Chronic exposure to ELF magnetic fields during night sleep with electric sheet: effects on diurnal melatonin rhythms in men

The possible effects of repeated night-time exposure to an extremely low frequency magnetic field (ELF-MF) on melatonin were investigated in nine healthy male subjects aged 23-37 yr. The 16-week experiment consisted of 3 weeks of pre-exposure, 11 weeks of night-time exposure to MF generated from a nonheated electric sheet (ES), and 2 weeks of post-exposure recovery observation. The average MF intensity (rms, mainly 50 Hz AC) on the surface of the sheet was 0.7 microT at the head, 8.3 microT at the waist, and 3.5 microT at the feet of the subject. For each of the urine samples collected 5 times a day on scheduled sampling days, the urinary excretion rate (ng/h) of melatonin was determined, and 24 h rhythms were extracted for each subject and each experimental period (pre-exposure, first half and latter half exposure, and post-exposure periods) by the method of complex cosine curve fitting. Although estimates of the peak height, acrophase, and total daily amount of melatonin were characterized by significant variations among individual subjects, they did not reveal any statistically significant difference between exposure periods and nonexposure periods. Thus, the present study indicates that any profound effect of the MF originating from an ES on nocturnal melatonin production and its circadian rhythm is unlikely.     

Cytogenetic effects of 50 Hz magnetic fields of different magnetic flux densities

Cytogenetic investigations were performed in human peripheral blood lymphocytes following exposure to 50 Hz magnetic fields alone or in combination with the chemical mutagen mitomycin C or with X-rays. It was found that magnetic fields up to 2500 microT did not significantly influence the chromosome aberration and sister chromatid exchange frequency. Also, the combined treatments failed to indicate the presence of any synergistic, potentiating, or antagonistic effect between the ELF magnetic fields and the mutagens. However, there were two exceptions: Cells exposed to 504 microT magnetic fields before and during cultivation displayed a statistically significant decrease in sister chromatid exchange frequency. Also, when cells were cultivated in the presence of 88.4 microT magnetic fields following X-ray exposures there was a significant increase in chromosome aberration frequency compared to X-ray exposure alone.     

Chronic exposure to ELF fields may induce depression

Exposure to extremely-low-frequency (ELF) electric or magnetic fields has been postulated as a potentially contributing factor in depression. Epidemiologic studies have yielded positive correlations between magnetic- and/or electric-field strengths in local environments and the incidence of depression-related suicide. Chronic exposure to ELF electric or magnetic fields can disrupt normal circadian rhythms in rat pineal serotonin-N-acetyltransferase activity as well as in serotonin and melatonin concentrations. Such disruptions in the circadian rhythmicity of pineal melatonin secretion have been associated with certain depressive disorders in human beings. In the rat, ELF fields may interfere with tonic aspects of neuronal input to the pineal gland, giving rise to what may be termed "functional pinealectomy." If long-term exposure to ELF fields causes pineal dysfunction in human beings as it does in the rat, such dysfunction may contribute to the onset of depression or may exacerbate existing depressive disorders.     

Nocturnal melatonin levels in human volunteers exposed to intermittent 60 Hz magnetic fields

Two double-blind laboratory-based studies were performed to determine whether a suppression of nocturnal melatonin similar to that observed in rodents occurs when humans are exposed to magnetic fields at night. In study 1, 33 men were exposed to sham, 10 mG, or 200 mG intermittent, circularly polarized magnetic fields from 2300 to 0700 h under controlled environmental and exposure test conditions. Overall, exposure had no effect on melatonin levels. Men with preexisting low levels of melatonin, however, showed significantly greater suppression of melatonin when they were exposed to light and also when they were exposed to the 200 mG magnetic-field condition. Study 2 directly tested the hypothesis that low-melatonin subjects show enhanced sensitivity when exposed to light and to 200 mG magnetic fields. After preexposure screening, each of 40 men slept in the exposure facility on two nights. On one night, the men were sham exposed. On the other night, they were exposed to the 200 mG field condition used previously. Again, exposure had no overall effect on melatonin levels. The original finding of enhanced sensitivity in low-melatonin subjects was not replicated in this study. We conclude that the intermittent exposure conditions used in these two studies were not effective in altering nocturnal melatonin release patterns in human volunteers. Further research is underway with regard to exposure parameters, hormonal and immune system measures, and individual differences. © 1996 Wiley-Liss, Inc.     

