were still regulating their weights, but at a higher value than before VMH lesioning.
- VMH lesioned rats turned out to be fussy eaters. They would overeat when the food tasted good, but if a small amount of quinine were added, making the food slightly bitter, they would refuse to eat it. Non-lesioned rats balked at eating the bitter food as well, but soon began consuming it when nothing else was available. VMH lesioned rats did not. This does not seem to fit the picture of a rat that is unable to quench its hunger. (By the way, even more recent evidence showed that becoming a finicky eater was not a direct result of the VMH lesions, but rather occurred as a result of being overweight: normal rats force-fed to become as overweight as VMH rats are equally finicky eaters.)
Evidence such as that presented above led to the formulation of an alternative hypothesis, known as the set-point theory. According to this view, body fat is regulated or controlled around a set point, so that deviations from set point produce changes that have the effect of restoring body fat (and therefore body weight) to the set-point value. A study of obese women who underwent a successful weight-loss program produced data that agree with this view. Although the women succeeded in bringing their weights down from in excess to 300 pounds to something close to normal weights for women their age, maintaining this state brought about problems. Their menstrual periods ceased, their metabolism fell, so that they felt cold and what little food they ate tended to get converted to fat rather than being burned, and they were obsessed with thoughts of food. All these changes are characteristic of people who are undergoing starvation, as in times of famine. These results are consistent with the view that the women were maintaining their body fat levels well below set point. This was turning on mechanisms to conserve energy, convert food into stored fat rather than expend it for fuel, and make food-related stimuli in the environment strongly attractive so that the women would eat.
Genetic versus Environmental Determinants of Body Weight
Present evidence suggests that both genetic and environmental factors are important in determining body weight. However, the genetic influence appears to be stronger. Studies comparing the weights of adopted children to those of their biological and adopted parents indicate that the children tend to resemble in weight their biological parents more than they do their adopted parents. Genetic factors such as those determining the number of fat cells in the body and the set point for fat-level seem to be very important. However, this is not to say that environment is without influence: studies of the children of asian immigrants to the United States indicate that these children, who have been raised in a culture offering high-calorie fast foods such as Big Macs and pizza, tend to weigh more by about 15 pounds than their counterparts back in the old country. Thus dietary habits and lifestyle to make a difference.