0021-972X/01/$03.00/0
The Journal of Clinical Endocrinology & Metabolism
Copyright © 2001 by The Endocrine Society
Vol. 86, No. 1
Printed in U.S.A.
Diminished Melatonin Secretion in the Elderly Caused
by Insufficient Environmental Illumination*
K. MISHIMA, M. OKAWA, T. SHIMIZU,
AND
Y. HISHIKAWA
Department of Neuropsychiatry (K.M., T.S., Y.H.), Akita University School of Medicine, Akita City
010-8543; and Division of Psychophysiology (M.O.), National Institute of Mental Health, National
Center of Neurology and Psychiatry, Ichikawa 272-0827, Japan
ABSTRACT
The pineal hormone melatonin has some circadian regulatory effects and is assumed to have a close relation with sleep initiation and
maintenance. Many previous reports have described age-related decreases in melatonin levels, especially in elderly insomniacs (EIs),
which may act as causal or exacerbating factors in sleep disturbances
in the elderly. Ten elderly residents with psychophysiological insomnia (mean age, 74.2 yr), 10 healthy residents of the same home [elderly
control (EC) group; mean age, 72.7 yr], and 10 healthy young control
subjects (mean age, 20.9 yr) living at home participated in this study.
The elderly persons, especially the EIs, were exposed to significantly
less environmental light and simultaneously suffered from signifi-
cantly diminished nocturnal melatonin secretion. Supplementary exposure to 4 h (1000 to 1200 h, 1400 to 1600 h) of midday bright light
in the EI group significantly increased melatonin secretion to levels
similar to those in the young control group without circadian phaseshifting. There was a tendency for the magnitude of the increase in
nocturnal melatonin secretion stimulated by bright light to parallel
amelioration of sleep disturbances in these subjects. The present
findings suggest that we need to pay attention to elderly individuals
who suffer under conditions of poor environmental light resulting in
disorganized circadian rhythms, including the sleep-wake cycle.
(J Clin Endocrinol Metab 86: 129 –134, 2001)
T
HE PINEAL HORMONE melatonin has a distinct daily
rhythm of secretion that is linked with sleep. Melatonin
concentration in blood is high during the nighttime and
nearly undetectable during the daytime. Melatonin secretion
is regulated by neuronal inputs from the suprachiasmatic
nucleus, which is believed to be involved in the regulation of
mammalian circadian rhythms (1, 2). In addition, melatonin
has been shown to play a critical role in circadian regulation
in both nocturnal and diurnal mammals (3). In rats, exogenously administered melatonin entrained their freerunning rest-activity rhythms according to phase response
curve properties (4). In humans, melatonin also has some
circadian regulatory effects, including acute hypothermic (5,
6), hypnogenic (7–10), and phase-shifting effects (11, 12), and
it is assumed to have close relation to sleep initiation and
maintenance (13, 14).
Aging is often associated with sleep-waking disorders (15,
16). Insomnia in the elderly is presumed to be based, in part,
on changes in the circadian time-keeping system. Previous
reports have indicated age-related decreases in melatonin
levels (17–23), especially in elderly insomniacs (EIs) (24) and
elderly persons with dementia who often show various types
of sleep problems (25–28). These findings let us assume that
reduction in melatonin secretion with aging may be a causal
or exacerbating factor in sleep disturbances observed in this
age group. Thus, supplementary administration of exogenous melatonin has been tried for sleep disorders in elderly
persons with (29 –31) and without (32, 33) dementia. However, the underlying mechanism of age-related decreases in
melatonin secretion remains unclear, and use of supplementary exogenous melatonin tends to be long-term, despite the
fact that potential side effects are not well-defined. In addition, one recent well-controlled study demonstrated no significant change in melatonin secretion in normal elderly persons. Zeitzer and co-workers (34) examined the amplitudes
of plasma melatonin levels during a constant routine in 34
healthy drug-free elderly subjects and were unable to detect
any significant age-related changes in mean 24-h average
melatonin levels or any other nocturnal melatonin secretion
profile parameters.
We demonstrate here that resident elderly persons can
suffer from insufficient environmental light and that supplementation with bright light at levels similar to those in the
young living at home can improve melatonin secretion and
sleep quality, suggesting that the discrepancies in previously
reported studies could be attributable, at least in part, to the
exposure of the experimental subjects to varying degrees of
environmental light.
Received July 20, 2000. Revision received September 7, 2000. Accepted September 10, 2000.
