Nasal versus Temporal Illumination of the Human Retina: Effects on Core Body Temperature, Melatonin, and Circadian Phase (original) (raw)
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Melatonin Suppression by Light in Humans Is Maximal When the Nasal Part of the Retina Is Illuminated
Journal of Biological Rhythms, 1999
This study investigated whether sensitivity of the nocturnal melatonin suppression response to light depends on the area of the retina exposed. The reason to suspect uneven spatial sensitivity distribution stems from animal work that revealed that retinal ganglion cells projecting to the suprachiasmatic nuclei (SCN) are unequally distributed in several species of mammals. Four distinct areas of the retinas of 8 volunteers were selectively exposed to 500 lux between 1:30 a.m. and 3:30 a.m. Saliva samples were taken before, during, and after light exposure in 1-h intervals. A significant difference in sensitivity was found between exposure of the lateral and nasal parts of the retinas, showing that melatonin suppression is maximal on exposure of the nasal part of the retina. The results imply that artificial manipulation of the circadian pacemaker to alleviate jet lag, to improve alertness in shift workers, and possibly to treat patients suffering from seasonal affective disorder shou...
BMC Research Notes, 2012
Background: A previous study reported a method for measuring the spectral transmittance of individual human eyelids. A prototype light mask using narrow-band "green" light (λ max = 527 nm) was used to deliver light through closed eyelids in two within-subjects studies. The first study investigated whether an individual-specific light dose could suppress melatonin by 40% through the closed eyelid without disrupting sleep. The light doses were delivered at three times during the night: 1) beginning (while subjects were awake), 2) middle (during rapid eye movement (REM) sleep), and 3) end (during non-REM sleep). The second study investigated whether two individualspecific light doses expected to suppress melatonin by 30% and 60% and delivered through subjects' closed eyelids before the time of their predicted minimum core body temperature would phase delay the timing of their dim light melatonin onset (DLMO). Findings: Compared to a dark control night, light delivered through eyelids suppressed melatonin by 36% (p = 0.01) after 60-minute light exposure at the beginning, 45% (p = 0.01) at the middle, and 56% (p < 0.0001) at the end of the night. In the second study, compared to a dark control night, melatonin was suppressed by 25% (p = 0.03) and by 45% (p = 0.009) and circadian phase, as measured by DLMO, was delayed by 17 minutes (p = 0.03) and 71 minutes (ns) after 60-minute exposures to light levels 1 and 2, respectively. Conclusions: These studies demonstrate that individual-specific doses of light delivered through closed eyelids can suppress melatonin and phase shift DLMO and may be used to treat circadian sleep disorders.
Extraocular Light Exposure Does Not Phase Shift Saliva Melatonin Rhythms in Sleeping Subjects
Journal of Biological Rhythms, 2002
Preliminary work in humans suggests that extraocular light can shift circadian phase. If confirmed, extraocular light may be of therapeutic benefit in the treatment of circadian-related sleep disorders with the advantage over ocular exposure that it can be administered while subjects are asleep. In sleeping subjects, however, the effect of extraocular light exposure on circadian phase has yet to be fully tested. Likewise, there is limited data on the acute effects of extraocular light on sleep and body temperature that may influence its clinical utility. Thirteen subjects [3F, 10M; mean (SD) age = 22.1 (3.0)y] participated in a protocol that totaled 7 nights in the laboratory consisting of a screening phase measurement night followed 1 week later by two counterbalanced experimental sessions each of 3 consecutive nights (habituation, treatment, and posttreatment phase measurement night) separated by 4 days. Saliva was collected for melatonin measurement every half hour from 1800 to 0300 h on the screening night and both the posttreatment phase measurement nights. On the treatment nights, continuous measures of rectal temperature and polysomnographic sleep were collected and overnight urine for measurement of total nocturnal urinary 6-sulphatoxymelatonin excretion. To test for the phase-delaying effects of extraocular light, subjects received either placebo or extraocular light (11,000 lux) behind the right knee from 0100 to 0400 h. Treatment had no significant effect on the onset of saliva melatonin secretion, phase of nocturnal core body temperature, or urinary 6sulfatoxymelatonin excretion, but a small increase was observed in wakefulness over the light administration period. In summary, extraocular light was not shown to delay circadian phase but was shown to increase wakefulness. The authors suggest that the present protocol has limited application as a treatment for circadian-related sleep disorders.
