What is biorhythm therapy?

Biological rhythms are the natural cycle of change in chemicals or functions in our body. It's like an internal master clock that coordinates the other.

What is biorhythm therapy?

Biological rhythms are the natural cycle of change in chemicals or functions in our body. It's like an internal master clock that coordinates the other. Effects · Treatment · Self-care · How it works Treatments for biological rhythm disorders vary and depend on the underlying cause. For example, jet lag symptoms are usually temporary and do not require medical treatment.

In cases of shift work disorder or mood disorders, changes in style. Talk to your doctor about more serious symptoms, such as fatigue, decreased mental acuity, or depression. Your doctor will be able to prescribe the right treatment and give you lifestyle suggestions. When lifestyle treatments and good sleep hygiene don't work, your doctor may prescribe medication.

Modafinil (Provigil) is for people who have difficulty with daytime wakefulness. For night shifts, it takes three to four nights for the body to adapt. Try to schedule your shifts in a row, if possible. This will reduce the amount of time to “train” your body for night shifts.

But working more than four 12-hour night shifts in a row can have harmful effects, according to the Cleveland Clinic. Learn about new approaches to treatment and read stories of people living with this condition in the best books on depression. What are biological rhythms? In essence, they are the rhythms of life. All forms of life on earth, including our bodies, respond rhythmically to the regular cycles of the sun, moon and seasons.

Hypertension or high blood pressure is a silent killer. Early high blood pressure causes no symptoms or discomfort. However, long-term high blood pressure without treatment can lead to strokes, heart disease, kidney disease, and eye damage. Medical scientists now know that a person's blood pressure varies according to the time of day (circadian rhythm).

Such variations may have important implications for the diagnosis, treatment and monitoring of patients with high blood pressure. The vasoconstrictive effects of catecholamines can also be improved in the morning due to the high levels of certain hormones that interact with catecholamines and increase their effects. Many medications for high blood pressure are designed to counteract the vasoconstrictive effects of these hormones. Most processes in the human body, such as brain function, are regulated by biological rhythms.

Altered biological rhythms affect mood, behavior, cognition, sleep and social activity and can lead to mental disorders. Altered rhythms are widely observable in patients with major depressive disorders (MDD) and pose risk of onset, comorbidity, antidepressant response, recurrence, cognition, social function, and physical health complications. Therefore, it is crucial to evaluate and manage the focus on biological rhythms for patients with MDD. There are several validated ways to assess biological rhythms, including 24-hour fluctuations in cortisol or melatonin, sleep monitoring, actigraphy, and self-report scales.

Chronotherapy, such as cognitive-behavioral therapy, interpersonal and social rhythm therapy, sleep deprivation, and bright light therapy, was widely reported for treatment in MDD patients. Monoamine antidepressants and lithium are attributed to the regulation of biological rhythm. And some rhythm-regulated agents have shown the effectiveness of antidepressants. Taking into account the crucial clinical importance of altered biological rhythms in MDD, we describe the mechanisms, clinical characteristics, measurements and treatments of biological rhythms in patients with MDD.

Try PMC Labs and let us know what you think. Studies show that alterations in the reciprocal relationship between molecular clocks and other neurotransmitter systems can cause alterations in brain functions and behaviors. For example, animals with the mutated Clock gene exhibit mania-like behaviors that can be rescued by expressing a functional Clock protein in the ventral tegmental área rich in dopamine-VTA (Royball et al. Alterations in neuropeptide Y receptors produce anxiety-like phenotypes (Karl et al., 200), while exposure to stress alters vasoactive intestinal peptide (VIP) mRNA expression and disrupts circadian rhythms (Handa et al.

