Even more than mountainside slides of mud or snow, naturally occurring forest fires promote the survival of aspen trees. Aspens' need for fire may seem illogical since aspens are particularly vulnerable to fires; whereas the bark of most trees consists of dead cells, the aspen's bark is a living, functioning tissue that—along with the rest of the tree—succumbs quickly to fire.

    The explanation is that each aspen, while appearing to exist separately as a single tree, is in fact only the stem or shoot of a far larger organism. A group of thousands of aspens can actually constitute a single organism, called a clone, that shares an interconnected root system and a unique set of genes. Thus, when one aspen—a single stem—dies, the entire clone is affected. While alive, a stem sends hormones into the root system to suppress formation of further stems. But when the stem dies, its hormone signal also ceases. If a clone loses many stems simultaneously, the resulting hormonal imbalance triggers a huge increase in new, rapidly growing shoots that can outnumber the ones destroyed. An aspen grove needs to experience fire or some other disturbance regularly, or it will fail to regenerate and spread. Instead, coniferous trees will invade the aspen grove's borders and increasingly block out sunlight needed by the aspens.

It was once believed that the brain was independent of metabolic processes occurring elsewhere in the body. In recent studies, however, we have discovered that the production and release in brain neurons of the neurotransmitter serotonin (neurotransmitters are compounds that neurons use to transmit signals to other cells) depend directly on the food that the body processes.

Our first studies sought to determine whether the increase in serotonin observed in rats given a large injection of the amino acid tryptophan might also occur after rats ate meals that change tryptophan levels in the blood. We found that, immediately after the rats began to eat, parallel elevations occurred in blood tryptophan, brain tryptophan, and brain serotonin levels. These findings suggested that the production and release of serotonin in brain neurons were normally coupled with blood-tryptophan increases. In later studies we found that injecting insulin into a rat’s bloodstream also caused parallel elevations in blood and brain tryptophan levels and in serotonin levels. We then decided to see whether the secretion of the animal’s own insulin similarly affected serotonin production. We gave the rats a carbohydrate-containing meal that we knew would elicit insulin secretion. As we had hypothesized, the blood tryptophan level and the concentrations of tryptophan and of serotonin in the brain increased after the meal.

Surprisingly, however, when we added a large amount of protein to the meal, brain tryptophan and serotonin levels fell. Since protein contains tryptophan, why should it depress brain tryptophan levels? The answer lies in the mechanism that provides blood tryptophan to the brain cells. This same mechanism also provides the brain cells with other amino acids found in protein, such as tyrosine and leucine. The consumption of protein increases blood concentration of the other amino acids much more, proportionately, than it does that of tryptophan. The more protein is in a meal, the lower is the ratio of the resulting blood-tryptophan concentration to the concentration of competing amino acids, and the more slowly is tryptophan provided to the brain. Thus the more protein in a meal, the less serotonin subsequently produced and released.