Luteinizing hormone following light exposure in healthy young men (original) (raw)
The Journal of Clinical Endocrinology & Metabolism, 2012
Melatonin is involved in a variety of diseases, including cancer, insomnia, depression, dementia, hypertension, and diabetes; its secretion is influenced by environmental light. Although daylight exposure increases nocturnal melatonin secretion in a controlled laboratory setting, whether it increases nocturnal melatonin secretion in an uncontrolled daily life setting remains unclear. Objective: We aimed to determine the association between daylight exposure in an uncontrolled daily life setting and urinary 6-sulfatoxymelatonin excretion. A cross-sectional study was conducted in 192 elderly individuals (mean age, 69.9 yr). We measured ambulatory daylight exposure using a wrist light meter in two 48-h sessions; furthermore, we measured overnight urinary 6-sulfatoxymelatonin excretion, an index of melatonin secretion, on the second night of each session. The median duration of daylight exposure of at least 1000 lux was 72 min (interquartile range, 37-124). Univariate linear regression analysis showed marginal to significant associations between log-transformed urinary 6-sulfatoxymelatonin excretion and age, current smoking status, benzodiazepine use, day length, log-transformed duration of daylight exposure of at least 1000 lux, and daytime physical activity. In a multivariate model, log-transformed duration of daylight exposure of at least 1000 lux was significantly associated with log-transformed urinary 6-sulfatoxymelatonin excretion (regression coefficient, 0.101; 95% confidence interval, 0.003-0.199; P ϭ 0.043). Furthermore, an increase in the duration of daylight exposure of at least 1000 lux from 37 to 124 min (25th to 75th percentiles) was associated with a 13.0% increase in urinary 6-sulfatoxymelatonin excretion (6.8 to 7.7 g). Conclusions: Daylight exposure in an uncontrolled daily life setting is positively associated with urinary 6-sulfatoxymelatonin excretion in the elderly. (J Clin Endocrinol Metab 97: 0000 -0000, 2012) M elatonin, a pineal gland hormone secreted predom- inantly at night, is involved in not only regulation of circadian rhythm but also prevention of a variety of diseases, including cancer, insomnia, depression, dementia, hypertension, and diabetes (1-11). Increased endogenous melatonin secretion might be associated with lower
Medical Hypotheses, 2004
The hypothesis that the suppression of melatonin (MLT) by exposure to light at night (LAN) may be one reason for the higher rates of breast and colorectal cancers in the developed world deserves more attention. The literature supports raising this subject for awareness as a growing public health issue. Evidence now exists that indirectly links exposures to LAN to human breast and colorectal cancers in shift workers. The hypothesis begs an even larger question: has medical science overlooked the suppression of MLT by LAN as a contributor to the overall incidence of cancer? The indirect linkage of breast cancer to LAN is further supported by laboratory rat experiments by David E. Blask and colleagues. Experiments involved the implanting of human MCF-7 breast cancer cell xenografts into the groins of rats and measurements were made of cancer cell growth rates, the uptake of Linoleic Acid (LA), and MLT levels. One group of implanted rats were placed in light-dark (12L: 12D) and a second group in light-light (12L:12L) environments. Constant light suppressed MLT, increased cancer cell growth rates, and increased LA uptake into cancer cells. The opposite was seen in the light-dark group. The proposed mechanism is the suppression of nocturnal MLT by exposure to LAN and subsequent lack of protection by MLT on cancer cell receptor sites which allows the uptake of LA which in turn enhances the growth of cancer cells. MLT is a protective, oncostatic hormone and strong antioxidant having evolved in all plants and animals over the millennia. In vertebrates, MLT is normally produced by the pineal gland during the early morning hours of darkness, even in nocturnal animals, and is suppressed by exposure to LAN. Daily entrainment of the human circadian clock is important for good human health. These studies suggest that the proper use and color of indoor and outdoor lighting is important to the health of both
Neuroscience Letters, 1997
Effects of bright light exposure at midday were examined on plasma melatonin rhythm in humans under controlled living conditions. Bright light of 5000 lx was provided from the ceiling at midday (1100-1700 h) for 3 consecutive days and the circadian rhythm in plasma melatonin was determined from the fourth to fifth day. The control study was performed in the same subjects who spend four days under dim light conditions (less than 200 lx). The subjects were allowed to sleep from 2400 to 0800 h. The onset phase, but not the end phase, of plasma melatonin rhythm was significantly phase-advanced by bright light exposure. Furthermore, the area under the curve of nocturnal melatonin rise was significantly larger under bright light exposure than under dim light. These findings indicate that midday exposure to bright light for 3 consecutive days changes the circadian organization of plasma melatonin rhythm in humans.
