The exact prevalence of delayed sleep phase syndrome in the general population is unknown. It is unclear what the prevalence of this disorder is; however, it may be more prevalent in adolescents and young adults (Weitzman et al., 1981; Pelayo et al., 1988; Regestein and Monk, 1995; AASM, 2005).
Night shift workers may be at higher risk for delayed sleep phase syndrome due to irregular circadian entrainment (Santhi et al., 2005). Similarly, individuals who live in extreme latitudes and are exposed to extended periods of light may also be at increased risk of suffering from delayed sleep phase syndrome (Lingjaerde et al., 1985; Pereira et al., 2005).
Biological, physiological, and genetic factors have been proposed to be responsible for causing delayed sleep phase syndrome. Behaviorally, late bedtimes and rise times delay an individual’s exposure to light, which may prevent entraining of the circadian clock. Furthermore, exposure to dim light in the late evening and at night, may also affect the circadian phase (Zeitzer et al., 2000; Gronfier et al., 2004).
Biological alterations to the endogenous circadian system also contribute to delayed sleep phase syndrome. Although levels of melatonin typically increase in the evening hours, individuals with this syndrome have a hypersensitivity to nighttime bright light exposure in the suppression of melatonin (Czeisler et al., 1981). It has also been hypothesized that the disorder may result from a circadian phase that has a reduced sensitivity to photic entrainment, or the free-running period of the circadian cycle is prolonged (Czeisler et al., 1981). Consistent with these hypotheses, polymorphisms in circadian genes influence the entraining and free-running period of the circadian cycle and may be associated with delayed sleep phase syndrome (Takahashi et al., 2000; Iwase et al., 2002; Hohjoh et al., 2003; Archer et al., 2003; Pereira et al., 2005). A recent study has also identified a candidate gene, human PER2, that results in familial advanced sleep phase syndrome (Xu et al., 2005).
Treatment for delayed sleep phase syndrome requires resynchronizing to a more appropriate phase to the 24-hour light-dark cycle. In addition to a structured sleep-wake schedule and good sleep hygiene practices, potential therapies include resetting the circadian pacemaker with bright light, melatonin, or a combination of both. However, studies that have investigated the efficacy of bright light have provided mixed results (Pelayo et al., 1988; Rosenthal et al., 1990; Akata et al., 1993; Weyerbrock et al., 1996), partially owing to limitations in their study design and the numbers of par-