Mutant mice lacking the Npas2 clock analog show deficits in learning pointed and contextual fear paradigms, suggesting that Npas2 plays a role in the acquisition of specific types of memory (Garcia et al. These examples illustrate that the SCN-mediated outputs of the circadian clock and the gene-mediated interaction of the clock with neurotransmitters and other neural processes are complex and likely play an important role in regulating a wide range of behaviors including sleep, emotion, motivation, alertness and cognition. We combine a critical evaluation of the literature with discussions of five main topics that focus on research questions and novel findings relevant to (the impact of molecular clocks on physiology and behavior; (interactions between circadian signals and cognitive functions); (the interface of rhythms circadians) with sleep and their relevance to normal and abnormal behaviors; (a clinical perspective on the relationship between circadian rhythm abnormalities and affective disorders, and (animal models of circadian rhythm abnormalities and mood disorders. We also discuss opportunities, gaps and challenges in the study of the association between altered circadian rhythms and psychiatric disorders and strategies for implementing the knowledge extracted from basic science studies in the clinical setting and vice versa.

A complex relationship has been identified between the symptoms of psychiatric illnesses, sleep and circadian rhythm dysfunction. Traditionally, sleep disruption has been considered a symptom of several psychiatric disorders, including bipolar disorder, schizophrenia, major depression, SAD, as well as mood, anxiety and substance use disorders (Benca, 199.However, it is still possible that sleep disorder reflects a biological impairment clock function that causes the development and maintenance of psychiatric disorders in susceptible individuals (Mansour et al. It is essential to analyze the effects of clock genes on circadian organization and sleep disruption and to understand their individual and synergistic contributions to mental disorders. In addition, many people at risk for mental disorders live in environments that have altered circadian rhythms, including irregular sleep schedules, meal times, or other temporary restrictions (Colten and Altevogt, 200.

The SNA functions like the primary central circadian oscillators in mammals (Stephan and Zucker, 1972; Moore and Eichler, 197.The CNS output is capable of producing sustained and synchronous cell rhythmicity in both central and peripheral tissues, resulting in the temporal organization of behavioral rhythms throughout the body (Liu et al. Circadian dysfunction associated with psychiatric diseases probably represents the decoupling of autonomic oscillators in the CNS or interruptions in the output of the SNS to other parts of the brain (Yang et al. Despite some promising early signs, sensitive sleep biomarkers specific to psychiatric disorders have not been validated (Yang et al. Although it is difficult to observe cellular circadian dysfunction in neurons, a simple system may be needed to untangle the complex interactions between CNS, sleep, and mood.

Fibroblasts are relatively easy to obtain and evaluate; therefore, examination of the effects of genetic alterations at the individual cell level could be linked to behavioral changes to reveal how intercellular coupling mechanisms are important for proper circadian clock gene function and solid (Welsh et al. Because intercellular coupling of circadian oscillators can compensate for genetic deficiencies in individual clock components, a greater understanding of coupling regulation could provide a novel insight into mechanisms for increasing resistance to a variety of genetic alterations that can disrupt behavior. In one study, fibroblasts from bipolar patients and healthy individuals were examined for rhythmic expression patterns of central clock genes, as well as mRNA expression levels of four kinases associated with clock function (Yang et al. Their results suggest that reduced amplitudes and levels of general expression of some circadian genes, and the decrease in the level of GSK3β phosphorylation, may lead to dysregulation of subsequent genes, which could explain some pathological features of bipolar disorder.

Therefore, the existence of rhythms in cultured fibroblasts and other tissues suggests their translational potential as peripheral markers of alterations in circadian rhythms in psychiatric disorders. Taken together, these and other molecular approaches combined with the further development of model systems are needed to identify novel mechanisms that could explain how circadian rhythms control behaviors under both normal and pathological conditions, and untangle the contributions of circadian processes treatment of psychiatric and sleep disorders. What are the mechanisms by which the circadian time system regulates cognition, memory and mood? A variety of neuroanatomical, neurophysiological, molecular and neurochemical mechanisms have been revealed. The neuroanatomical circuit that mediates the circadian regulation of excitation is a multi-synaptic pathway between the CNS and LC noradrenergic neurons (Aston-Jones et al.

