Association Between Mobile Phone Radiation Exposure and the Secretion of Melatonin and Cortisol, Two Markers of the Circadian System: A Review.

The extremely important use of mobile phones in the world, at all ages of life, including children and adolescents, leads to significant exposure of these populations to electromagnetic waves of radiofrequency. The question, therefore, arises as to whether exposure to these radiofrequencies (RFs) could lead to deleterious effects on the body's biological systems and health. In the current article, we review the effects, in laboratory animals and humans, of exposure to RF on two hormones considered as endocrine markers: melatonin, a neurohormone produced by the pineal gland and cortisol, a glucocorticosteroid synthesized by the adrenal glands. These two hormones are also considered as markers of the circadian system. The literature search was performed using PubMed, Medline, Web of Sciences (ISI Web of Knowledge), Google Scholar, and EMF Portal. From this review on RF effects on cortisol and melatonin, it appears that scientific papers in the literature are conflicting, showing effects, no effects, or inconclusive data. This implies the need for additional research on higher numbers of subjects and with protocols perfectly controlled with follow-up studies to better determine whether the chronic effect of RF on the biological functioning and health of users exists (or not). Bioelectromagnetics. 2021;42:5-17. © 2020 Bioelectromagnetics Society.

Seven-day human biological rhythms: An expedition in search of their origin, synchronization, functional advantage, adaptive value and clinical relevance.

This fact-finding expedition explores the perspectives and knowledge of the origin and functional relevance of the 7 d domain of the biological time structure, with special reference to human beings. These biological rhythms are displayed at various levels of organization in diverse species - from the unicellular sea algae of Acetabularia and Goniaulax to plants, insects, fish, birds and mammals, including man - under natural as well as artificial, i.e. constant, environmental conditions. Nonetheless, very little is known about their derivation, functional advantage, adaptive value, synchronization and potential clinical relevance. About 7 d cosmic cycles are seemingly too weak, and the 6 d work/1 d rest week commanded from G-d through the Laws of Mosses to the Hebrews is too recent an event to be the origin in humans. Moreover, human and insect studies conducted under controlled constant conditions devoid of environmental, social and other time cues report the persistence of 7 d rhythms, but with a slightly different (free-running) period (τ), indicating their source is endogenous. Yet, a series of human and laboratory rodent studies reveal certain mainly non-cyclic exogenous events can trigger 7 d rhythm-like phenomena. However, it is unknown whether such triggers unmask, amplify and/or synchronize previous non-overtly expressed oscillations. Circadian (~24 h), circa-monthly (~30 d) and circannual (~1 y) rhythms are viewed as genetically based features of life forms that during evolution conferred significant functional advantage to individual organisms and survival value to species. No such advantages are apparent for endogenous 7 d rhythms, raising several questions: What is the significance of the 7 d activity/rest cycle, i.e. week, storied in the Book of Genesis and adopted by the Hebrews and thereafter the residents of nearby Mediterranean countries and ultimately the world? Why do humans require 1 d off per 7 d span? Do 7 d rhythms bestow functional advantage to organisms? Is the magic ascribed to the number 7 of relevance? We hypothesize the 7 d time structure of human beings is endogenous in origin - a hypothesis that is affirmed by a wide array of evidence - and synchronized by sociocultural factors linked to the Saturday (Hebrews) or Sunday (Christian) holy day of rest. We also hypothesize they are representative, at least in part, of the biological requirement for rest and repair 1 d each 7 d, just as the circadian time structure is representative, in part, of the biological need for rest and repair each 24 h.

[Internal clock desynchronization and public health consequences]. / Désynchronisation de l'horloge interne : des conséquences en santé publique.

Internal clock desynchronization and public health consequences. The internal clock which is located in the suprachiasmatic nuclei of the hypothalamus is controled by genetic factors (clock genes) and environmental factors (light-dark and sleepwake alternations). Light is the major component of the clock control. Clock desynchronization occurs when the clock is no longer in phase with the environment resulting in a phase shift (phase advance or phase delay) which can produce fatigue, sleep and mood disorders. Chronic exposure to light at night results in a clock desynchronization with concomitant health issues. This paper reports on the effects of the chronic desynchronization experienced by shiftworkers and nightworkers (which is a public health issue) and also by a large number of children and adolescents who sleep for 7-8 h instead of 9-10 h per night in relation with their use at night of electronic media. This sleep debt can lead to fatigue, behavioral problems and poor academic achievement.

Désynchronisation de l'horloge interne : des conséquences en santé publique. L'horloge interne, localisée dans les noyaux suprachiasmatiques de l'hypothalamus, est sous le contrôle de facteurs génétiques (les gènes d'horloge) et de facteurs environnementaux (les alternances de lumière-obscurité et de veille-sommeil). La lumière est l'élément déterminant du fonctionnement et de la régulation de l'horloge. L'horloge est désynchronisée lorsqu'il n'y a plus de relations de phase entre l'heure biologique (l'horloge) et l'heure astronomique (la montre). On observe alors un déplacement (en avance ou en retard) de la phase des rythmes circadiens conduisant à des troubles du sommeil, de l'humeur, et à de la fatigue, etc. L'exposition chronique à la lumière la nuit entraîne une désynchronisation avec les troubles décrits ci-dessus. Cet article rapporte, d'une part, les effets de la désynchronisation chronique des travailleurs postés et de nuit (une véritable question de santé publique) et, d'autre part, le nombre croissant d'enfants et adolescents qui dorment 7-8 heures par nuit au lieu des 9-10 heures en raison de l'utilisation abusive, tard le soir, de médias électroniques. Cette dette de sommeil entraîne fatigue, troubles comportementaux, mauvais résultats scolaires.

