Animal and human studies indicate that diet can alter plasma and brain concentrations of neurotransmitter precursors, with possible implications for the synthesis and release of brain neurotransmitters. The best known example is serotonin, whose synthesis is limited by the availability of its precursor, tryptophan, in the brain. Consuming tryptophan or a carbohydrate-rich, protein-poor meal increases brain levels of tryptophan and serotonin. Although a carbohydrate meal itself lacks tryptophan, the meal causes insulin to be secreted. Insulin, in turn, decreases plasma levels of large neutral amino acids that would ordinarily compete with tryptophan for transport across the blood-brain barrier. Resulting brain changes in serotonin provide a plausible mechanism whereby diet could affect behaviour. Research on human subjects suggests that ingesting tryptophan or carbohydrate can reduce subjective alertness and possibly influence some aspects of objective performance. Effects on sleep latency and on pain perception have also been detected. Behavioral effects may come about via the action of tryptophan on brain serotoninergic pathways, although other mechanisms may operate and must still be ruled out before the mechanism is certain.