Acute exposure to 50 Hz magnetic fields with harmonics and transient components: lack of effects on nighttime hormonal secretion in men

The purpose of this study was to examine whether low frequency magnetic field (MF) influences nighttime secretion of hormones, particularly melatonin. Ten healthy males stayed in the experimental room (2.7 m cube with 3 axis Merritt coils) on two separate nights. On one night, subjects were exposed to linearly polarized 50 Hz, 20 microT sinusoidal MF with the third (30%) and the fifth (10%) harmonics and repetitive transient waves (1 burst/s of 1 kHz waves, exponentially attenuated with a duration of 50 ms; initially 100 microT peak), and the other night was for blind control. During the nights (2000-0800 h, including sleeping time, 2300-0700 h), blood samples were collected from the subjects at 1 h intervals for determining the levels of plasma hormones (melatonin, growth hormone (GH), cortisol, prolactin) and at 10 min intervals from 2200 to 0200 h for observing the GH surge induced by sleep. Statistical analyses revealed no significant difference between the 2 nights in the profiles of the four hormones, and the result suggested that extremely low frequency (ELF) or intermediate frequency (IF) MF to which humans are exposed residentially has no acute effect on nighttime secretion of hormones, particularly melatonin.     

Melatonin rhythm observed throughout a three-cycle bright-light stimulus designed to reset the human circadian pacemaker.

Exposure to light and darkness can rapidly induce phase shifts of the human circadian pacemaker. A type 0 phase response curve (PRC) to light that has been reported for humans was based on circadian phase data collected from constant routines performed before and after a three-cycle light stimulus, but resetting data observed throughout the entire resetting protocol have not been previously reported. Pineal melatonin secretion is governed by the hypothalamic circadian pacemaker via a well-defined neural pathway and is reportedly less subject to the masking effects of sleep and activity than body temperature. The authors reasoned that observation of the melatonin rhythm throughout the three-cycle light resetting trials could provide daily phase-resetting information, allowing a dynamic view of the resetting response of the circadian pacemaker to light. Subjects (n = 12) living in otherwise dim light (approximately 10-15 lux) were exposed to a noncritical stimulus of three cycles of bright light (approximately 9500 lux for 5 h per day) timed to phase advance or phase delay the human circadian pacemaker; control subjects (n = 11) were scheduled to the same protocols but exposed to three 5-h darkness cycles instead of light. Subjects underwent initial and final constant routine phase assessments; hourly melatonin samples and body temperature data were collected throughout the protocol. Average daily phase shifts of 1 to 3 h were observed in 11 of 12 subjects receiving the bright light, supporting predictions obtained using Kronauer's phase-amplitude model of the resetting response of the human circadian pacemaker. The melatonin rhythm in the 12th subject progressively attenuated in amplitude throughout the resetting trial, becoming undetectable for >32 hours preceding an abrupt reappearance of the rhythm at a shifted phase with a recovered amplitude. The data from control subjects who remained in dim lighting and darkness delayed on average -0.2 h per day, consistent with the daily delay expected due to the longer than 24-h intrinsic period of the human circadian pacemaker. Both temperature and melatonin rhythms shifted by equivalent amounts in both bright light-treated and control subjects (R = 0.968; p<0.0001; n = 23). Observation of the melatonin rhythm throughout a three-cycle resetting trial has provided a dynamic view of the daily phase-resetting response of the human circadian pacemaker. Taken together with the observation of strong type 0 resetting in humans in response to the same three-cycle stimulus applied at a critical phase, these data confirm the importance of considering both phase and amplitude when describing the resetting of the human circadian pacemaker by light.     