Address all correspondence and requests for reprints to: Kazuo
Mishima, M.D., Department of Neuropsychiatry, Akita University
School of Medicine, 1-1-1 Hondo, Akita City 010-8543, Japan. E-mail:
mishima@psy.med.akita-u.ac.jp.
* Supported in part by a Special Coordination Fund for Promoting
Science and Technology from the Science and Technology Agency and
by a Grant-in-Aid for Cooperative Research from the Ministry of Public
Welfare of Japan.
Subjects and Methods
Experimental subjects
Study subjects were 10 elderly residents of a nursing home with
psychophysiological insomnia [EI group; males/females (M/F) ⫽ 4/6;
66 – 82 yr old, average age ⫽ 74.2 yr], 10 healthy residents of the same
home [elderly control (EC) group; M/F ⫽ 5/5; 65– 80 yr old, average
age ⫽ 70.7 yr], and 10 healthy college students [young control (YC)
group; M/F ⫽ 10/0; 19 –23 yr old, average age ⫽ 20.9] living at home.
Subjects in the EI group were required to satisfy Lushington et al. criteria
129
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MISHIMA ET AL.
(35) based on the International Classification of Sleep Disorders criteria
for psychophysiological insomnia (36) and criteria for sleep maintenance
insomnia by Waters et al. (37). That is, according to The Pittsburgh Sleep
Quality Index (38) and 7-day sleep diary, EIs were selected if they
reported a mean wake time after sleep onset (WASO, the accumulated
time awake after the sleep onset) more than 30 min, total sleep time (TST)
less than 6 h, and sleep efficacy (the total time asleep as a percentage of
the total time in bed) less than 85%. All subjects gave informed consent.
With the exception of 4 elderly subjects in the EI group who were using
short-acting benzodiazepines, no subject took any medication, such as
␤-blocker or antiphlogistic, that might modify sleep states or melatonin
secretion levels. The 4 patients who took benzodiazepines (7.5 mg zopiclone for 2 subjects, 0.5 mg etizolam for 1 subject, and 0.125 mg
triazolam for 1 subject) had been on medication continuously at fixed
dosages for at least 6 weeks before participating in our study, and
continued the treatment during the study. All elderly subjects underwent brain magnetic resonance imaging and/or computed tomography,
as well as Mini Mental State (MMS) examinations, and subjects with
moderate-to-severe ischemic and/or atrophic changes in the brain, and
MMS scores of 20 or less, were excluded from the study. Average ⫾ sem
of MMS scores for the EI and EC groups were 23.6 ⫾ 0.83 (range, 21–30)
and 24.4 ⫾ 0.64 (range, 22 to 30), respectively.
Protocol
The study was performed in Akita City (39° 42⬘ N) located in the
northern part of Japan. The study comprised a 2-week baseline period
(day 1 to day 14) for the three groups, followed immediately by a 4-week
light exposure period (day 15 to day 42) for the EI group. The EI group
was exposed to bright light for 4 h each day, from 1000 h to 1200 h and
from 1400 h to 1600 h, in a light room where full-spectrum fluorescent
tubes were placed across the entire ceiling so that subjects were exposed
to light without behavioral restriction, at an intensity of approximately
2500 lux at eye level when seated anywhere in the room. Throughout the
study, all elderly subjects followed self-determined schedules, with the
exception of some common daily events such as meals at 0700 h, 1200 h,
and 1730 h and bathing between 1600 h and 1700 h. All subjects in the
YC group followed self-determined schedules at home. Light during the
time in bed was kept below 25 lux; 0 lux was used during sleeping times,
as identified by wrist actigraph data. To maintain consistency between
the three groups, with respect to the influences of weather on rhythm
properties and light conditions, monitoring was performed simultaneously in three subjects from each group.
Evaluation of environmental light condition
Light exposure was simultaneously monitored, at 1-min intervals, in
each subject, from day 6 to day 12 in the baseline period and during the
last 7 days in the light-exposure period, using a thin patch-type photosensor (Matsushita Electric Works, Ltd., Osaka, Japan) that was calibrated to measure light intensities from 1–10,000 lux (r ⫽ 0.99999) and
that was applied to each subject’s forehead or to glass frames connected
to a small ambulatory illuminorecorder (Gram Ltd., Tokyo, Japan). This
device allowed us to evaluate entry of incidental environmental light
into the retina. Parameters for light condition were defined as follows:
total light exposure (Ltotal), the area under the light intensity curve
calculated for each subject by summing the total light intensity values
during wake time; bright light exposure time (L ⬎ 1000), the number of
minutes of light exposure above 1,000 lux during wake time.
