|Everybody sleeps in a specific position. The basic position is the fetus when the body is rolled in with arms and legs to form a minimum surface. This position is a left over from the time in the mother’s womb. It is a very comfortable position when alone children sleep that way.
When growing up the position is changing. Females often start to hold on to something in the night, a pillow, bear and later a partner. The position is often fetus-like. Many people start in a “flat on the back” position. But after a while, this is not comfortable any longer and turn on the side. During the night everyone turns many times, this proves already that.
1 / a person keeps searching for a comfortable position but even when one is found it is not kept for a long time.
2 / Sleep shows its active state by turning around
The sleep position must be relaxed during the night, the body needs space to move. Even when sleeping with a partner this must be considered from both sides. There are many different postures for sleeping. Most people sleep on the side. In the side position, it seems that breathing is a little easier than on the back.
Laying on the belly is not comfortable for most people, especially not for females with big breast. The belly position depends on the comfort of the mattress and is, for instance, impossible in a hangmat.
Movement stimulates sleep. Sleep activate movements. The interaction between sleep and motion is clear but it is a fact that when the movement is good, sleep improves and the mental capacity increases. In other words, movement increases the total value of life with a measurable amount of energy and joy.
Sleep gives a lot; renewed energy, clear neural systems, better concentration, healthier blood circulation, growth and recuperation of all tissue and more stable emotions.
Memory development and storage is an important and fragile circuit during the aging process. Older people develop “empty spots” in memory. These “empty spots” are memories which are partial, incomplete, disturbed, not correct or otherwise. An important part of this seems to be related to the level and quality of sleep and activity. The lesser activity and lower quality of sleep, the more memory elements seemed to be affected.
The changes in the quantity of a certain neurotransmitter as well as how the post-synaptic terminal responds to this change are underlying mechanisms of brain plasticity. During sleep, there are remarkable changes in modulatory neurotransmitters throughout the brain. Acetylcholine is an excitatory neurotransmitter that is seen to increase to near waking levels during REM sleep while compared to lower levels during slow-wave sleep. Evidence has shown that the functioning of the hippocampus-dependent memory system (episodic memory and autobiographical memory) is directly affected by cholinergic changes throughout the wake-sleep cycle.
High levels of ACh would promote information attained during wakefulness to be stored in the hippocampus. This is accomplished by suppressing previous excitatory connections while facilitating encoding without interference from previously stored information. During NREM sleep, and especially slow-wave (SW) sleep, low levels of ACh would cause the release of this suppression and allow for spontaneous recovery of hippocampal neurons resulting in the facilitation of memory consolidation.
|Chemistry of sleep
Melatonin is commonly called the sleep hormone. Created from the inhibitory neurotransmitter serotonin, melatonin is secreted by the pineal gland according to the circadian rhythm and availability of serotonin. Melatonin production increases as it gets dark to create the sleepy feeling. During the day, melatonin secretion is low to aid in alertness; however, there is a smaller increase in the afternoon (between 1:00 pm and 4:00 pm) that may explain common daytime sleepiness. During aging, the production tends to increase slowly.
Like melatonin, cortisol follows the circadian rhythm. Cortisol is often considered to be the stress hormone, as it increases in response to stress. However, cortisol also plays important roles in the immune response, blood pressure, conversion of norepinephrine to epinephrine, and metabolism of carbohydrates, proteins, and fats. Chronic circadian disruption and reduced sleep time are associated with elevated cortisol and increased obesity.
Cortisol increases the production of glucose from protein (gluconeogenesis), helping to maintain optimal blood sugar levels. This is especially helpful when sleeping. During the night when the body is in a fasting state, cortisol increases glucose availability for the body to use for energy and repair. Thus, cortisol levels are highest in the morning after waking. As per the circadian rhythm, the morning peak gradually decreases throughout the day, reaching its lowest point around midnight.
Adenosine is a neurotransmitter with many functions, including regulating sleep-wake homeostasis. Adenosine levels increase while awake, and the body breaks adenosine down during sleep. Without sleep, increasing adenosine levels can cause the sleepy feeling, eventually prompting to give in to overwhelming sleepiness.
Ghrelin and leptin
Ghrelin is an important hormone that tells the brain to consume food. Leptin is another hormone that has the opposite effect and tells the body that it is full. Studies from the University of Luebeck and the University of Chicago reveal that a lack of sleep increases ghrelin levels and decreases leptin levels, which drives up food cravings.
Human growth hormone is a critical anti-aging hormone. This hormone makes it easier to build muscle, burn fat, and have a healthy immune system. The body produces growth hormone during deep sleep, and as one age, the production goes down. A study in the Journal of Psychiatry & Neuroscience showed that another way to produce less growth hormone is by sleep loss.
(GHRH, somatoliberin) is the hypothalamic peptide hormone that specifically stimulates synthesis and release of growth hormone (GH, somatotropin) by somatotrope cells of the anterior pituitary gland. GHRH is an important regulator of cellular functions in many cells and organs. The ability of GHRH analogs to increase and preserve insulin secretion by beta-cells in isolated pancreatic islets. The hypothalamic growth hormone-releasing hormone is one of the “humoral factors” that is critical for growth hormone secretion. GHRH undergoes rapid enzymatic degradation in blood.
Pituitary adenylate cyclase-activating polypeptide (PACAP) is a 38-amino acid peptide. PACAP belongs to the vasoactive intestinal polypeptide (VIP)-glucagon-growth hormone releasing factor-secretin family. PACAP is widely distributed in the brain and peripheral organs, notably in the endocrine pancreas, gonads, and respiratory and urogenital tracts. The diverse functions of PACAP include regulation of proliferation, differentiation, and apoptosis in some cell populations. In addition, PACAP regulates metabolism and the cardiovascular, endocrine, and immune systems, although the physiological event(s) that coordinates PACAP responses remains to be identified.
PACAP is as effective as GRF in releasing GH from cultured pituitary cells.
The functional role of galanin remains largely unknown; however, galanin is predominantly involved in the modulation and inhibition of action potentials in neurons. Galanin has been implicated in many biologically diverse functions, including nociception, waking and sleep regulation, cognition, feeding, regulation of mood, regulation of blood pressure, it also has roles in development as well as acting as a trophic factor. A study (Association of galanin and major depressive disorder in the Chinese Han population. [Yong-Jun Wang, Hui Li, Yu-Tao Yang, Chang-Le Tie, Feng Li, Zhi-Qing David Xu, Chuan-Yue Wang] it also has other effects.
VIP – Vasoactive intestinal polypeptide
Vasoactive intestinal polypeptide (VIP), a 28-amino-acid polypeptide secreted by cells throughout the intestinal tract. It stimulates the secretion of electrolytes and water by the intestinal mucosa. Studies have indicated that VIP is capable of acting as a neurotransmitter, inducing a relaxation effect in some tissues. On a molar basis, VIP is 50-100 times more potent than acetylcholine as a vasodilator. VIP release in the body is stimulated by high frequency (10-20 Hz) nerve stimulation and by cholinergic agonists, serotonin, dopaminergic agonists, prostaglandins (PGE, PGD), and nerve growth factor. endogenously released or exogenous VIP can significantly increase the heart rate and has a more potent effect on heart rate than does norepinephrine. The leading hypothesis of VIP function points to the neurons using VIP to communicate with specific postsynaptic targets to regulate circadian rhythm.