Static and extremely low frequency electromagnetic field exposure: Reported effects on the circadian production of melatonin

The circadian rhythm of melatonin production (high melatonin levels at night and low during the day) in the mammalian pineal gland is modified by visible portions of the electromagnetic spectrum, i.e., light, and reportedly by extremely low frequency (ELF) electromagnetic fields as well as by static magnetic field exposure. Both light and non-visible electromagnetic field exposure at night depress the conversion of serotonin (5HT) to melatonin within the pineal gland. Several reports over the last decade showed that the chronic exposure of rats to a 60 Hz electric field, over a range of field strengths, severely attenuated the nighttime rise in pineal melatonin production; however, more recent studies have not confirmed this initial observation. Sinusoidal magnetic field exposure also has been shown to interfere with the nocturnal melatonin forming ability of the pineal gland although the number of studies using these field exposures is small. On the other hand, static magnetic fields have been repeatedly shown to perturb the circadian melatonin rhythm. The field strengths in these studies were almost always in the geomagnetic range (0.2 to 0.7 Gauss or 20 to 70 μtesla) and most often the experimental animals were subjected either to a partial rotation or to a total inversion of the horizontal component of the geomagnetic field. These experiments showed that several parameters in the indole cascade in the pineal gland are modified by these field exposures; thus, pineal cyclic AMP levels, N-acetyltransferase (NAT) activity (the rate limiting enzyme in pineal melatonin production), hydroxyindole-O-methyltransferase (HIOMT) activity (the melatonin forming enzyme), and pineal and blood melatonin concentrations were depressed in various studies. Likewise, increases in pineal levels of 5HT and 5-hydroxyindole acetic acid (5HIAA) were also seen in these glands; these increases are consistent with a depressed melatonin synthesis. The mechanisms whereby non-visible electromagnetic fields influence the melatonin forming ability of the pineal gland remain unknown; however, the retinas in particular have been theorized to serve as magnetoreceptors with the altered melatonin cycle being a consequence of a disturbance in the neural biological clock, i.e., the suprachiasmatic nuclei (SCN) of the hypothalamus, which generates the circadian melatonin rhythm. The disturbances in pineal melatonin production induced by either light exposure or non-visible electromagnetic field exposure at night appear to be the same but whether the underlying mechanisms are similar remains unknown.     

No association between occupational exposure to ELF magnetic field and urinary 6-sulfatoximelatonin in workers

A suppression in melatonin secretion is one of the mechanisms proposed to explain the possible adverse effects of extremely low frequency magnetic fields (ELF-MF), but the results of research are inconclusive. This study investigated the effect of occupational ELF-MF exposure on 6-sulfatoximelatonin (6-OHMS). Exposure was monitored for three complete work shifts in 59 workers using personal exposure meters. Environmental exposure was also evaluated. Urinary 6-OHMS in morning samples, an indicator of night-time melatonin production, was measured. Urine was collected twice on Friday and the following Monday. Workers were classified according to ELF exposure as low exposed (0.2 microT): 6-OHMS did not differ between groups (P > .05) in either Friday or Monday urine samples. In addition, 6-OHMS was not related to exposure under multivariate analysis. The ratio between 6-OHMS in Monday versus Friday samples was also calculated to test the hypothesis of a possible variation in pineal function after 2 days, interruption of occupational ELF-MF exposure: again no exposure-related difference was observed. Our results do not support the hypothesis that occupational exposure to ELF-MF significantly influences melatonin secretion.     

Effects of combined DC and AC magnetic fields on germination of hornwort seeds

Seeds of hornwort (Cryptotaenia japonica Hassk) were exposed to sinusoidally time-varying extremely low frequency (ELF) magnetic fields (AC fields) in combination with the local geomagnetic field (DC field). Exposure lasted 24 h/day for 16 days. Three directions of the AC magnetic fields were considered; the vertical (magnetic flux density B ACV, the directions parallel B ACparallel), and perpendicular B ACperpendicular to the direction of total geomagnetic field (magnetic flux density BG) in the geomagnetic plane (GP). Controls consisted of seeds exposed to zero AC magnetic fields in combination with the DC magnetic field. The B ACV in combination with BG effectively promoted the germination of hornwort seeds when applied at 750 microT (RMS) at 7 Hz or 500 microT (RMS) at 14 Hz from among the cases of individual frequencies f = 3.5, 7.0, 10.5, 14.0 Hz at 500 and 750 microT. The B ACparallel promoted the germination of hornwort seeds more effectively than the B ACperpendicular in combination with BG when 500 and 750 microT at 7 Hz were applied.     