Evaluation of sleep quality calculated by actigraph data
Throughout the study period, wrist activity was monitored with an
actigraph (AMI Inc., Ardsley, NY) around the nondominant wrist of
each subject. Actigraph data were analyzed for computer-calculated
sleep-wake determinations (39). Nighttime sleep parameters for each
subject were defined as follows: sleep onset time (SOT), clock time of the
onset of sleep; sleep efficacy (SE), the total time asleep as a percentage
of the total time in bed; awake time (AT), the total number of waking
episodes that continued for at least 10 min during the sleep period;
WASO (accumulated time); and sleep latency (SL), the time between
bedtime and the sleep onset.
JCE & M • 2001
Vol. 86 • No. 1
Evaluation of melatonin secretion rhythm
Blood sampling for RIA of serum melatonin was performed on the
days 13–14 and on days 42– 43. Blood was collected every hour for 24 h,
starting from 8 h before the average SOT determined for days 6 –12 in
the baseline period for 3 groups (, and for days 35– 41 in the lightexposure period for the EI group) via iv catheter that had been placed
in a forearm vein under dim light (⬍25 lux) to avoid masking effect on
melatonin levels. The blood sample was immediately centrifuged (3000
rpm for 15 min), and serum was separated and frozen (below ⫺75 C) for
later RIA. Parameters for melatonin rhythm were defined as follows:
rhythm amplitude (AMP), the difference between peak and low values;
nocturnal melatonin secretion volume (AUCn), the area under the melatonin time-concentration curve calculated for each subject by summing
the total melatonin levels from 4 h before to 8 h after bedtime; daytime
melatonin secretion volume (AUCd), the area under the melatonin timeconcentration curve with the exception of AUCn; dim light melatonin
onset time (DLMOn), the evening time at which serum melatonin concentrations reached 8.1 pg/mL, which was 3 times the detection limit of
the RIA kit used in this study; dim light melatonin offset time (DLMOff),
the morning time at which serum melatonin concentrations decreased
below 8.1 pg/mL; the duration of nocturnal rise (Duration), the duration
during which serum melatonin concentration was kept higher than 8.1
pg/mL; and the midtime of nocturnal rise (Midtime), the midtime between DLMOn and Off time). The DLMOn, DLMOff, and Midtime were
expressed as a time relative to 0000 h, defined as average SOT determined for day 6 –12 (day 35– 41) in the baseline period (in the lightexposure period).
Statistics
For statistical analysis, we used the Kruskal-Wallis test, followed by
the Mann-Whitney U or Wilcoxon test, to identify the significant intergroup differences in light, sleep, and melatonin parameters among three
groups. Pearson correlation analysis was used to examine association
between changes in melatonin and sleep parameters induced by midday
light exposure. Results were evaluated at the P ⬍ 0.05 significance level
and are shown as the mean and sem values.
Results
Sleep parameters in the baseline period
Sleep parameters and their values for the last 7 days of the
baseline period (excluding the last day for melatonin sampling) are shown in Table 1. The EI group showed significantly lower values of TST and SE, as well as significantly
higher values of AT, WASO, and SL, compared with the
corresponding values in the YC group. The EC group also
showed significantly lower values of TST and SE, as well as
significantly higher values of AT and WASO, compared with
the corresponding values in the YC group. Furthermore, the
EI group showed significantly lower values of TST and SE,
as well as significantly higher values of AT and WASO,
compared with the corresponding values in the EC group.
Melatonin rhythm parameters in the baseline period
The melatonin secretion rhythm parameters in the baseline
period are also shown in Table 1. AMP and AUCn in the EI
group and AMP in the EC group were significantly reduced,
compared with the corresponding values in the YC group.