The behavioral state of arousal and wakefulness is induced by stimulation of the frontal cortex by noradrenergic neurotransmission arising from LC (Aston-Jones and Bloom, 1981; González and Aston-Jones, 200. Decreases in noradrenergic activity, as well as serotonergic activity, are associated with depression. In rats, prolonged light deprivation leads to loss of noradrenergic fibers in the frontal cortex, decreased amplitude of sleep-wake rhythms, and delayed onset of activity periods (Gonzalez and Aston-Jones, 200. In addition, long-term light deprivation induces apoptosis of LC noradrenergic neurons and increases immobility in the forced swimming test, an indicator of a depressive-like condition; treatment with the antidepressant, desipramine, alleviates both effects (González and Aston-Jones, 200.

These profound effects of light deprivation may help explain the mechanisms underlying the improvement of depression through bright light. In addition to altering cognition and its neural substrates, exposure to the short-day photoperiod influences affective state. For example, male Siberian hamsters housed on a short-term regime exhibit elevated behaviors similar to anxiety and depression (Prendergast and Nelson, 200. These behaviors are influenced not only by acute exposure to the short-day photoperiod, but also by prenatal exposure to melatonin in the womb, suggesting that photoperiodic exposure of the mother during gestation can organize the developing brain through exposure to melatonin rhythms of the mother, which influences the later adult affective responses (Workman et al.

It is also interesting to note that short-day photoperiodic induction of anxiety- and depression-like behaviors is associated with increased serotonin transport in the midbrain, consistent with the therapeutic use of selective serotonin reuptake inhibitors (SSRIs) to combat anxiety and depression in humans. In summary, circadian rhythms and environmental photoperiod influence cognition and affective behavior through multiple mechanisms, including regulation of noradrenergic innervation of the cortex, clock gene expression in the CNS and hippocampus, density of the dendritic column, and serotonin transport. Animals that exhibit mutations of the clock gene, or animals exposed to various photoperiods, can be used as experimental models to probe the interaction of circadian signals with cognition and affective state. The application of chronobiological principles to the treatment of psychopathophysiological conditions has led to the development of new non-pharmacological therapies (eg,.

Sleep is one of the most important behaviors influenced by the circadian system, and specific changes in sleep patterns, as well as circadian rhythms, have been described in a number of neuropsychiatric disorders, most notably mood disorders. Recent work suggests that the relationship between circadian rhythms and sleep may contribute to normal and abnormal behaviors. Although circadian rhythms certainly influence the timing of sleep and wakefulness throughout the day, there are other factors that regulate sleep patterns, including environmental and developmental effects. However, perhaps the most important determinant of sleep behavior is the homeostatic drive to sleep; the longer an organism is awake, the greater the pressure to sleep.

The homeostatic process of sleep is thought to regulate the amount of sleep obtained and is likely related to sleep function; knowing why sleep is necessary for the brain is critical to understanding the relationships between sleep and circadian rhythms. Tononi and Cirelli have proposed that sleep reverses the “costs of being awake”, which accumulate from the accumulation of synaptic force in the brain through the long-term empowerment (LTP) process and include increased energy utilization, increased neuropil density, increased need for cellular supplies and saturation of the ability to learn (Tononi and Cirelli, 200. Prolonged wakefulness decreases the ability to induce more LTP in several models, which in turn should inhibit learning (Vyazovskiy et al. The relationship of LTP during wakefulness to increased production of slow waves in sleep is probably relevant for depression, as the most effective antidepressants increase the expression of plasticity-related genes (reviewed in Duman, 2002; Payne et al.

Therefore, an increase in synaptic potentiation may explain the antidepressant effects of acute sleep deprivation, and the reduction of synaptic scale by slow waves during sleep, the rapid reversal of these antidepressant effects even in short periods of recovery sleep. In addition, depression is characterized by decreases in slow-wave sleep and slow-wave activity, suggesting the possibility that abnormalities in sleep homeostasis are somehow related to depression. Possible mechanistic links between the circadian system and homeostatic sleep regulation include the Period (Per) genes, so named for their role in determining the length of the circadian rhythm period. Individuals with a variable-number polymorphism of Per3 tandem repeats show high slow-wave sleep and slow-wave activity and more severe cognitive declines in response to sleep deprivation than unaffected individuals (Viola et al.