Familial advanced sleep-phase syndrome: A short-period circadian rhythm variant in humans.

Biological circadian clocks oscillate with an approximately 24-hour period, are ubiquitous, and presumably confer a selective advantage by anticipating the transitions between day and night. The circadian rhythms of sleep, melatonin secretion and body core temperature are thought to be generated by the suprachiasmatic nucleus of the hypothalamus, the anatomic locus of the mammalian circadian clock. Autosomal semi-dominant mutations in rodents with fast or slow biological clocks (that is, short or long endogenous period lengths; tau) are associated with phase-advanced or delayed sleep-wake rhythms, respectively. These models predict the existence of familial human circadian rhythm variants but none of the human circadian rhythm disorders are known to have a familial tendency. Although a slight 'morning lark' tendency is common, individuals with a large and disabling sleep phase-advance are rare. This disorder, advanced sleep-phase syndrome, is characterized by very early sleep onset and offset; only two cases are reported in young adults. Here we describe three kindreds with a profound phase advance of the sleep-wake, melatonin and temperature rhythms associated with a very short tau. The trait segregates as an autosomal dominant with high penetrance. These kindreds represent a well-characterized familial circadian rhythm variant in humans and provide a unique opportunity for genetic analysis of human circadian physiology.     

Systematic review of light exposure impact on human circadian rhythm

Light is necessary for life, and artificial light improves visual performance and safety, but there is an increasing concern of the potential health and environmental impacts of light. Findings from a number of studies suggest that mistimed light exposure disrupts the circadian rhythm in humans, potentially causing further health impacts. However, a variety of methods has been applied in individual experimental studies of light-induced circadian impacts, including definition of light exposure and outcomes. Thus, a systematic review is needed to synthesize the results. In addition, a review of the scientific evidence on the impacts of light on circadian rhythm is needed for developing an evaluation method of light pollution, i.e., the negative impacts of artificial light, in life cycle assessment (LCA). The current LCA practice does not have a method to evaluate the light pollution, neither in terms of human health nor the ecological impacts. The systematic literature survey was conducted by searching for two concepts: light and circadian rhythm. The circadian rhythm was searched with additional terms of melatonin and rapid-eye-movement (REM) sleep. The literature search resulted to 128 articles which were subjected to a data collection and analysis. Melatonin secretion was studied in 122 articles and REM sleep in 13 articles. The reports on melatonin secretion were divided into studies with specific light exposure (101 reports), usually in a controlled laboratory environment, and studies of prevailing light conditions typical at home or work environments (21 studies). Studies were generally conducted on adults in their twenties or thirties, but only very few studies experimented on children and elderly adults. Surprisingly many studies were conducted with a small sample size: 39 out of 128 studies were conducted with 10 or less subjects. The quality criteria of studies for more profound synthesis were a minimum sample size of 20 subjects and providing details of the light exposure (spectrum or wavelength; illuminance, irradiance or photon density). This resulted to 13 qualified studies on melatonin and 2 studies on REM sleep. Further analysis of these 15 reports indicated that a two-hour exposure to blue light (460 nm) in the evening suppresses melatonin, the maximum melatonin-suppressing effect being achieved at the shortest wavelengths (424 nm, violet). The melatonin concentration recovered rather rapidly, within 15 min from cessation of the exposure, suggesting a short-term or simultaneous impact of light exposure on the melatonin secretion. Melatonin secretion and suppression were reduced with age, but the light-induced circadian phase advance was not impaired with age. Light exposure in the evening, at night and in the morning affected the circadian phase of melatonin levels. In addition, even the longest wavelengths (631 nm, red) and intermittent light exposures induced circadian resetting responses, and exposure to low light levels (5–10 lux) at night when sleeping with eyes closed induced a circadian response. The review enables further development of an evaluation method of light pollution in LCA regarding the light-induced impacts on human circadian system.     

