Original ArticlesSuppression of melatonin by 2000-lux light in humans with closed eyelids
Introduction
The anatomical structures involved in the regulation of human body rhythms by light consist of retinal photoreceptors, the retinohypothalamic tract and the main body clock, the hypothalamic suprachiasmatic nuclei (SCN) (Reuss 1996). The intrinsic rhythmicity of the clock is usually adjusted by environmental lighting conditions to correspond to the solar day. From the SCN, the information on time controls various body functions including the rhythmic secretion of melatonin from the pineal gland. In addition to its effects on the melatonin rhythm, light has a direct suppressing influence on nocturnal melatonin synthesis. Both effects are mediated via the retinohypothalamic pathways and the SCN (Moore and Klein 1973). The secretion of melatonin has a special role in the control of daily rhythms since it feeds back to the SCN and, like light, is able to reset the phase of the clock via specific receptors Lewy et al 1996, Weaver and Reppert 1996.
Only recently, it was discovered that the retinohypothalamic tract to the SCN may not be the only way for light to influence body rhythms. A hypothesis of an alternative humoral pathway from skin to clock was tested by Campbell and Murphy (1998) who found that a 13000-lux 3-hour light pulse, directed to the popliteal skin, caused phase shifts in the rhythms of body temperature and the melatonin onset time.
Although the mechanisms by which light affects body functions are not completely understood, therapeutic applications are expanding in use. It has been demonstrated that properly timed light exposures have beneficial effects in circadian rhythm disorders caused by shift work or time zone transitions Boulos et al 1995, Eastman et al 1995. In addition, light is considered therapeutic in psychiatry, especially in seasonal affective diseases (Lee et al 1997) and in circadian sleep disorders (Terman et al 1995). It is uncertain whether the suppression of melatonin secretion by light has any role in these therapeutic applications. The suppression is however, a good indicator for ensuring that the retinal illumination is mediated via the hypothalamus.
In the present study, we tested whether a 60-min 2000-lux light exposure to the face with closed eyelids was able to suppress nocturnal melatonin secretion in healthy subjects. The question of light penetration through closed eyelids or the facial skin has practical implications: are our daily rhythms regulated by light during sleep? Are the alterations of lighting in the bedroom at night significant for the rhythms? Does it make any difference whether the windows are covered in the morning or not? It has been suggested that light therapy might be effective when applied to sleeping subjects (Wirz-Justice et al 1997). Does light in such situations really reach the brain? Finally, the finding that light exposure to the popliteal skin can be mediated to the circadian system makes one wonder why facial light exposure is insufficient, e.g., in a number of blind people who fail to maintain the daily rhythms that are synchronized with the light/dark cycles (e.g., Orth et al 1979, Sack et al 1992, Lockley et al 1997, Palm et al 1997).
Section snippets
Methods and materials
Eight healthy subjects (3 males, 5 females, aged 20–53 years) gave informed consent after the nature of the study had been explained. The study plan was accepted by the ethical committee of the Institute. The volunteers came to the laboratory for 3 sessions: first for the determination of the control pattern of melatonin in dim light with the eyes open, then for the light exposure either with the eyes open or closed. All sessions took place at 1-week intervals in November. During those weeks
Results
There was a rise of melatonin in all 8 volunteers during the dim–light control session. The range of the highest melatonin concentrations was 18–65 ng/l. The suppressive effect of 2000-lux light on melatonin levels was evident in all subjects when they were exposed to light with their eyes open. The average remaining concentration at the end of exposure was less than half of the prelight level and about a third of the corresponding control concentration (Figure 1, Table 1). When the subjects
Discussion
It has been shown that 6–17-lux (photopic) or 28–86-lux (scotopic) illuminance of monochromatic light of 509 nm is sufficient to suppress melatonin within 60 min in humans (Brainard et al 1988). These threshold illuminances were determined in specially controlled conditions (dilated pupils, volunteers’ heads kept motionless, and light beam directed uniformly on the retina). In other studies, higher illuminances (300, 350, and 500 lux) have been needed to suppress melatonin levels significantly
Acknowledgements
Taina Hätönen was financially supported by Finnish Sleep Research Society, Helsinki, Finland.
References (29)
- et al.
Mechanisms in the eye that mediate the biological and therapeutic effects of light in humans
- et al.
Dose-response relationship between light irradiance and the suppression of plasma melatonin in human volunteers
Brain Res
(1988) - et al.
Pathophysiological mechanism of seasonal affective disorder
J Affect Disord
(1997) - et al.
Natural light exposure of young adults
Physiol Behav
(1986) - et al.
Suppression of nocturnal plasma melatonin and 6–sulphatoxymelatonin by bright and dim light in man
Horm Metabol Res
(1987) - et al.
Light treatment for sleep disordersConsensus report. VII. Jet lag
J Biol Rhythms
(1995) - et al.
Extraocular circadian phototransduction in humans
Science
(1998) - et al.
Suppression of melatonin secretion in some blind patients by exposure to bright light
N Engl J Med
(1995) - et al.
Light treatment for sleep disordersConsensus report. VI. Shift work
J Biol Rhythms
(1995) - et al.
Bright light suppresses melatonin in blind patients with neuronal ceroid-lipofuscinoses
Neurology
(1998)