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Natural Rhythms and Sleep Regulation Correlation

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Researchers have known that living organisms, including humans, have an internal biological clock that this predictable change in the light environment allows organisms helps them predict and adapt their activity-rest rhythms and physiology to specific times of the day-night cycle.

Despite the fact the circadian system of the organism acts independently of external cues, but as mentioned environmental conditions, such as light, temperature, and food, reset the body clock through multiple pathways. Environmental temperature cycles reset the body clock through cellular heat shock signaling and humoral/neural pathways. Food availability is also a potent time giver and entrains peripheral clocks through nutrient-sensing and hormonal pathways. The superchiasmatic nucleus (SCN) of the hypothalamus of the brain is synchronized by light/dark cycles and arranges and by peripheral clocks. The circadian clock in the SCN is governed to external cues, and it coordinates the peripheral clock by sending signals to peripheral tissues such as liver, skeletal muscle, adipose tissue, and pancreas, through hormones and neurotransmitters.

Three basic processes underlie sleep regulation: first biological mechanisms control is a homeostatic process mediating the rise of sleep tendency during waking and its dissipation during sleep; another mechanisms control is an ultradian process occurring within the sleep episode and represented by the alternation of the two basic sleep states, non-REM sleep and REM sleep. And third mechanisms control a circadian process, a clocklike mechanism that is basically independent of prior sleep and waking and determines the alternation of periods with high and low sleep propensity.

The circadian clock drives many outputs, which include the sleep/ wake and metabolic cycles as well as hormonal changes. Proper alignment between light, the circadian clock, and output behaviors produces a temporal order in organisms that is essential for survival. The circadian clock partitions sleep to occur at a particular time of the day-night cycle, whereas a homeostatic mechanism tracks sleep need.

Sleep and behavioral activity has a strong effect on levels of numerous hormones (e.g., melatonin, growth hormone). sleep to occur in the part of the circadian cycle, the time of minimum core body temperature and maximum melatonin concentration should occur towards the end of the sleep period [6, 7]. Core temperature usually reaches its minimum around 4:30-5:00am in the morning in human adults, and melatonin (normally completely absent during daylight hours) typically begins to be produced around 8:00-9:00pm at night and stops around 7:00-8:00am in the morning. The deepest tendency to sleepiness occurs in the middle of the night, around 2:00-3:00am, along with a shorter and shallower period of sleepiness about twelve hours later, around 2:00-3:00 in the afternoon (fig1).

Melatonin is not required for sleep in humans. For example, patients who have had their pineal gland removed for medical reasons often experience little disturbance in their sleep–wake cycle [10]. Nevertheless, several studies have examined the ability of exogenous melatonin to promote sleep in humans, often with conflicting results. The melatonin system has a well-established role in regulating the circadian clock and the rhythms the clock controls. In pre-clinical studies, melatonin has shown great promise for treatment of insomnia or circadian rhythm sleep disorder (CRSDs). However, the physicochemical and pharmacokinetic properties of melatonin have slowed realization of that potential. The development of selective melatonin agonists with improved properties has enhanced the prospects of manipulating the melatonin system to treat patients with a range of sleep disorders.

Nocturnal exposure to light has been shown to affect the expression of specific genes in the SCN known as clock genes, such as period (per). The level of per expression within cells of the SCN determines the phase of the circadian clock. Thus, exposure to bright light in the evening causes a phase delay in the circadian clock, whereas similar exposure in the late night causes a phase advance. Because the SCN clock controls pineal melatonin release, such phase shifts will be manifest as changes in the timing of melatonin secretion. Indeed, the level of circulating melatonin is one of the most reliable measures of the phase of the circadian clock in humans.