Biological effects of power frequency magnetic fields: Neurochemical and toxicological changes in developing chick embryos

BACKGROUND: There are several reports that indicate a linkage between exposure to power frequency (50 - 60 Hz) magnetic fields with abnormalities in the early embryonic development of the chicken. The present study was designed to understand whether power frequency electromagnetic fields could act as an environmental insult and invoke any neurochemical or toxicological changes in developing chick embryo model. METHODS: Fertilized chicken eggs were subjected to continuous exposure to magnetic fields (50 Hz) of varying intensities (5, 50 or 100 microT) for a period of up to 15 days. The embryos were taken out of the eggs on day 5, day 10 and day 15. Neurochemical (norepinephrine and 5-hydroxytryptamine) and amino acid (tyrosine, glutamine and tryptophan) contents were measured, along with an assay of the enzyme glutamine synthetase in the brain. Preliminary toxicological investigations were carried out based on aminotransferases (AST and ALT) and lactate dehydrogenase activities in the whole embryo as well as in the liver. RESULTS: The study revealed that there was a significant increase (p < 0.01 and p < 0.001) in the level of norepinephrine accompanied by a significant decrease (p < 0.01 and p < 0.001) in the tyrosine content in the brain on day 15 following exposure to 5, 50 and 100 microT magnetic fields. There was a significant increase (p < 0.001) in glutamine synthetase activity resulting in the significantly enhanced (p < 0.001) level of glutamine in the brain on day 15 (for 100 microT only). The possible mechanisms for these alterations are discussed. Further, magnetic fields had no effect on the levels of tryptophan and 5-hydroxytryptamine in the brain. Similarly, there was no effect on the activity of either aminotransferases or lactate dehydrogenase in the whole embryo or liver due to magnetic field exposure. CONCLUSIONS: Based on these studies we conclude that magnetic field-induced changes in norepinephrine levels might help explain alterations in the circadian rhythm, observed during magnetic field stress. Also, the enhanced level of glutamine can act as a contributing factor for developmental abnormalities.     

Measurement of the individual exposure to 50 and 16 2/3 Hz magnetic fields within the Bavarian population.

This study investigates the individual magnetic field exposures at 16 2/3 and 50 Hz of 1952 people, selected from the Bavarian population. Personal flux density meters ("Field Watcher FW2A") were worn by the participants for 24 h. Every second, the flux density was recorded for both frequencies and for the three spatial axes (dynamic range per axis: several nT up to 100 microT at 50 Hz, 150 microT at 16 2/3 Hz). For 50 Hz fields, the mean of the 1,952 individual means was 0.101 microT and that of the individual medians was 0.047 microT. High level exposures occurred mainly during working hours. Only 2.4% of the subjects showed individual medians higher than 0.2 microT. About 53% of all volunteers were working on the day of recording. Levels for craftsmen (n = 148; mean individual mean: 0.166 microT) were generally higher than those for office workers (n = 624; mean individual mean: 0.107 microT). Flux densities exceeding 100 microT at 50 Hz were measured in 31 persons. The total time with such extreme exposures amounts to nearly 21 min, less than 0.001% of the total time for all measurements (5.3 years). To our knowledge, this is the first exposure study where 16 2/3 Hz magnetic fields (caused by electrified railways) have additionally been monitored over 24 h. For persons living next to railway lines, the mean individual mean (0.156 microT) and mean individual median (0.102 microT) were calculated. Over all, the mean exposures are only 0.1% of the magnetic flux density limit for 50 Hz (100 microT) and about 0.05% of the limit (300 microT) for 16 2/3 Hz recommended by the International Commission on Non-Ionizing Radiation Protection.     