European Journal of Endocrinology, 1994
Lemmer B, Brühl T, Witte K, Pflug B, Köhler W, Touitou Y. Effects of bright light on circadian patterns of cyclic adenosine monophosphate, melatonin and cortisol in healthy subjects. Eur J Endocrinol 1994; 130:472–7. ISSN 0804–4643 Bright light is known as a strong zeitgeber on human circadian rhythms and influences several endocrine and neuroendocrine functions. In the present study we examined the influence of a 3-h bright light stimulus, given at different times during the day (morning or evening), on circadian patterns of cyclic adenosine monophosphate (cAMP), melatonin and cortisol. Two groups of synchronized healthy volunteers (lights on: 05.00–23.00 h) were exposed to bright light (2500 lux) for 3 h over 6 days either in the morning (05.00–08.00 h) or in the evening (18.00–21.00 h). The results showed a significant phase advance in the circadian rhythms of melatonin and cortisol when bright light was given in the morning but not when given in the evening. Rhythm in plasma cAM...
Biomedical Journal, 2016
Background: Continuous light or darkness has various effects on different systems. In the present research work, the effects of constant light and darkness exposure of male rats and oral administration of exogenous melatonin on the serum levels of melatonin have been studied. Methods: Thirty adult male Wistar rats were divided into six groups of: (1) Control, (2) melatonin, (3) light, (4) light and melatonin, (5) darkness, and (6) darkness and melatonin. All groups were placed according to light conditions for 10 days. Melatonin was administered orally after a period of 10 days to Groups 2, 4, and 6 (10 mg/kg of body weight). Serum levels of melatonin were measured using ELISA. Results: The results showed the significant difference on serum melatonin in darkness, no light, and control groups. Although serum levels of melatonin were different in melatonin groups, the difference is not significant. Conclusions: We concluded that being exposed to continuous darkness leads to an increase in serum melatonin.
Melatonin effects on luteinizing hormone in postmenopausal women: a pilot clinical trial NCT00288262
BMC women's health, 2006
In many mammals, the duration of the nocturnal melatonin elevation regulates seasonal changes in reproductive hormones such as luteinizing hormone (LH). Melatonin's effects on human reproductive endocrinology are uncertain. It is thought that the same hypothalamic pulse generator may both trigger the pulsatile release of GnRH and LH and also cause hot flashes. Thus, if melatonin suppressed this pulse generator in postmenopausal women, it might moderate hot flashes. This clinical trial tested the hypothesis that melatonin could suppress LH and relieve hot flashes. Twenty postmenopausal women troubled by hot flashes underwent one week of baseline observation followed by 4 weeks of a randomized controlled trial of melatonin or matched placebo. The three randomized treatments were melatonin 0.5 mg 2.5-3 hours before bedtime, melatonin 0.5 mg upon morning awakening, or placebo capsules. Twelve of the women were admitted to the GCRC at baseline and at the end of randomized treatment f...
Journal of Molecular Neuroscience, 1999
The role of melatonin in the regulation of human reproduction remains unclear. In the present study, we examined the influence of exogenous melatonin on pulsatile luteinizing hormone (LH), diurnal rhythm of testosterone, and endogenous melatonin profile in six healthy young adult males. To test the hypothesis that the effect of melatonin on LH or testosterone secretory patterns may be mediated through the benzodiazepine-(BNZ) γ-amino-butyric acid (GABA) receptor complex, a benzodiazepine receptor antagonist (Flumazenil) was administered. The study design comprised four 10-h (4:00 PM-2:00 AM) testing periods. During each experimental period, subjects were given an oral dose of placebo, or 3 mg melatonin or 10 mg flumazenil, at 5:00 PM, in a randomized, double-blind, partially repeated Latin square design in the following combinations: placebo-placebo, placebo-melatonin, flumazenil-placebo, and flumazenil-melatonin. The following day, serum samples were obtained every 20 min between 4:00 PM and 2:00 AM in a controlled light-dark environment for the determination of LH and melatonin levels. Serum testosterone concentrations were determined every 20 min between 7:00 and 8:00 AM and 7:00 and 8:00 PM. A significant decrease in mean serum LH levels (p < 0.02) was observed in the melatonin-treated groups as compared with placebo-flumazenil groups. There was no change in LH pulse frequency, testosterone levels, or in melatonin onset time and amplitude. No additional effect of flumazenil on LH or testosterone levels was observed.
