Response of the melatonin cycle to phototherapy for Seasonal Affective Disorder

Terman, Michael; Terman, Jiuan Su; Quitkin, Frederic M.; Cooper, Thomas B.; Lo, Ee-Sing; German, J. M.; Stewart, Jonathan W.; McGrath, Patrick J.

doi:10.1007/bf01250238

Cited by 66 publications

(21 citation statements)

References 23 publications

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“…According to the well replicated phase response curve to light exposure, exposure to bright light in the morning results in a phase advance whereas exposure to bright light in the evening induces a phase delay, with mid-day exposure having no effect [Van Cauter et al, 1994; Khalsa et al, 2003]. There is evidence for [Lewy et al, 1987; Terman et al, 1988; Lewy et al, 1998; Lewy et al, 2006] and against [Wirz-Justice et al, 1993] the phase shift hypothesis. In particular, studies attempting to unmask sleep and environment from circadian factors in SAD resulted in conflicting results.…”

Section: Discussionmentioning

confidence: 99%

Seasonality of mood and behavior in the Old Order Amish

Raheja

Stephens

Mitchell

et al. 2013

Journal of Affective Disorders

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Background/Objective We examined seasonality and winter seasonal affective disorder (SAD) in the Old Order Amish of Lancaster County, Pennsylvania, a unique population that prohibits use of network electric light in their homes. Methods We estimated SAD using the Seasonal Pattern Assessment Questionnaire (SPAQ) in 1,306 Amish adults and compared the frequencies of SAD and total SAD (i.e., presence of either SAD or subsyndromal-SAD) between men and women, young and old, and awareness of (ever vs. never heard about) SAD. Heritability of global seasonality score (GSS) was estimated using the maximum likelihood method, including a household effect to capture shared environmental effects. Results The mean (± SD) GSS was 4.36 (± 3.38). Prevalence was 0.84% (95% CI: 0.36 – 1.58) for SAD and 2.59% (95% CI: 1.69 – 3.73) for total SAD. Heritability of GSS was 0.14 ± 0.06 (SE) (p = 0.002) after adjusting for age, gender, and household effects. Limitations Limitations include likely overestimation of the rates of SAD by SPAQ, possible selection bias and recall bias, and limited generalizability of the study. Conclusions In the Amish, GSS and SAD prevalence were lower than observed in earlier SPAQ-based studies in other predominantly Caucasian populations. Low heritability of SAD suggests dominant environmental effects. The effects of awareness, age and gender on SAD risk were similar as in previous studies. Identifying factors of resilience to SAD in the face of seasonal changes in the Amish could suggest novel preventative and therapeutic approaches to reduce the impact of SAD in the general population.

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Section: Discussionmentioning

confidence: 99%

Seasonality of mood and behavior in the Old Order Amish

Raheja

Stephens

Mitchell

et al. 2013

Journal of Affective Disorders

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“…An early study found relatively long sleep episodes to occur when sleep was initiated at a phase of high core body temperature, while shorter episodes were found with sleep onsets near Tmm (Czeisler et al, 1980). Cases of extreme circadian phase delay-with the onset of melatonin production after midnight-have been noted in winter depressives (e.g., Terman et al, 1988). If a patient maintains a normal bedtime, with sleep onset earlier relative to a delayed core body temperature rhythm, hypersomnia could result given the association of spontaneous awakening with the morning rise in temperature (Zulley et al, 1981).…”

Section: Role Of Circadian and Sleep Processes In Hypersomniamentioning

confidence: 97%

Light Treatment for Sleep Disorders: Consensus Report

et al. 1995

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Advanced and delayed sleep phase disorders, and the hypersomnia that can accompany winter depression, have been treated successfully by appropriately timed artificial bright light exposure. Under entrainment to the 24-h day-night cycle, the sleep-wake pattern may assume various phase relationships to the circadian pacemaker, as indexed, for example, by abnormally long or short intervals between the onset of melatonin production or the core body temperature minimum and wake-up time. Advanced and delayed sleep phase syndromes and non-24-h sleep-wake syndrome have been variously ascribed to abnormal intrinsic circadian periodicity, deficiency of the entrainment mechanism, or--most simply--patterns of daily light exposure insufficient for adequate phase resetting. The timing of sleep is influenced by underlying circadian phase, but psychosocial constraints also play a major role. Exposure to light early or late in the subjective night has been used therapeutically to produce corrective phase delays or advances, respectively, in both the sleep pattern and circadian rhythms. Supplemental light exposure in fall and winter can reduce the hypersomnia of winter depression, although the therapeutic effect may be less dependent on timing.

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“…It is believed that light plays an important role, by providing entrainment of circadian rhythms and by suppressing melatonin during the day (Cassone et al, 1993). In patients with affective disorders, there have been indications of circadian as well as seasonal variation in illness, which may be reflected in melatonin production (Terman et al, 1988). …”

Section: Introductionmentioning

confidence: 99%

Subsensitive melatonin suppression by dim white light: possible biological marker of panic disorder

Nathan

Burrows

Norman

1998

Int. J. Neuropsychopharm.

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Light is involved in providing entrainment of circadian rhythms and the suppression of the pineal hormone melatonin. In patients with affective disorders, there have been indications of circadian as well as seasonal variation in illness, which may be reflected in melatonin production. Varying sensitivity to light has been noted within healthy individuals as well as in some patients with affective disorders. Recent evidence suggests that patients with panic disorder may have an altered and phase-delayed melatonin rhythm. The present study examined the nocturnal plasma melatonin rhythm in patients with panic disorder, and also examined their melatonin sensitivity to dim light. The melatonin rhythm was examined in 6 patients with panic disorder and 8 controls. The melatonin sensitivity to dim white light (200 lx) was examined in 8 patients with panic disorder and 63 controls and was compared to that of a group of 7 patients with other anxiety disorders. Patients with panic disorder demonstrated a trend towards higher and delayed peak melatonin levels compared to controls. Patients with panic disorder also had a subsensitive melatonin suppression by dim white light, compared to controls and patients with other anxiety disorders (p<0.005). The phase-delayed circadian rhythm observed in patients with panic disorder may be secondary to the subsensitivity of the melatonin response to light. It is hypothesized that the subsensitivity may be due to abnormal neurotransmitter/receptor systems involved in regulation of melatonin suppression and circadian rhythmicity, and may lead to phase- delayed circadian rhythms. The melatonin subsensitivity to light may be used as a biological marker of panic disorder.

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Response of the melatonin cycle to phototherapy for Seasonal Affective Disorder

Cited by 66 publications

References 23 publications

Seasonality of mood and behavior in the Old Order Amish

Seasonality of mood and behavior in the Old Order Amish

Light Treatment for Sleep Disorders: Consensus Report

Subsensitive melatonin suppression by dim white light: possible biological marker of panic disorder

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