Biophysical mechanisms: a component in the weight of evidence for health effects of power-frequency electric and magnetic fields

Comparatively high exposures to power-frequency electric and magnetic fields produce established biological effects that are explained by accepted mechanisms and that form the basis of exposure guidelines. Lower exposures to magnetic fields (< 1 microT average in the home) are classified as "possibly carcinogenic" on the basis of epidemiological studies of childhood leukemia. This classification takes into consideration largely negative laboratory data. Lack of biophysical mechanisms operating at such low levels also argues against causality. We survey around 20 biophysical mechanisms that have been proposed to explain effects at such low levels, with particular emphasis on plausibility: the principle that to produce biological effects, a mechanism must produce a "signal" larger than the "noise" that exists naturally. Some of the mechanisms are impossible, and some require specific conditions for which there is limited or no evidence as to their existence in a way that would make them relevant to human exposure. Others are predicted to become plausible above some level of field. We conclude that effects below 5 microT are implausible. At about 50 microT, no specific mechanism has been identified, but the basic problem of implausibility is removed. Above about 500 microT, there are established or likely effects from accepted mechanisms. The absence of a plausible biophysical mechanism at lower fields cannot be taken as proof that health effects of environmental electric and magnetic fields are impossible. Nevertheless, it is a relevant consideration in assessing the overall evidence on these fields.     

A replication study of human exposure to 60-Hz fields: effects on neurobehavioral measures.

The purpose of this study was to reproduce and extend an earlier investigation of the effects of human exposure to combined, 60-Hz electric and magnetic fields. This paper presents the neurobehavioral results. Thirty men participated in one training session and four testing sessions. Subjects were randomly assigned to two groups. The 18 subjects in Group I were exposed (9 kV/m, 20 microT) and sham exposed in two counterbalanced orders. In Group II, half of 12 subjects were exposed (9 kV/m, 20 microT) every session, and the remaining half were sham exposed every session. The study was doubly blinded. Measures of cardiac interbeat interval, event-related brain potentials, and performance were obtained before, during, and after exposures. As in the earlier study, exposure to the combined field resulted in a statistically significant slowing of heart rate, in changes in late components of event-related brain potentials, and in decreased errors on a choice reaction-time task. In addition, field effects on several other measures approached statistical significance. The physiological measures obtained during exposure indicated that effects were greatest soon after the field was switched on, and again when it was switched off. The data indicate that changes in exposure level may be more important than duration of exposure for producing effects in human beings.     

The influence of 1.2 microT, 60 Hz magnetic fields on melatonin- and tamoxifen-induced inhibition of MCF-7 cell growth

We independently examined the findings of Harland and Liburdy, who reported that 1.2 microT(rms), 60 Hz magnetic fields could significantly reduce the inhibitory action of physiological levels of melatonin (10(-9) M) and of pharmacological levels of tamoxifen (10(-7) M) on the growth of MCF-7 human breast cancer cells in vitro. We used two testing protocols. In the melatonin study, the cell numbers per dish on day 7 of treatment were determined using a hemocytometer assay. In the tamoxifen study we used an expanded protocol, employing an alternative cell counting assay to characterize the cell numbers per dish on days 4, 5, 6, and 7. In both the melatonin and tamoxifen studies, cells were plated on 35 mm dishes and placed in each of two exposure chambers inside 5% CO(2) incubators. One exposure chamber was energized to produce 1.2 microT(rms), 60 Hz magnetic fields and the other chamber was not energized. Treatment was continuous until assays were performed. Cells were harvested at selected times, and enumerated without knowledge of treatment. In the melatonin study, the experiment was repeated three times, whereas in the tamoxifen study, each experiment was repeated nine times. In the melatonin study, cell numbers per dish were significantly reduced (by 16.7%) in the melatonin treated cultures after 7 days of incubation compared to control cultures, whereas in the presence of 1.2 microT(rms), 60 Hz magnetic fields, the melatonin treated cultures had the same cell populations as the control cultures. In the tamoxifen study, tamoxifen reduced the cell growth by 18.6 and 25% on days 6 and 7, respectively, in the chamber not energized, while in 1.2 microT(rms), 60 Hz fields, tamoxifen reduced the cell growth only by 8.7 and 13.1%, respectively. These results are consistent with those reported by Harland and Liburdy. A critical element of this successful replication effort was the constructive communication established and maintained with the original investigators. Bioelectromagnetics 22:122-128, 2001. Published 2001 Wiley-Liss, Inc.     