Nocturnal melatonin secretion is not suppressed by light exposure behind the knee in humans
Neuroscience Letters, 1999
Ocular light exposure can phase shift circadian rhythms and suppress nocturnal melatonin production. A recent ®nding suggests that extraocular light can also produce phase shifts in humans. We investigated whether extraocular light could also suppress melatonin secretion in humans. We assayed the salivary melatonin of 16 subjects during a baseline night and an experimental night in dim light (10±20 lux). The experimental night included either: (1) 3-h ocular light exposure (1000 lux, n 6); (2) 3-h extraocular light exposure behind the knee (13 000 lux, n 7) or (3) constant dim light exposure (10±20 lux, n 3). Melatonin suppression occurred with ocular light but not with extraocular light or constant dim light. q
Scientific Reports, 2019
We studied the dynamics of melatonin suppression and changes in cortisol levels in humans in response to light exposure at night using high-frequency blood sampling. twenty-one young healthy participants were randomized to receive either intermittent bright (~9,500 lux) light (IBL), continuous bright light (CBL) or continuous dim (~1 lux) light (VDL) for 6.5 h during the biological night (n = 7 per condition). Melatonin suppression occurred rapidly within the first 5 min and continued until the end of each IBL stimuli (t 1/2 = ~13 min). Melatonin recovery occurred more slowly between IBL stimuli (half-maximal recovery rate of ~46 min). Mean melatonin suppression (~40%) and recovery (~50%) were similar across IBL stimuli. Suppression dynamics under CBL were also rapid (t 1/2 = ~18 min), with no recovery until the light exposure ended. There was a significant linear increase of cortisol levels between the start and end of each IBL stimulus. Under CBL conditions cortisol showed trimodal changes with an initial linear activating phase, followed by an exponential inhibitory phase, and a final exponential recovery phase. These results show that light exposure at night affects circadian driven hormones differently and that outcomes are influenced by the duration and pattern of light exposure. Melatonin secretion is acutely suppressed by light exposure at night 1,2. While the intensity 3,4 , duration 5 and spectral sensitivity 4,6-8 of this response is well characterized in humans, the precise temporal dynamics of this response has not been studied in detail. Findings from studies of several animal models suggest that this response is rapid (t 1/2 ~2-10 min) 9-14 , which is consistent with the rapid attenuation of enzymatic activity in the melatonin biosynthetic pathway 10,15. The onset of melatonin suppression and the onset of melatonin recovery begin within ~5-15 min of the start and end of the light pulse, respectively. Recovery to baseline levels can be up to several hours in both humans and rats 11,16,17. The suppression and recovery intervals in rats are accurate because high-frequency (every 15 min) microdialysis based sampling was used to measure melatonin in the extracellular space of the pineal gland 11. In humans, however, the recovery-interval estimation of several hours may be less accurate since low-frequency sampling (hourly) was used after the light pulse ended 17. Unlike birds and reptiles 18-20 , the mammalian pineal gland is not directly light sensitive. Instead, a multisynaptic retinal-hypothalamic-pineal pathway carries photic signals from the eye to the suprachiasmatic nucleus (SCN), and to the pineal gland via the paraventricular nucleus of the hypothalamus, intermediolateral nucleus of the spinal cord and the superior cervical ganglion 21. SCN lesion or transection of the multisynaptic pathway abolishes light-induced suppression of melatonin 22,23. Another multisynaptic pathway has been identified leading from the SCN to the adrenal cortex 24. Similar to melatonin, the circadian rhythm of glucocorticoids is also regulated by the SCN 25,26. Light exposure in mice increases corticosterone levels via this sympathetic pathway without activating the hypothalamic-pituitary-adrenal axis 27. The effects of light exposure on cortisol levels in humans are less clear, however. When humans were kept on a 3-h day, with 1 h of sleep in the dark and 2 h of wakefulness in the light in each 3-h interval, mean cortisol secretion was highest during the first hour of waking following
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.