Seasonal affective disorder and season-dependent abnormalities of melatonin suppression by light

Thompson, Christopher; Stinson, Deborah; Smith, A. M.

doi:10.1016/0140-6736(90)92202-s

Cited by 102 publications

(61 citation statements)

References 20 publications

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“…A supersensitivity in SAD patients has been noted previously (Thompson et al 1990;McIntyre et al 1990). According to one hypothesis, winter depressives are supersensitive to light and become ill in the winter because centers in the brain that monitor seasonal changes in day length respond inappropriately to artificial light (Wehr 1992).…”

Section: Discussionmentioning

confidence: 71%

“…However a study by Murphy et al (1990) found no difference in the sensitivity of melatonin to bright light between controls and SAD patients. It was suggested that the lack of significance seen in the latter study was due to a lack of a dim light control night, and the fact that the test was not repeated in summer (Thompson et al 1990). This may not be a factor as the present study found significant differences between the groups, and no control dim light test night was conducted, nor was the test repeated in summer.…”

Section: Discussionmentioning

confidence: 74%

“…However, the supersensitivity observed in SAD may be a state marker of the disorder as supersensitivity only persists in winter months (Thompson et al 1990). More studies are warranted to determine if the supersensitivity to light is a trait marker of BD.…”

Section: Discussionmentioning

confidence: 99%

“…Patients with seasonal affective disorder (SAD) may also show a supersensitive response to dim or bright light compared to controls (Thompson et al 1990;McIntyre et al 1990). Supersensitivity was only found in the winter months suggesting an abnormal seasonal and state dependent variation in the suppression of melatonin by light in SAD.…”

mentioning

confidence: 99%

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Melatonin Sensitivity to Dim White Light in Affective Disorders

Nathan

Burrows

Norman

1999

Neuropsychopharmacology

108

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Section: Discussionmentioning

confidence: 71%

Section: Discussionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Melatonin Sensitivity to Dim White Light in Affective Disorders

Nathan

Burrows

Norman

1999

Neuropsychopharmacology

108

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“…There is overwhelming evidence that melatonin exerts its chronobiotic effects via the SCN (Cassone et al 1986). On the other hand, there are many hints pointing to the assumption that the SCN`s sensitivity for light and melatonin varies with time (Thompson et al 1990;Owen and Arendt 1992;Dubocovich et al 1996) as well as under the influence of various modulators (Medanic and Gillette 1992;Rea et al 1994;Duncan et al 1998). It also varies between states (McIntyre et al 1990), but moreover between individuals (Lewy et al 1985;McArthur et al 1996).…”

Section: Discussionmentioning

confidence: 99%

A New Concept for Melatonin Deficit On Pineal Calcification and Melatonin Excretion

Kunz

1999

Neuropsychopharmacology

139

102

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Even though exogenous melatonin has proven to influence sleep and circadian parameters, low endogenous melatonin is not related to sleep disturbances, nor does it predict response to melatonin replacement therapy. In this manuscript, we present a new concept towards a definition of a melatonin deficit. The purpose of the study was to introduce a marker for an intra-individual decrease in melatonin production. Therefore, we developed a method to quantify the degree of pineal calcification (DOC) usingIn mammals, the circadian timing system has proven to be involved in the daily variation of almost any physiological and psychological variable evaluated so far (Weitzman et al. 1978;Wirz-Justice 1987;Johnson et al. 1992;Dijk and Czeisler 1995;Boivin et al. 1997). The rhythm of the circadian pacemaker comprised in the nuclei suprachiasmatici (SCN) becomes entrained to the environmental 24-hour rhythm, predominantly by two zeitgebers, light and melatonin (Dawson and Armstrong 1996).Melatonin influences the circadian phase in humans inversely compared to light. In particular, this drug delays circadian rhythms when administered in the morning and advances them when administered in the afternoon or early evening according to a phase response curve (PRC), which is nearly opposite in phase to the PRC's for light exposure (Lewy et al. 1992). Melatonin has proven to exert a chronobiotic mode of action (Dawson and Armstrong 1996) by its ability to facilitate the post-flight adaptation to jet-lag (Arendt et al. 1986), to phase advance the sleep of patients suffering from a phase-delay syndrome (Dahlitz et al. 1991;Tzischinsky et al. 1993), and to re-entrain the sleep-wake cycle of patients with a non-24-hour rhythm, such as in the blind, to the environmental light-dark cycle (Arendt et al. 1988;Lapierre and Dumont 1995;McArthur et al. 1996).However, in only one of the clinical studies (Haimov et al. 1995), in which exogenous melatonin proved usefulness, did low endogenous melatonin excretion predict response (Garfinkel et al. 1995;Hughes et al. 1998 Lushington et al. 1998;Youngstedt et al. 1998). Furthermore, normative data as to the amount of melatonin secretion demonstrate a huge inter-individual variability in humans (Dawson et al. 1992;Bergiannaki et al. 1995;Smith et al. 1997). Thus, existing normative data on melatonin excretion in a "healthy population" might only be considered normal in the sense that they are representative for the normal scatter. But since there is yet no pathology that can be attributed to either high or low melatonin levels, "normative" in this context may not necessarily indicate being healthy. The question arises, does a melatonin deficit or a hypopinealism exist at all?In a previously reported pilot-study we showed that the degree of pineal calcification (DOC) correlated positively to the incidence of chronic daytime tiredness as well as the subjective perception of sleep disturbances (Kunz et al. 1998). The basic assumption in that study was the hypothesis that an increasing degree of pineal c...

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Melatonin sensitivity to dim white light in different seasons

Nathan

Burrows

Norman

1999

Hum. Psychopharmacol. Clin. Exp.

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It is well known that the pineal hormone melatonin is suppressed by light. The melatonin suppression by dim light has also been suggested as a possible trait marker of bipolar disorder. However, there is large inter individual differences in the light responses. It is possible that methodological factors may contribute to the variable responses observed. Most studies in the past have been conducted in different seasons under different lighting conditions. It is possible the external lighting conditions may affect the melatonin suppression to dim light. Hence we examined the melatonin suppression by dim light in (1) a large group of subjects randomly tested once in one of the four seasons (part one) and (2) small group of subjects tested in all seasons (part two). Subjects were placed in a dark room from 2100 h to 0230 h. Light exposure was between midnight and 0100 h in a sitting position. Blood samples were collected at regular intervals for measurement of plasma melatonin. No statistically significant seasonal differences in the percentage suppression of melatonin were found in both parts of the study (p>0·5). The study suggests that seasonal changes in external lighting do not affect the melatonin suppression by dim light in healthy controls. Copyright © 1999 John Wiley & Sons, Ltd.

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Seasonal affective disorder and season-dependent abnormalities of melatonin suppression by light

Cited by 102 publications

References 20 publications

Melatonin Sensitivity to Dim White Light in Affective Disorders

Melatonin Sensitivity to Dim White Light in Affective Disorders

A New Concept for Melatonin Deficit On Pineal Calcification and Melatonin Excretion

Melatonin sensitivity to dim white light in different seasons

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