AUCn in the EC group shows a decreasing tendency, compared with that in the YC group (P ⫽ 0.082), as well as a
increasing tendency, compared with that in the EI group and
compared with the EC group (P ⫽ 0.080). There were no
significant differences in AMP between the EC and EI
groups. There were no significant differences in AUCd,
ILLUMINATION AFFECTS MELATONIN SECRETION
131
TABLE 1. Sleep, melatonin and light parameters in the baseline and light exposure periods
Parameters
Sleep parameters
TST (min)
SE (%)
AT (times)
WASO (min)
SL (min)
Melatonin parameters
AMP (pg/mL)
AUCn (pg/mL䡠h)
AUCd (pg/mL䡠h)
DLMOn (h:min)
DLMOff (h:min)
Duration (h:min)
Midtime (h:min)
Light parameters
Ltotal (lux/h䡠103)
L ⬎ 1000 (min)
YC (n ⫽ 10) Baseline
EC (n ⫽ 10) Baseline
444.1 ⫾ 8.14
91.9 ⫾ 0.91
2.85 ⫾ 0.31
21.5 ⫾ 3.10
13.1 ⫾ 1.45
EI (n ⫽ 10)
Baseline
Light exposure
405.0 ⫾ 13.1a
80.03 ⫾ 2.14b
5.45 ⫾ 0.46b
44.4 ⫾ 4.70b
19.33 ⫾ 3.76
349.0 ⫾ 15.0b,c
71.3 ⫾ 1.89b,c
7.96 ⫾ 0.88b,d
64.3 ⫾ 5.00b,d
24.3 ⫾ 2.73b
375.1 ⫾ 17.0
76.9 ⫾ 2.77
5.57 ⫾ 0.43e
49.2 ⫾ 4.70
21.9 ⫾ 3.60
43.0 ⫾ 5.50
272.9 ⫾ 33.5
86.3 ⫾ 17.5
⫺1:56 ⫾ 24.3
8:05 ⫾ 15.7
10:01 ⫾ 25.8
3:05 ⫾ 15.9
26.2 ⫾ 4.60a
184.4 ⫾ 28.7
65.9 ⫾ 3.89
⫺2:05 ⫾ 15.7
7:47 ⫾ 15.4
9:52 ⫾ 25.9
2:51 ⫾ 8.62
18.5 ⫾ 6.15b
139.1 ⫾ 35.4a
72.2 ⫾ 4.75
⫺1:49 ⫾ 22.3
7:19 ⫾ 26.6
9:07 ⫾ 35.6
2:45 ⫾ 17.0
35.1 ⫾ 7.54e
231.9 ⫾ 46.5e
72.7 ⫾ 5.08
⫺2:01 ⫾ 25.1
8:03 ⫾ 34.2
10:05 ⫾ 43.4
3:01 ⫾ 20.6
29.2 ⫾ 2.18
115.2 ⫾ 13.5
14.9 ⫾ 0.66b
47.5 ⫾ 9.60b
12.1 ⫾ 0.54b,d
39.5 ⫾ 8.40b
29.4 ⫾ 0.54f
267.4 ⫾ 5.70f
P ⬍ 0.05 vs. YC group.
P ⬍ 0.01 vs. YC group.
P ⬍ 0.01 vs. EC group.
d
P ⬍ 0.05 vs. EC group.
e
P ⬍ 0.05 vs.. baseline period.
f
P ⬍ 0.001 vs.. baseline period.
a
b
c
DLMOn, DLMOff, Duration, and Midtime among the three
groups. Four subjects in the EI group who took benzodiazepines showed no significant difference in either AMP or
AUCn, compared with the corresponding value in the other
six subjects in the EI group (34.5 ⫾ 5.7 vs. 35.2 ⫾ 5.2 pg/mL,
and 226.2 ⫾ 33.3 vs. 230.68 ⫾ 30.39 pg/mL䡠h, respectively).
Luminous condition in the baseline period
Values of parameters of light condition in the baseline
period are also shown in Table 1. Average Ltotal values,
measured at eye level during wake time in both the EI and
EC groups, were significantly lower than that measured in
the YC group. There was also significant difference in Ltotal
between the EI and EC groups. Average L ⬎ 1000 values,
measured at eye level during wake time in both the EI and
EC groups, were significantly lower than that measured in
the YC group. There was no significant difference in L ⬎ 1000
between the EI and EC groups.