However, circadian rhythms, to the extent that they have been evaluated, do not appear to be abnormal in these individuals. The homeostatic and circadian aspects of sleep regulation show profound changes during development, although it is not clear whether these are independent of each other or whether the developing circadian and homeostatic sleep regulatory mechanisms interact. For example, significant maturative changes in sleep patterns after birth occur in mammals, including the development of typical sleep waveforms (e.g. slow waves and sleep spindles), as well as the appearance of circadian rhythms.

Studies in rats have shown that although the delta rhythm and other typical EEG characteristics of quiet sleep (NREM) and active (REM) do not appear until postnatal day 11, the overall organization of the cycle between quiet and active sleep can be detected at least several days earlier and remains stable (Seelke and Blumberg, 200. However, the general temporal organization of sleep and wakefulness episodes changes throughout the postnatal period. Adult mammals, including rats, cats and humans, show brief wakefulness episodes during the sleep period showing a distribution of the power law, while the durations of sleep sessions are exponentially distributed (Lo et al. However, in studies of developing rats, on postnatal day 2, both sleep and wakefulness session duration are distributed in an exponential pattern, and waking session durations do not change to the adult power law distribution until about postnatal day 15 (Blumberg et al.

Although the mechanistic basis for the organization of sleep-wake patterns throughout the sleep period is unknown, the consistency of these patterns in adult mammal species suggests similarities in the underlying neural control of sleep organization, which may include both homeostatic and circadian. features. Age and brain development affect the activity of slow waves during sleep; during childhood, when the brain synaptic density is higher, slow waves show the highest slopes and the highest activity. During adolescence, slow wave activity decreases (Jenni and Carskadon, 200), possibly in relation to synaptic pruning that occurs during this period of development.

In addition, the rate of accumulation of sleep pressure, indicated by slow wave activity, is faster in children than in adolescents (Jenni et al. Hormonal influences are also important for the development of sleep cycles. Puberty may be associated with lengthening of the intrinsic period of the circadian clock (Carskadon et al. Studies in degus, a diurnal rodent, show that modulation of the circadian system in adolescence may be related to puberty, since the progressive delay in the onset of activity after lights on that normally occurs during adolescence does not occur in animals gonadectomized before puberty ( Hummer et al.

Interestingly, phase delay in adolescent humans and rodents is reversed in young adulthood. As noted above, human adolescence is also associated with a decrease in slow-wave sleep, and it is possible that changes in both homeostatic sleep processes and circadian rhythms may contribute to the tendency of adolescents to show a delayed sleep phase. Adolescence is also a time associated with sleep deprivation, even more so in industrialized societies, as a result of delayed bedtime and early start of school. People who are more likely to delay circadian rhythms in adolescence may be more likely to have sleep restrictions.

Epidemiological evidence suggests that adolescents with sleep deprivation are more likely to develop depressive symptoms (Fredriksen et al. In rodents, chronic sleep restriction results in decreased sensitivity to 5HT1A receptors, and although these experiments were performed on adult animals, they suggest that sleep loss may affect neural systems involved in mood and behavior, as well as rhythm regulation circadians (Novati et al. It is clear that there is a need for longitudinal human studies to understand the normal and abnormal patterns of seasonal and circadian rhythms in humans, including the effects of gender on these rhythms. It is also not known whether circadian and seasonal rhythms are controlled by similar mechanisms and how they might interact.

The effects of the environment on rhythm development, particularly during childhood and adolescence, is another critical area for research, as factors that contribute to abnormal development, such as exposure to light and sleep deprivation, can permanently alter the brain systems involved in behavior regulation. Finally, there are promising ways to improve the diagnosis of neuropsychiatric disorders and the identification of people at risk using new sleep technologies. For example, using a high-density EEG (256 channels), it is possible to determine the sources and travel paths of the individual slow waves. Initial analyses of slow wave origin patterns and dissemination through the cortex show local abnormalities in stroke patients (Murphy et al.