The circadian clock partitions sleep to occur at a particular time of the day-night cycle, whereas a homeostatic mechanism tracks sleep need. This homeostatic drive accumulates during periods of wakefulness and diminishes with sleep. The combination of circadian mechanism and homeostatic sleep drive determines the length of sleep. It was assumed for many years that light influences sleep only secondarily through changes in circadian photoentrainment. However, several studies have now demonstrated that light directly affects both sleep onset and homeostatic sleep drive. So the circadian clock and sleep may closely interact to allow organisms to adapt to their environments. This interaction can be used to explain why changes in the light environment, such as those associated with shift-work, shortened day lengths in winter, and transmeridian travel are associated with general changes in health including mental health issues such as seasonal affective disorder, depression, and cognitive dysfunction. The effects of light on the circadian system have been thoroughly studied, with a focus on how changes in the light environment lead to changes in circadian rhythms that, in turn, influence sleep and contribute to alterations in mood and cognitive function. Circadian genes may play an important role in the control of multiple biological processes, including DNA repair, oxidative stress, maintenance of genomic stability, cell proliferation, and apoptosis. Therefore, they may have important relevance to the carcinogenic process. Alteration of circadian disorders, cardiovascular diseases, obesity, impaired glucose tolerance, alcohol abuse, and cancer.

It has been widely observed that a molecular feedback loop exists for specific clock genes that act as positive and as well negative regulators of the biological clock. Moreover, circadian genes expression among humans is reported to be similar to that observed in rodent peripheral tissue, although tissue-specific clock genes expression patterns were also observed. The daily variations in expression of clock genes associated with different rhythmicity and maximal or minimal expression in various peripheral tissues of the human organism are the strongest for peripheral blood leukocytes, probably due to the presence of various cell populations in that tissue. However, blood leukocytes subpopulations may be useful for the investigation of human circadian rhythms as circadian genes are expressed with the peak level occurring during the habitual time of activity.

The DSM-V defines Circadian Rhythm Sleep-Wake Disorder as follows: A persistent or recurrent pattern of sleep disruption that is primarily due to an alteration of the circadian system or to a misalignment between the endogenous circadian rhythm and the sleep-wake schedule required by an individual’s physical environment or social or professional schedule. The International Classification of Diseases (ICD-10-CM, 2014) lists 6 subtypes of circadian rhythm sleep disorder: delayed sleep phase type, free-running type, advanced sleep phase type, irregular sleep-wake type, shift work type, jet lag type.

The sleep disruption leads to excessive sleepiness or insomnia, or both. The sleep disturbance causes clinically significant distress or impairment in social, occupational, and other important areas of functioning. Researchers have known that living organisms, including humans, have an internal biological clock that this predictable change in the light environment allows organisms helps them predict and adapt their activity-rest rhythms and physiology to specific times of the day-night cycle. Despite the fact the circadian system of the organism acts independently of external cues, but as mentioned environmental conditions, such as light, temperature, and food, reset the body clock through multiple pathways. Environmental temperature cycles reset the body clock through cellular heat shock signaling and humoral/neural pathways. Food availability is also a potent time giver and entrains peripheral clocks through nutrient-sensing and hormonal pathways.

The superchiasmatic nucleus (SCN) of the hypothalamus of the brain is synchronized by light/dark cycles and arranges and by peripheral clocks. The circadian clock in the SCN is governed to external cues, and it coordinates the peripheral clock by sending signals to peripheral tissues such as liver, skeletal muscle, adipose tissue, and pancreas, through hormones and neurotransmitters.

Three basic processes underlie sleep regulation: first biological mechanisms control is a homeostatic process mediating the rise of sleep tendency during waking and its dissipation during sleep; another mechanisms control is an ultradian process occurring within the sleep episode and represented by the alternation of the two basic sleep states, non-REM sleep and REM sleep. And third mechanisms control a circadian process, a clocklike mechanism that is basically independent of prior sleep and waking and determines the alternation of periods with high and low sleep propensity.

The circadian clock drives many outputs, which include the sleep/ wake and metabolic cycles as well as hormonal changes. Proper alignment between light, the circadian clock, and output behaviors produces a temporal order in organisms that is essential for survival. The circadian clock partitions sleep to occur at a particular time of the day-night cycle, whereas a homeostatic mechanism tracks sleep need.

Sleep and behavioral activity has a strong effect on levels of numerous hormones (e.g., melatonin, growth hormone). sleep to occur in the part of the circadian cycle, the time of minimum core body temperature and maximum melatonin concentration should occur towards the end of the sleep period. Core temperature usually reaches its minimum around 4:30-5:00am in the morning in human adults, and melatonin (normally completely absent during daylight hours) typically begins to be produced around 8:00-9:00pm at night and stops around 7:00-8:00am in the morning. The deepest tendency to sleepiness occurs in the middle of the night, around 2:00-3:00am, along with a shorter and shallower period of sleepiness about twelve hours later, around 2:00-3:00 in the afternoon.