Midday exposure to bright light
During the light exposure time in the light room, the light
intensity at eye level was controlled for each EI subject
(range, 2205–2501; mean, 2406 ⫾ 30.2 lux). Average Ltotal
during the light exposure period was not significantly different from that in the YC group during the baseline period
(P ⫽ 0.596). Midday bright light exposure for 4 weeks significantly decreased AT, increased SE (P ⫽ 0.083), and decreased WASO (P ⫽ 0.066) in the EI group (Table 1). The
midday bright light exposure also increased the AMP and
AUCn without any significant changes in DLMOn, DLMOff,
and Midtime in the EI group (Table 1, Fig. 1). There was a
tendency for increased AMP to be associated with increased
SE (r ⫽ 0.56, P ⫽ 0.096) and for increased AMP to be associated with decreased AT (r ⫽ 0.60, P ⫽ 0.066) induced by
FIG. 1. Daily profiles of serum melatonin secretion for the YC, EC,
and EI groups. Horizontal bars indicate the time, relative to 0000 h,
defined as the average SOT for the last 7 days in the baseline and light
exposure periods. Values are shown as mean ⫾ SEM. The white line
and shaded area cover mean ⫾ SEM of the daily melatonin secretion
profile for the YC group. Bars showing SEM for the EC group were
omitted for convenience. AMP in the EC (P ⬍ 0.05) and EI (P ⬍ 0.01)
groups were significantly reduced, compared with the YC group. The
midday bright light exposure significantly increased the AMP (P ⬍
0.05) and the area under the melatonin time-concentration (P ⬍ 0.05)
in the EI group.
light exposure (Fig. 2). There was also a tendency for increased AUCn to be associated with decreased AT (r ⫽ 0.57,
P ⫽ 0.086) induced by light exposure.
132
MISHIMA ET AL.
FIG. 2. Relation between increase in AMP and (a) increase in SE and
(b) decrease in AT induced by midday exposure to bright light. Horizontal bars indicate differences in the AMP value between the light
exposure and baseline periods (dif AMP), and vertical bars indicate
differences in SE and AT values between the light exposure and
baseline periods (dif SE and dif AT, respectively).
Discussion
In the present study, the resident elderly subjects, especially the EIs, were shown to suffer from diminished nocturnal secretion of melatonin, compared with YC subjects
living at home. These findings are consistent with many
previous reports of age-related (17–23) and insomnia-related
(24, 33, 40) decreases in melatonin secretion. Some previous
studies have reported that benzodiazepines could suppress
nocturnal melatonin secretion levels (41– 44); however, small
doses of short-acting benzodiazepines, prescribed for 4 EIs,
exhibited no obvious effects on melatonin secretion levels (at
least in the present study).
We also found that these resident elderly persons were
exposed to significantly lower levels of environmental light,
compared with the YCs. It is noteworthy that supplementary
exposure of bright light at midday for EIs induced significant
increases in AMP and nocturnal melatonin secretion, resulting in levels of melatonin secretion similar to those in YCs.
Based on these data, we suggest that the diminished secretion of melatonin in the elderly subjects in this study was
attributable, at least in part, to their poor environmental
illumination. In addition, the improvement in sleep main-
JCE & M • 2001
Vol. 86 • No. 1
tenance, as represented by decreased AT and WASO and
increased SE induced by midday exposure to bright light,
tended to parallel the improvement in nocturnal melatonin
secretion but without significant circadian phase-shifting as
represented by DLMOn, DLMOff, and Midtime. These findings indicate that reduced secretion of melatonin observed in
poor light conditions may cause sleep maintenance disturbances. In experimental and/or therapeutic trials, melatonin
has been given in doses ranging from 0.1–10 mg (45), which
often yields nonphysiological profiles of serum melatonin
concentration (6). Some previous studies have demonstrated
that melatonin supplementation at night significantly improved sleep problems in EIs (32, 33). However, considering
possible side effects of long-term melatonin administration,
exposure to midday light may provide a more desirable,
potent, safe, and self-directed therapeutic tool for EIs with
diminished melatonin secretion.
The present findings pose some important issues concerning environmental light conditions and the related physiological and/or chronobiological significance. First, we need
to note elderly individuals who suffer from poor light conditions during both phase-shifting (morning and evening)
and nonphase-shifting periods, which result in disorganized
circadian rhythms, including the sleep-wake cycle. Timed
exposure to bright light ranging from 2500 lux to 13000 lux
has been revealed to induce marked suppression of melatonin secretion (46) and strong circadian phase-resetting effect (47– 49) in humans. Dimmer light exposure of 1000 lux
or less could also induce similar effects; however, their magnitude have been shown to distinctly decrease in intensitydependent manners (50, 51). In addition, light intensity of
1000 lux, defined as a cutoff point of bright vs. dim light in
the present study, is thought to reflect exposure to sunlight
both in the summer and winter, and it is rare to record light
intensity of 1000 lux or more under indoor light conditions
(52). These findings let us assume that elderly persons, especially EIs, spending most of their daily life under room
light, could receive insufficient light intensity to adjust their
circadian timing system. Actually, the inadequate exposure
to environmental light that affected the resident elderly persons in this study were thought to result from the high
incident angle of sunlight (decreased sunlight intensities
through windows), withdrawal of residents into their rooms,
and/or little time spent outdoors. Such conditions may exist
for inactive elderly persons residing at home.