A more sophisticated topographic analysis of sleep-related waveforms may be useful in determining patients at risk for a variety of diseases. For example, more than 90% of schizophrenic subjects show a dramatic reduction in sleep spindles, suggesting dysfunction in the thalamus reticular nucleus (Ferrarelli et al. If specific “fingerprints” of sleep EEG can be determined for neuropsychiatric disorders, they can provide an opportunity to identify people at risk. Additional preclinical studies involving animal models of circadian gene dysfunction would be useful, as well as clinical studies that further explore the relationship between circadian dysfunction and disease states.

Prospective studies should examine circadian function and alteration in patients with mood disorders, early in the course of their disease and in young people at risk for bipolar disorder. Comparisons of the effects of therapeutic strategies, including mood stabilizers (eg,. Mechanistic studies are needed to elucidate the neural basis of social rhythm therapy in bipolar disorder and other therapeutic interventions with suspected effects on the circadian system, the consequences of altered circadian rhythms on mental health and the interaction between the clock gene polymorphisms and changes in emotion and cognition. It would also be important to evaluate circadian rhythms in neurotransmitter systems in patients with mood disorders and patterns of mood variation (including circadian vs.

Homeostatic components) in both unipolar and bipolar patients. Finally, model systems for studying the change in mania-depression-eutimia that occurs in bipolar disorder would facilitate studies beyond current models that only focus on steady-state conditions. In recent years, ethylnitrosourea (ENU) mutagenesis has been used in mice to discover genes involved in sleep and circadian rhythms. This technique has led to the identification of a series of mutations that produce abnormalities in circadian rhythms, sleep time and rebound.

This includes the identification of the Clock gene, which is one of the central components of the circadian machinery (King et al. Interestingly, some of these circadian and sleep mutants have abnormalities in additional neurobehavioral measures indicative of anxiety and mood-related changes. In addition, mice that have a mutation in the Clock gene spend less time in all phases of sleep and have several symptoms indicative of a metabolic disorder (Naylor et al. This includes weight gain, particularly with a high-fat diet, and changes in the expression of food-related hormones and peptides in the body.

According to these findings, simply feeding mice a high-fat diet alters the circadian period and attenuates the diurnal pattern of eating behavior (Kohsaka et al. This could be important for the development of a number of obesity-related disorders. Clock mutant mice are not the only mice that have a behavioral profile similar to that of human mania. By determining which additional genes contribute to a maniac-like phenotype, we can more specifically determine how the circadian system interacts with other systems to produce mood changes.

In addition to the dopaminergic system, the glutamatergic system has been suggested as a possible regulator of manic behavior. In fact, glutamate 6 (GluR) -deficient mice are hyperactive, have an increased response to amphetamine, have low anxiety-related behaviors, and have lower depression-like behavior (Shaltiel et al. These mice are also more aggressive than wild-type mice. Treatment with lithium was able to reduce his hyperactivity, increase anxiety and reduce his aggressive behavior.

Interestingly, however, lithium further reduced its immobility in the forced swimming test (a measure of depression-like behavior) rather than bringing mice back to wild-type levels as seen with Clock mutants. Lithium treatment had no effect on GluR5 levels in the hippocampus of GluR6-inactivated animals, suggesting that this is not the mechanism by which lithium restores normal activity and anxiety-related behavior in these mice (Shaltiel et al. It is not clear whether GluR6 is involved in the regulation of circadian rhythms, but it is interesting that GluR6 knockouts share similar phenotypes with Clock mutants. It is possible that GluR6 and Clock regulate each other in some way, or that the loss of both genes leads to common effects on neural activity.

In summary, animal models may be useful for identifying genes involved in the regulation of complex behaviors and psychiatric disorders. In addition, circadian genes appear to be involved in the regulation of mood, sleep and metabolism, perhaps through their functions outside the CNS. If these diseases are caused by altered rhythms, it would be useful to design medications that can restore these rhythms and treat the disorder. This is an exciting time in the fields of circadian and affective disorders, and there is no doubt that more promising work lies ahead.