Possible Behavioral Consequences of Light-Induced Changes in Melatonin Availabilitya
Annals of the New York Academy of Sciences, 1985
Melatonin is a hormone secreted at night by the human pineal organ. This nocturnal release of melatonin, in humans and other species, is rapidly suppressed by exposure to sufficiently bright light.' Melatonin was first isolated and its structure identified by Lerner and his coworkers over 25 years ago.* Until very recently, however, the effects of this hormone on human behavior had not been closely examined. Some studies had suggested that melatonin had hypnotic-like proper tie^;'.^ others, however, failed to document such effectss The influence of exogenously administered melatonin on animal behavior is still unclear and often contradictory. For example, Holmes and Sugden6 reported that melatonin increased sleep in the rat, whereas Mendelson et al.' have reported a decrease in time spent sleeping after melatonin administration. Other studies with rats have indicated that melatonin has anxiety reducing properties (to the extent that such effects can be inferred from animal behavior).*.9 If melatonin does have different effects on different species this may be attributable to differences in daily patterns of activity displayed by such species (diurnal, nocturnal, or crepuscular).' Although the behavioral effects of melatonin on animals remain uncertain at this time, the effects on humans have recently been clarified. These recent human studies, including one conducted in our laboratory, will be discussed. A possible relationship between light exposure, human alertness, and circadian patterns of activity, as mediated by melatonin, will also be discussed. In these recent human studies melatonin has been administered in various doses, acutely and chronically, a t various times of the day to healthy male and female volunteers. Vollrath et al.." in a double-blind crossover study administered melatonin (1.7 mg) intranasally to six male and four female volunteers. It was observed (apparently based on a self-report questionnaire) that seven subjects fell asleep within 1 or 2 hours of melatonin administration, whereas only one slept after placebo administration. Although standard methods for quantifying sleep or sleepiness (i.e. EEG recordings or standardized self-report mood questionnaires) were not used, the consistency of the findings is strong support for melatonin having hypnotic properties uThis work was supported by NIH Grants 2R01-HD11722 and 2M01-RR00088 as well as dPresent address: Univ.-Kinderklinik. Waehringer Geurtel74-76, A
Journal of Pineal Research, 1994
Different patterns of light exposure in relation to melatonin and cortisol rhythms and sleep of night workers. J. Pineal Res. 1994:16:127-135. Abstract: There is strong evidence to suggest that circadian psychophysiological adaptation processes are modified by light, depending on its intensity and timing. To characterize such modifications and determine whether they are associated with an alteration in the dayhight pattern of melatonin excretion, measurements were obtained around the clock in 14 permanent night workers, each studied over a 48 hr period in the field. The light exposure behavior of these workers was studied with a newly developed light dosimetry by measuring light intensity at eye level. Physical activity was continuously registered and sleep indices were obtained by sleep logs and activity markings. Circadian rhythms of melatonin and cortisol were analysed from salivary samples collected for 24 hr at 2 hr intervals. The interindividual variation of melatonin acrophase determined by cosinor analysis was greater than 180 degrees (from around midnight to noon) and that of cortisol was about 135 degrees (from early morning to afternoon). Hormonal phase positions coincided significantly with light exposure: the more bright light pulses in the morning (maximum lux between 0600 and 0900), the less were the melatonin and cortisol acrophases shifted into the day. There was also a negative correlation between melatonin acrophase shift and duration of the overall light exposure above 1500 lux. Morning light maximum and sleep onset correlated highly significantly. Night workers were divided into those with less than ('non-shifters', n = 9) and more than 6 hr deviation from midnight ('shifters', n = 5) of the melatonin acrophase. The group comparison revealed a marked difference of the mean melatonin concentrations at night, and at 0700. Shifters did not experience bright light exposure in the morning and showed a tendency towards shorter overall exposure of light above 1500 lux. In conclusion, light avoidance behavior during morning hours, as observed in 5 out of 14 night workers, coincided significantly with a phase delay of melatonin acrophase. Light avoidance also correlated with an earlier sleep onset and a tendency to longer sleep hours. Thus our data suggest that the interaction of a phase shifted activity cycle and the lighvdark exposure leads in the field situation to different degrees of adaptation to the prevailing activitykest requirements, depending on dose and phase position of bright light exposure.
Complex effects of melatonin on human circadian rhythms in constant dim light
Journal of biological rhythms, 1997
In humans, the pineal hormone melatonin can phase shift a number of circadian rhythms (e.g., "fatigue," endogenous melatonin, core body temperature) together with the timing of prolactin secretion. It is uncertain, however, whether melatonin can fully entrain all human circadian rhythms. In this study, the authors investigated the effects of daily melatonin administration on sighted individuals kept in continuous very dim light. A total of 10 normal, healthy males were maintained in two separate groups in partial temporal isolation under constant dim light (< 8 lux) with attenuated sound and ambient temperature variations but with knowledge of clock time for two periods of 30 days. In these circumstances, the majority of individuals free run with a mean period of 24.3 h. In a double-blind, randomized crossover design, subjects received 5 mg melatonin at 20:00 h on Days 1 to 15 (Melatonin 1st) followed by placebo on Days 16 to 30 (Placebo 2nd) or vice versa (Placebo 1st, Melatonin 2nd) during Leg 1 with treatment reversed in Leg 2. The variables measured were melatonin (as 6sulphatoxymelatonin), rectal temperature, activity, and sleep (actigraphy and logs). In the experiment, 9 of the 10 subjects free ran with Placebo 1st, whereas Melatonin 1st stabilized the sleep-wake cycle to 24 h in 8 of 10 individuals. In addition, 2 individuals showed irregular sleep with this treatment. In some subjects, there was a shortening of the period of the temperature rhythm without synchronization. Melatonin 2nd induced phase advances (5 of 9 subjects), phase delays (2 of 9 subjects), and stabilization (2 of 9 subjects) of the sleep-wake cycle with subsequent synchronization to 24 h in the majority of individuals (7 of 9). Temperature continued to free run in 4 subjects. Maximum phase advances in core temperature were seen when the first melatonin treatment was given approximately 2 h after the temperature acrophase. These results indicate that melatonin was able to phase shift sleep and core temperature but was unable to synchronize core temperature consistently. In the majority of subjects, the sleepwake cycle could be synchronized.