Melatonin is not required for sleep in humans. For example, patients who have had their pineal gland removed for medical reasons often experience little disturbance in their sleep–wake cycle. Nevertheless, several studies have examined the ability of exogenous melatonin to promote sleep in humans, often with conflicting results. The melatonin system has a well-established role in regulating the circadian clock and the rhythms the clock controls. In pre-clinical studies, melatonin has shown great promise for treatment of insomnia or circadian rhythm sleep disorder (CRSDs). However, the physicochemical and pharmacokinetic properties of melatonin have slowed realization of that potential. The development of selective melatonin agonists with improved properties has enhanced the prospects of manipulating the melatonin system to treat patients with a range of sleep disorders.

Nocturnal exposure to light has been shown to affect the expression of specific genes in the SCN known as clock genes, such as period (per). The level of per expression within cells of the SCN determines the phase of the circadian clock. Thus, exposure to bright light in the evening causes a phase delay in the circadian clock, whereas similar exposure in the late night causes a phase advance. Because the SCN clock controls pineal melatonin release, such phase shifts will be manifest as changes in the timing of melatonin secretion. Indeed, the level of circulating melatonin is one of the most reliable measures of the phase of the circadian clock in humans.

The circadian clock partitions sleep to occur at a particular time of the day-night cycle, whereas a homeostatic mechanism tracks sleep need. This homeostatic drive accumulates during periods of wakefulness and diminishes with sleep. The combination of circadian mechanism and homeostatic sleep drive determines the length of sleep. It was assumed for many years that light influences sleep only secondarily through changes in circadian photoentrainment. However, several studies have now demonstrated that light directly affects both sleep onset and homeostatic sleep drive.

So the circadian clock and sleep may closely interact to allow organisms to adapt to their environments. This interaction can be used to explain why changes in the light environment, such as those associated with shift-work, shortened day lengths in winter, and transmeridian travel are associated with general changes in health including mental health issues such as seasonal affective disorder, depression, and cognitive dysfunction. The effects of light on the circadian system have been thoroughly studied, with a focus on how changes in the light environment lead to changes in circadian rhythms that, in turn, influence sleep and contribute to alterations in mood and cognitive function. Circadian genes may play an important role in the control of multiple biological processe, including DNA repair, oxidative stress, maintenance of genomic stability, cell proliferation, and apoptosis.

Therefore, they may have important relevance to the carcinogenic process. Alteration of circadian disorders, cardiovascular diseases, obesity, impaired glucose tolerance, alcohol abuse, and cancer. It has been widely observed that a molecular feedback loop exists for specific clock genes that act as positive and as well negative regulators of the biological clock. Moreover, circadian genes expression among humans is reported to be similar to that observed in rodent peripheral tissue, although tissue-specific clock genes expression patterns were also observed. The daily variations in expression of clock genes associated with different rhythmicity and maximal or minimal expression in various peripheral tissues of the human organism are the strongest for peripheral blood leukocytes, probably due to the presence of various cell populations in that tissue. However, blood leukocytes subpopulations may be useful for the investigation of human circadian rhythms as circadian genes are expressed with the peak level occurring during the habitual time of activity.

The DSM-V defines Circadian Rhythm Sleep-Wake Disorder as follows: A persistent or recurrent pattern of sleep disruption that is primarily due to an alteration of the circadian system or to a misalignment between the endogenous circadian rhythm and the sleep-wake schedule required by an individual’s physical environment or social or professional schedule. The International Classification of Diseases (ICD-10-CM, 2014) lists 6 subtypes of circadian rhythm sleep disorder: delayed sleep phase type, free-running type, advanced sleep phase type, irregular sleep-wake type, shift work type, jet lag type. The sleep disruption leads to excessive sleepiness or insomnia, or both. The sleep disturbance causes clinically significant distress or impairment in social, occupational, and other important areas of functioning.

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