The ability of circadian oscillators in the CNS to produce sustained and synchronous cell rhythmicity in both central and peripheral tissues and to produce efficient integration of molecular and behavioral rhythms throughout the body indicates the importance of using systems-level and integrative approaches. elucidate the neural bases underlying the role of circadian oscillators in learning and memory, attention, arousal, affect, anxiety and motivation under both normal and pathological conditions. A better understanding of the role of circadian regulation of complex behaviors may be aided by the development of biomarkers that reflect alterations in brain circadian rhythms and behaviors relevant to mental health. For example, cultured human fibroblasts derived from biopsies express sustained circadian rhythms similar to cultured SCN neurons from rodents.

Therefore, studies examining their translational potential as biomarkers may reveal mechanisms of circadian rhythm disturbances in psychiatric disorders. Simultaneous studies of circadian rhythms in fibroblasts and genetic polymorphisms related to circadian control can make it easier to compare people with bipolar disorder and people at risk for the disease. It has been hypothesized that cyclical changes in the metabolic states of cells may play a role in regulating biological rhythms and sleep. The interaction between neural metabolic cycles and circadian rhythms may be important for neural plasticity and learning and memory processes.

It would be interesting to explore whether this interaction regulates the sleep-wake cycle and the functioning of neural systems early and throughout development, especially during key transitional phases associated with marked changes in brain function and behavior. There is a pressing need for more in-depth studies that address the gaps between neural circuits and behaviors relevant to mental health. For example, it would be pertinent to clarify whether neural projections from the SCN to the LC mediate changes in the amplitude of circadian rhythms, and whether this circuit plays a role in the circadian regulation of arousal, affect, and cognitive function. Further research on this circuit is warranted to elucidate the transitional changes between focused attention and behavioral flexibility that are accommodated in a multifunctional system in the LC.

It will also be important to further explore the interaction of the SNA with other complex networks, including the hippocampus, dorsal raphe and amygdala, to determine whether circadian oscillations in these regions are necessary for the expression of circadian rhythms in the memory recall process. fear of learning and extinction, and symptoms of anxiety and depression. Studies on the interaction between CLOCK protein and VTA dopaminergic neurons provide an excellent model for studying mania-like phenotypes. Because in the VTA of CLOCK mutants, CLOCK could be involved in the regulation of locomotor activity, dopaminergic neuron activity and anxiety-like behaviors, examining the interaction of the clock network with monoaminergic neural circuits will facilitate the definition of systems underlying regulation of mood and complex behaviors.

In addition, a more systematic characterization of Clock mutants and other circadian mutants in both sexes is likely to facilitate the discovery of new behavioral phenotypes related to clock genes and uncover the role of dysfunctional clock genes in altered emotional behaviors. Further studies are needed to elucidate the role, regulatory factors, and underlying genetic and cellular mechanisms of sleep and circadian rhythms in the context of higher-order brain functions during periods of developmental transition, between species, sexes and throughout life. Novel studies demonstrating a close relationship between cortical plasticity and slow-wave sleep activity have greatly improved the understanding of the role of sleep in neural plasticity, emotion, learning and memory. Further study is needed to elucidate how developmental changes in sleep and circadian rhythms can be critical for the regulation of higher-order brain functions, including cognition, emotion, and affect.

It would also be important to better understand the role of sleep and circadian rhythms in defining critical periods in the development of these higher-order brain functions that may be more sensitive to changes in rhythms and sleep. Studies investigating how disruptions in the social spirit produce alterations in circadian rhythms that may increase vulnerability to mood disorders warrant more integrative and systems-level approaches. For example, it would be important to investigate whether the underlying mechanisms of dysfunctions in biological rhythms are related to interruptions in the clock network that synchronizes the phase relationship between sleep and higher-order brain functions. Treatments for bipolar disorder that combine drug therapy with interpersonal and social rhythm therapy demonstrate that social rhythm stabilization accelerates recovery from acute bipolar depression and delays the recurrence of manic and depressive episodes.

