Women should sleep early as they wake up early, a natural body rhythm for women based on the study done by a team from McGill University had 15 men and 11 women come and spend 36 hours in the lab. They subjected the participants to a “cat nap” paradigm, where they’d raise and lower the lights, so that the participants slept for an hour and rose for an hour. They measured levels of melatonin, the central sleep hormone and other, subjective variables, like wakefulness and sleepiness.
The pineal gland produces melatonin, a serotonin derived hormone which modulates sleep patterns in both circadian and seasonal cycles. It helps maintain circadian rhythm and regulate reproductive hormones. Menopausal women have less melatonin and as we age we produce less of this hormone.
About Melatonin
Circadian rhythm
In animals, the primary function is regulation of day-night cycles. Human infants’ melatonin levels become regular in about the third month after birth, with the highest levels measured between midnight and 8:00 am.[48] Human melatonin production decreases as a person ages.[49] Also, as children become teenagers, the nightly schedule of melatonin release is delayed, leading to later sleeping and waking times.[50]
Antioxidant
Besides its function as synchronizer of the biological clock, melatonin is a powerful free-radical scavenger and wide-spectrum antioxidant as discovered in 1993.[51] In many less-complex life forms, this is its only known function.[26] Melatonin is an antioxidant that can easily cross cell membranes[52] and the blood–brain barrier.[5][53]This antioxidant is a direct scavenger of radical oxygen and nitrogen species including OH•, O•2−, and NO•.[54][55] Melatonin works with other antioxidants to improve the overall effectiveness of each antioxidant.[55] Melatonin has been proven to be twice as active as vitamin E, believed to be the most effective lipophilic antioxidant.[56]An important characteristic of melatonin that distinguishes it from other classic radical scavengers is that its metabolites are also scavengers in what is referred to as the cascade reaction.[26] Also different from other classic antioxidants, such as vitamin C and vitamin E, melatonin has amphiphilic properties. When compared to synthetic, mitochondrial-targeted antioxidants (MitoQ and MitoE), melatonin proved to be a comparable protector against mitochondrial oxidative stress.[57]
Immune system
While it is known that melatonin interacts with the immune system,[58][59] the details of those interactions are unclear. Antiinflammatory effect seems to be the most relevant and most documented in the literature.[60] There have been few trials designed to judge the effectiveness of melatonin in disease treatment. Most existing data are based on small, incomplete clinical trials. Any positive immunological effect is thought to be the result of melatonin acting on high-affinity receptors (MT1 and MT2) expressed in immunocompetent cells. In preclinical studies, melatonin may enhance cytokine production,[61] and by doing this, counteract acquired immunodeficiences. Some studies also suggest that melatonin might be useful fighting infectious disease[62] including viral, such as HIV, and bacterial infections, and potentially in the treatment of cancer.
In rheumatoid arthritis patients, melatonin production has been found increased when compared to age-matched healthy controls.
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Possible effect of melatonin on sleep-related postural mechanisms
Experimental and clinical evidences indicate that endocrine mechanisms, particularly involving the pineal gland, exert a role in the development of postural deficits leading to the occurrence of idiopatic scoliosis (IS). In particular, experiments performed in bipedal animals have shown that removal of the pineal gland, which secretes melatonin (M), induced a scoliosis, and that in such preparations, administration of this hormone prevented the development of this deformity (cf. 131). It appears also that adolescents with IS showed a reduced level of serum M with respect to age-related control subjects. The possible mechanisms involved in the M regulation of the tonic contraction of the axial musculature have been discussed.
It is known that the pineal gland is implicated in the control of circadian rhythms, including the sleep-waking cycle, and that during this cycle there are prominent changes in postural activity, which affect not only the limbs, but also the axial musculature. These changes are characterized by a decrease followed by a suppression of postural activity, which occur particularly during transition from wakefulness to synchronized sleep and, more prominently, to rapid eye movement (REM) sleep.
Episodes of postural atonia may also occur during the cataplectic episodes, which are typical of narcolepsy. Cholinergic and/or cholinoceptive neurons located in the dorsal pontine reticular formation (pRF) and the related medullary inhibitory reticulospinal (RS) system, intervene in the suppression of posture during REM sleep, as well as during the cataplectic episodes which occur in narcolepsy.
These structures are under the modulatory (inhibitory) influence of the dorsomedial and the dorsolateral pontine tegmentum, where serotoninergic raphe nuclei (RN) neurons and noradrenergic locus coeruleus (LC) neurons are located. We postulated that M may act not only on the circadian pacemaker, but also directly on the pontine tegmental structures involved in the regulation of posture during the animal states indicated above.
This hypothesis is supported by the facts that:
- 1) the dorsal pRF may contain specific binding sites for M;
- 2) this structure is particularly sensitive to M in adolescents, as well as in adult subjects affected by narcoleptic disturbances leading to cataplexy;
- 3) M increases the release of serotonin (5-HT), a neurotransmitter which enhances the postural tone by acting on the dorsal pRF: on the other hand, deficits in M levels may lower the activity of the serotoninergic raphe system, thus leading to a decrease or suppression of postural activity similar to that occurring either during REM sleep or during the cataplectic episodes typical of narcoleptic patients;
- 4) IS patients may show episodes of sleep apnea, a phenomenon which has been attibuted to a reduced tonic contraction of primary and accessory respiratory muscles during REM, resulting from a reduced release of 5-HT at dorsal pontine level.
It has been postulated that, if the reduced M and 5-HT levels are subliminal to produce a complete suppression of posture under the conditions reported above, the reduced postural tone, which results from this condition may lead to the development of IS, due to hypotonia which affects the axial musculature.
M secretion could be regulated not only by the activity of the serotoninergic raphe neurons projecting to the pineal gland, but probably also by the activity of noradrenergic LC neurons.
It is likely that the development of IS, which results from a reduced level of M and 5-HT, may occur provided that the noradrenergic LC inhibition of the pontine structures is impaired. Such impairment could depend upon genetic factors, similar to those postulated to play a role in narcolepsy.
In conclusion, the possibility exists that an impaired activity of brain monoaminergic systems may lead to disfunction in the production of M, which is apparently an important factor in the etiopathogenesis of IS.
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