Second, we need to recognize the physiological significance of environmental midday light. Sufficient and welltimed morning and evening exposure to light according to
the human phase-response curve is essential for maintaining
proper mutual phase position (47– 49). However, the physiological significance of midday light exposure without significant circadian phase-shifting is unclear. Hashimoto et al.
(53) found that midday exposure to bright light for 3 consecutive days had a phase-resetting effect on melatonin
rhythm without changing the AMP, under isolated conditions in young subjects. In the present study, more long-term
exposure to midday bright light induced remarkable increases in circadian AMPs in elderly persons despite lack of
circadian phase-shifting, even under entrained conditions. In
future studies, these amplitude-modifying effects should be
ILLUMINATION AFFECTS MELATONIN SECRETION
confirmed, with respect to other physiological markers of
circadian rhythms, such as core body temperature.
Third, the present study may help to explain the contradictory data regarding age-related decreases in melatonin
secretion. The discrepancy between previous studies concerning melatonin secretion properties in elderly persons
may be attributable, at least in part, to the environmental
light condition surrounding the experimental subjects.
Twenty older women and 14 older men participating in a
well-controlled study by Zeitzer et al. (34) showed no agerelated changes in melatonin secretion. The subjects in that
study were not institutionalized, and they underwent extensive medical screening to assess physical and mental
health, including sleep patterns and medications. It is possible that these super-healthy elderly subjects spend their
daily lives under light conditions sufficient to maintain melatonin secretion at levels similar to those of young persons.
Although serum melatonin secretion rhythm is often used as
a stable marker of circadian output, the present findings
suggest that we need to consider the environmental light
conditions of the experimental subjects when evaluating
their melatonin rhythms as a circadian marker.
The mechanism behind increased nocturnal melatonin secretion after midday exposure to bright light is unclear. One
explanation is that repeated light stimuli could enhance the
oscillatory amplitude of the circadian clock (54) via the suprachiasmatic nucleus. Bright light was shown to modify
both the phase and the amplitude of the circadian system. In
young subjects, a 3-cycle light stimulus induced strong circadian phase shifting, with different effects on circadian amplitude that depended on the initial phase of the stimulus
application (54). The effect of long-term exposure to midday
light stimulus in elderly persons remains unclear. However,
a previous study revealed that a 2-week exposure to bright
light daily from 0900 h to 1100 h could induce significant
increases in the AMP of core body temperature in EIs (55).
One possible explanation is that midday bright light modifies brain serotonergic function, resulting in increased secretion of melatonin, which is a major metabolite of serotonin
(5-HT) in the pineal gland. Some data from rodent (56) and
human (57) studies have suggested that light can alter the
processing of brain 5-HT signals. Penev et al. (56) showed that
exposure of hamsters to light during their subjective midday
significantly attenuated the phase-shifting effect caused by a
5-HT1a agonist. Lam et al. (57) showed, in humans, that rapid
depletion of the 5-HT precursor tryptophan reversed the
antidepressant effect of bright light therapy in patients with
seasonal affective disorder, suggesting that the therapeutic
effect of bright light may involve a serotonergic mechanism.
It is possible that the significant increase in melatonin synthesis, observed in the present study, is caused by altered
5-HT metabolism induced by long-term exposure to bright
light.
Environmental light not only acts as a mediator of visual
perception, but it also influences the phase/amplitude of
circadian rhythms, which tend to run at a period of about
(but not exactly) 24 h (48, 58). Generally, environmental light
is thought to be sufficient to maintain the circadian timekeeping system, except in special situations such as physiological blindness, experimental isolation, or space flight.
133
However, findings of the present and some previous studies
(28, 59 – 61) suggest that many elderly people spend less time
in bright light because of living arrangements or seasonal
factors. For elderly persons who live with few social time
cues, the possibility that poor daytime conditions could affect
various brain functions, including circadian and serotonergic
systems, should be evaluated.
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