Finally, our findings may affect the way we treat chronic insomnia. The insomnia phenotype with short sleep duration may respond better to treatments that primarily aim at decreasing physiological hyperarousal and increasing sleep duration, such as medication or other biological treatments.30 Previous studies have shown that sedative antidepressants such as trazodone or doxepin, used at low dosages, down-regulate the activity of the HPA axis, decrease cortisol levels, and increase sleep duration.30,89,90 Needless to state that biological treatments should be part of a multidimensional approach that combines behavioral changes, i.e., sleep hygiene, and psychological interventions, i.e., cognitive-behavioral therapy (CBT), when indicated. The second phenotype, i.e., insomnia with normal sleep duration, may respond better to treatments that primarily aim at decreasing cognitive-emotional arousal, changing sleep-related beliefs and behaviors, and altering sleep misperception, such as CBT.91 Psychotherapeutic medication may be indicated based on the presence of comorbid psychiatric conditions, i.e., anxiety or depressive disorders. The differential treatment response of these two phenotypes should be tested in future placebo-controlled clinical trials. In any event, the treatment of insomnia with objective short sleep duration should become a priority given its severity and its effects on physical health. Finally, in the prevention of chronic insomnia, our strategies should focus on (1) those with premorbid cognitive-emotional hyperarousal and short sleep duration, (2) stress-related poor sleep with short objective sleep duration, and (3) a family history of sleep problems.