Hormons effect on sleep

Stages of sleep: is divided into non-REM sleep and REM sleep (rapid eyes movements). There are 3 phases of the non-REM sleep (NREM) sleep process and another of REM sleep.

-Non REM phase:

It is the first state of sleeping in which we enter and for most adults it will be the place that occupies 75% of the totality of your sleep.

The No Rem stage is divided into 3 phases, in which the characteristics of the sleep are modeled, these are the following:

Non-REM stage – Phase I

It is the stage where we feel drowsy or we are asleep. The waking state is disappearing since the Alpha rhythm also does it. At the moment muscle tone does not relax completely. The Beta waves disappear.

Non-REM stage – Phase II

It is the stage where although we are asleep, the dream is light, the Alpha rhythm disappears more and more, muscle tone continues to exist. We experience the entrance to the theta waves little by little.

Stage No REM – Phase III

This is the stage of deep sleep, the encephalographic rhythm is very low, muscle tone is maintained or may be greatly diminished. Delta waves appear in our brain. It is also called slow wave sleep and is the one that predominates during the first third of the night and represents between 15 and 25% of total sleep in young people, in older adults, particularly men, there can be a total absence of slow wave sleep.

Dreams are more common at this stage than at other stages of NREM sleep, although only fragments are remembered, or nothing at all.
Actually these stages differ in that the muscular atony is gradually increased and brain waves are gradually changing depending on the relaxation of the body.

-REM phase:

This is the paradoxical dream phase, since during this phase the brain has an activity that resembles that which occurs when we are awake. Also during this phase rapid eye movements are seen. The body is in atony.

What we dream about occurs during this phase. Currently, there is no clear theory of why ocular movement occurs during the REM phase.

After going through these stages, for about 70 to 120 minutes, the first REM (Rapid Eye Movement) phase usually occurs. The time it takes to start this phase will give us REM latency. REM sleep occupies 20% of the total sleep time in adults, although it varies with age, being greater in children(in babies it is 50% of the total) and in it there are discharges of rapid eye movements and a complete abolition of muscle tone, respiratory rate and pulse become faster and irregular.

Subsequently, the different phases of sleep alternate cyclically throughout the night, during the first part, non-REM sleep predominates and during the second, the REM periods become longer. During normal sleep, waking periods appear so brief that they may not be remembered the next day.

The physiological characteristics of dream activity vary throughout the different stages of sleep. During REM sleep, weird and bizarre images appear, we find that dreams are longer, more emotional than in non-REM stages, which correlates with the different physiology of these phases.

Obstructive sleep apnea (OSA)) does not seem to have a direct effect on testosterone, after adjusting for age and obesity. However, a possible indirect causal process may exist mediated by the effect of OSAS on obesity.

The treatment of moderate to severe OSAS with continuous positive airway pressure (CPAP) does not increase testosterone levels reliably in most studies. In contrast, a reduction in weight makes it predictable and linearly in proportion to the amount of weight lost. In addition to a very transient detrimental effect, treatment with testosterone does not adversely affect OSA, treated.

Data on the effect of sleep quality on testosterone may depend on whether testosterone is given as a substitute or in supra-therapeutic doses. Experimental data suggest that testosterone can modulate individual vulnerability to subjective symptoms of sleep restriction.

Low testosterone can affect the quality of sleep in general, which improves with replacement dose. Large doses of exogenous testosterone and anabolic or androgenic steroid abuse are associated with abnormalities of sleep duration.

The Endocrine System:

Collection of glands that secrete hormones in the circulatory system and are taken to another organ) has a complex importance in sleep.

The secretion of some hormones increases during sleep (for example, growth hormone, prolactin and luteinizing hormone), while the secretion of other hormones is inhibited (for example, thyroid-stimulating hormone and cortisol).

Some hormones are directly linked to a particular stage of sleep. Growth hormone is usually secreted in the first hours after the onset of sleep and is usually released during slow wave sleep (SWS).

Cortisol is linked to the circadian rhythm and reaches its peak at the end of the afternoon, regardless of the person’s sleep state or the darkness and light cycle. Melatonin is released in the dark and is suppressed by light. The secretion of thyroid hormone occurs late at night.

Adenosine: adenosine, is a substance that accumulates with metabolic activation; that is, during the waking period. This substance is stored in the anterior hypothalamus, better known as the sleep homeostat site. Therefore the production of sleep occurs due to the disinhibition of the neurons of this area, derived from the inhibitory work of adenosine.

Serotonin: in relation to sleep, it has been shown that serotonin levels are higher in the waking state, these levels decrease during slow sleep and REM sleep, which is why serotonin prepares the body for sleep by failing to act in certain areas.

Melatonin is a hormone that is synthesized from the serotonin neurotransmitter in the pineal gland; which is responsible for regulating circadian rhythms under the control of certain nuclei, since this substance is associated with levels of light and darkness, rising during darkness and more specifically during sleep; therefore it can be said that melatonin favors and regulates the moment in which the sleep happens.

Histamine: histamine is that transmitter that participates in the inhibition of certain neurons, being responsible for the withdrawal of the systems of diencephalic awakening. This process constitutes the sleep-wake switch. These systems of awakening are responsible for the tonic function during the waking period, acting to counteract the pressure exerted by the accumulation of adenosine.

Noradrenaline: Noradrenaline (NA) is involved in both the control of wakefulness and REM sleep. A considerable increase in noradrenaline induces the waking state; therefore REM sleep appears or begins to occur as long as NA activity decreases. In this way, noradrenaline should be considered as the inhibitory transmitter of REM sleep, when we speak of inhibition for the case of NA, we refer specifically to the control of the tonic state, characteristic of this stage.

Acetylcholine: acetylcholine, is a transmitter that acts during the state of wakefulness and REM sleep, its main function is the triggering and maintenance of REM sleep, providing a modulating effect on it.

Considerable research has linked endocrine dysfunction and sleep dysfunction (specifically insomnia). It has been proposed that the overactivity (or hyperdrive) of the hypothalamic-pituitary-adrenal (HPA) axis, the over-activation of hormonal interaction between a part of the brain and the adrenal gland, may affect sleep function, perhaps in response to stress, and subsequently increase the secretion of cortisol and norepinephrine, thus promoting wakefulness.

Diabetes is a specific disease that affects the ability of the endocrine system to produce the hormone insulin and, in turn, is affected by sleep. It has been proven that adults who have 5 or less hours of sleep per night were 2.5 times more likely to have diabetes, compared to people who sleep 7 to 8 hours per night, also, people who sleep for 9 or more hours are more likely to suffer from diabetes, therefore insufficient sleep, as well as excessive sleep are not healthy when it comes to insulin.

Orexin plays an important role in the metabolism of glucose (including through its participation in the production of a circadian rhythm of glucose), preventing or promoting insulin resistance.

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