Understanding the neurobiological underpinnings of the effects of social spirit on mood and behavior would shed light on how stabilizing social rhythms may be relevant for people at risk for bipolar disorder and how it can improve outcomes in those who have already been diagnosed with bipolar disorder this disease. In summary, we review here several important questions, strengths and areas of gap relevant to research on the neurobiological foundations of the interaction of circadian rhythms with higher-order brain function and behavior. The review discusses promising research directions and strategies for expanding basic, translational and clinical studies on circadian rhythms to help bridge the gaps between genes, circuits and behavior. Studies that focus on the interaction between biological clocks and neural circuits that consider differences between normal and abnormal conditions, diagnostic subgroups, sex and gender, and gene-environment-development interactions are likely to facilitate the translation of basic scientific knowledge about biology watches in the clinical setting, and to improve understanding of how alterations in this relationship contribute to psychiatric disorders.

Beth-Anne Sieber (NINDS) for their interesting discussions on the manuscript, and Ms. Laura Fonken (Ohio State University) and Ms. April Harrison (NIMH) for their technical assistance. National Center for Biotechnology Information, USA.

UU. National Library of Medicine 8600 Rockville Pike, Bethesda MD, 20894, USA. Treatments for medical conditions that are administered with respect to natural biological cycles regulated by the body clock. It has been considered that when the same dose of a drug is administered to a given living organism, the drug will always exert the same action on the organism and give rise to the same response, regardless of the time of administration.

However, this understanding may be too simple, since the living organism itself continuously displays various types of circadian rhythm (biological rhythm that has a period of about 24 hours). It can be assumed that the body's response to a drug may also fluctuate concomitantly with these biological fluctuations. Many drugs have been examined on the basis of this assumption. As a result, it has been shown that there is a circadian fluctuation in the effects of many drugs, depending on the time of drug administration (TODA).

As far as psychotropic drugs are concerned, studies have just been initiated on the above-mentioned subject. Clarification of this topic may lead to a better understanding of the mechanism of action of these drugs and of the function of the brain. In addition, it can also provoke the development of a new method of treatment, including the determination of single daily doses of drugs in clinical practice. This article deals with circadian fluctuation in the effect of psychotropic drugs or on the susceptibility of the living organism to these drugs.

Biorhythms are based on the idea that cycles, which can be calculated and graphed, can be used to make predictions about your life. Without them, biorhythms became another pseudoscientific statement that people are willing to accept without the required evidence. The practice of consulting biorhythms was popularized in the 1970s by a series of books by Bernard Gittelson, including Biorhythm A Personal Science, Biorhythm Charts of the Famous and Infamous, and Biorhythm Sports Forecasting. Another type of pseudoscience, called biorhythms, originated in the 19th century and became popular in the 60s, 70s and 80s.

In the 1960s, 70s and 80s, many people accepted the idea; however, most scientific research has found that predictions made with biorhythms were equivalent to random, so its validity decreased. Those who push biorhythm calculators and books to a gullible audience are guilty of making fraudulent claims. Both the theoretical basis and the practical scientific verification of the theory of biorhythm are lacking. In the early 1900s, a professor named Hermann Swoboda claimed to have created cycles of biorhythms independently.

A 1978 study on the incidence of industrial accidents found no empirical or theoretical support for the biorhythm model. Biorhythms are considered a pseudoscience, meaning they don't have the same scrutiny and objective research compared to the other sciences. Articles on biorhythms are found in scientific journals, but most studies (99 out of 13) indicate that biorhythms are not valid and that they are not better at predicting than chance. Skeptical evaluations of the various biorhythm proposals led to a series of criticisms that criticized the issue published in the 1970s and 1980s.

Biorhythm programs were a common application on personal computers; and in the late 1970s, there were also portable biorhythm calculators on the market, Kosmos 1 and Casio Biolator. According to the theory of biorhythms, a person's life is influenced by rhythmic biological cycles that affect his ability in various domains, such as mental, physical and emotional activity. There are biorhythms and remedies for falling asleep, at least for people with marginal sleep problems, such as mild insomnia. .

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Floyd Bellafiore
Floyd Bellafiore

Award-winning music advocate. Devoted travel junkie. Certified social media evangelist. Award-winning web buff. Hardcore internet fanatic. Incurable zombie specialist.

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