[Internal clock desynchronization, light and melatonin]. / Désynchronisation de l'horloge interne, lumière et mélatonine.

The internal clock is synchronized by environmental factors. In humans the main factors are the light-dark alternation, the sleep-wake cycle, and social life. Rhythm desynchronization occurs when the clock is no longer in phase (harmony) with the environment, resulting in a phase shift (phase advance or phase delay) which can produce fatigue, sleep disorders and mood disorders. Clock desynchronization is related to a a loss of adaptation between the clock and synchronizers, to an inability of the clock to be entrained, or to a dysfunction of the clock itself Shiftwork and nightwork, transmeridian flights, depressive states and other psychiatric disorders, as well as blindness, aging and intake in some medications and psychoactive agents like alcohol are among the numerous causes of rhythm desynchronization. Melatonin and light exposure are able to control and resynchronize the clock. The phase response curve (PRC) clearly demonstrates that light exposure and/or melatonin administration are able to shift (advance or delay, depending on their timing) and thereby reset the clock.

Sleep and rhythm consequences of a genetically induced loss of serotonin.

BACKGROUND: A genetic deficiency in sepiapterin reductase leads to a combined deficit of serotonin and dopamine. The motor phenotype is characterized by a dopa-responsive fluctuating generalized dystonia-parkinsonism. The non-motor symptoms are poorly recognized. In particular, the effects of brain serotonin deficiency on sleep have not been thoroughly studied. OBJECTIVE: We examine the sleep, sleep-wake rhythms, CSF neurotransmitters, and melatonin profile in a patient with sepiapterin reductase deficiency. PATIENT: The patient was a 28-year-old man with fluctuating generalized dystonia-parkinsonism caused by sepiapterin reductase deficiency. METHODS: A sleep interview, wrist actigraphy, sleep log over 14 days, 48-h continuous sleep and core temperature monitoring, and measurement of CSF neurotransmitters and circadian serum melatonin and cortisol levels before and after treatment with 5-hydroxytryptophan (the precursor of serotonin) and levodopa were performed. RESULTS: Before treatment, the patient had mild hypersomnia with long sleep time (704 min), ultradian sleep-wake rhythm (sleep occurred every 11.8 +/- 5.3 h), organic hyperphagia, attentionlexecutive dysfunction, and no depression. The serotonin metabolism in the CSF was reduced, and the serum melatonin profile was flat, while cortisol and core temperature profiles were normal. Supplementation with 5-hydroxytryptophan, but not with levodopa, normalized serotonin metabolism in the CSF, reduced sleep time to 540 min, normalized the eating disorder and the melatonin profile, restored a circadian sleep-wake rhythm (sleep occurred every 24 +/- 1.7 h, P < 0.0001), and improved cognition. CONCLUSION: In this unique genetic paradigm, the melatonin deficiency (caused by a lack of its substrate, serotonin) may cause the ultradian sleep-wake rhythm.

Twenty-four-hour profiles of urinary excretion of calcium, magnesium, phosphorus, urea, and creatinine in healthy prepubertal boys.

OBJECTIVES: Available data on 24-h urinary solute excretion in healthy children are sparse. We thus documented the daily and overnight variations of urinary electrolytes (calcium, magnesium, and phosphorus), urea, and creatinine in prepubertal (Tanner stage I) boys. DESIGN AND METHODS: Nine voluntary healthy prepubertal boys aged 10.8+/-0.11 years participated in this study. Concentrations of variables were quantified in daytime samples (collected between 07:00 h+/-30 min and 21:00 h+/-30 min) and nighttime samples (collected between 21:00 h+/-30 min and 07:00 h+/-30 min) in spring, during a period of 24-h every 3 h. RESULTS: Significant differences were found between daytime and nighttime excretion of calcium (p<0.05), magnesium (p<0.001), phosphorus (p<0.01), and urea (p<0.05), with high concentrations during the night. The 24-h solute/creatinine ratio was 0.072+/-0.008 mg/mg for calcium, 0.069+/-0.008 mg/mg for magnesium, 0.698+/-0.070 mg/mg for phosphorus, and 0.017+/-0.001 g/mg for urea. Statistically significant correlation analyses showed that urea and creatinine were positively associated with body mass index (BMI) (R=0.790, p=0.0113 for urea; R=0.889, p=<0.0013 for creatinine) and weight (R=0.717, p=0.0297 for urea; R=0.978, p=<0.001 for creatinine). The other urinary variables were independent of BMI and body mass. CONCLUSION: These data are of interest for the diagnosis of certain renal disease in prepubertal children.

Promoting adjustment of the sleep-wake cycle by chronobiotics.

Chronobiotics are substances that adjust the timing of internal biological rhythms. Many classes of drugs have been claimed to possess such properties and arouse growing interest as the circumstances for their use in sleep disturbances caused by circadian rhythms alterations (delayed or advanced sleep-phase syndromes, non-24-h sleep-wake disorders, jet lag, shift work sleep disorders and so on) have become progressively more frequent. Amongst the substances potentially presenting chronobiotic properties, a consensus seems to be reached on the possible use of melatonin or its agonists to shift the phase of the human circadian clock, but optimizing the dose, formulation and especially the time of administration require further studies.