动物内源褪黑素调控生物节律的研究进展

内源褪黑素对人类和其他哺乳动物的节律行为具有调控功能。生物节律是自然进化赋予生命的基本特征之一,生物体的生命活动受到生物节律的控制与影响。在哺乳动物中,节律调控中心是松果体,其主要功能是合成和分泌褪黑素。褪黑素广泛参与生物体节律行为的调节,本文从褪黑素的产生和作用机制,分别阐述褪黑素对昼夜节律行为和多种年节律行为的调控作用,同时明确褪黑素与生物钟及神经内分泌系统的直接作用和反馈互动的复杂集合,进一步揭示褪黑素调控生物节律的重要作用,以期为褪黑素的基础研究以及未来探究生物体的生物钟内源性发生机制提供参考。     

Melatonin and Human Rhythms

Melatonin signals time of day and time of year in mammals by virtue of its pattern of secretion, which defines 'biological night.' It is supremely important for research on the physiology and pathology of the human biological clock. Light suppresses melatonin secretion at night using pathways involved in circadian photoreception. The melatonin rhythm (as evidenced by its profile in plasma, saliva, or its major metabolite, 6-sulphatoxymelatonin [aMT6s] in urine) is the best peripheral index of the timing of the human circadian pacemaker. Light suppression and phase-shifting of the melatonin 24 h profile enables the characterization of human circadian photoreception, and circulating concentrations of the hormone are used to investigate the general properties of the human circadian system in health and disease. Suppression of melatonin by light at night has been invoked as a possible influence on major disease risk as there is increasing evidence for its oncostatic effects. Exogenous melatonin acts as a 'chronobiotic.' Acutely, it increases sleep propensity during 'biological day.' These properties have led to successful treatments for serveal circadian rhythm disorders. Endogenous melatonin acts to reinforce the functioning of the human circadian system, probably in many ways. The future holds much promise for melatonin as a research tool and as a therapy for various conditions.     

Melatonin and Human Rhythms

Melatonin signals time of day and time of year in mammals by virtue of its pattern of secretion, which defines ‘biological night.’ It is supremely important for research on the physiology and pathology of the human biological clock. Light suppresses melatonin secretion at night using pathways involved in circadian photoreception. The melatonin rhythm (as evidenced by its profile in plasma, saliva, or its major metabolite, 6‐sulphatoxymelatonin [aMT6s] in urine) is the best peripheral index of the timing of the human circadian pacemaker. Light suppression and phase‐shifting of the melatonin 24 h profile enables the characterization of human circadian photoreception, and circulating concentrations of the hormone are used to investigate the general properties of the human circadian system in health and disease. Suppression of melatonin by light at night has been invoked as a possible influence on major disease risk as there is increasing evidence for its oncostatic effects. Exogenous melatonin acts as a ‘chronobiotic.’ Acutely, it increases sleep propensity during ‘biological day.’ These properties have led to successful treatments for serveal circadian rhythm disorders. Endogenous melatonin acts to reinforce the functioning of the human circadian system, probably in many ways. The future holds much promise for melatonin as a research tool and as a therapy for various conditions.     

Melatonin and human rhythms

Melatonin signals time of day and time of year in mammals by virtue of its pattern of secretion, which defines 'biological night.' It is supremely important for research on the physiology and pathology of the human biological clock. Light suppresses melatonin secretion at night using pathways involved in circadian photoreception. The melatonin rhythm (as evidenced by its profile in plasma, saliva, or its major metabolite, 6-sulphatoxymelatonin [aMT6s] in urine) is the best peripheral index of the timing of the human circadian pacemaker. Light suppression and phase-shifting of the melatonin 24 h profile enables the characterization of human circadian photoreception, and circulating concentrations of the hormone are used to investigate the general properties of the human circadian system in health and disease. Suppression of melatonin by light at night has been invoked as a possible influence on major disease risk as there is increasing evidence for its oncostatic effects. Exogenous melatonin acts as a 'chronobiotic.' Acutely, it increases sleep propensity during 'biological day.' These properties have led to successful treatments for serveal circadian rhythm disorders. Endogenous melatonin acts to reinforce the functioning of the human circadian system, probably in many ways. The future holds much promise for melatonin as a research tool and as a therapy for various conditions.