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This is an old revision of this page, as edited by Doc James (talk | contribs) at 11:49, 24 January 2020 (→Out of place). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

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"Melatonin is rapidly absorbed and distributed, reaching peak plasma concentrations after 60 minutes of administration, and is then eliminated. Melatonin has a half life of 35–50 minutes."

How does that work? — Preceding unsigned comment added by Drsruli (talk • contribs) 14:47, 22 July 2019 (UTC)[reply]


Melatonin should be described as a neurotransmitter

That Melatonin acts as a neurotransmitter is implicit on this page in that it's part of the "neurotransmitters" series, and also that the *effects* of Melatonin receptors being engaged is described in the "Functions" section, however it is never clearly stated. See: Serotonin page functions section. --Whilom Chime (talk) 17:09, 4 December 2016 (UTC)[reply]

It is actually a hormone, not a neurotransmitter that has effects on more distant cells, not just adjacent cells connected by synapses. I have edited the lead so that it now stated that it is a hormone in the lead sentence. Boghog (talk) 18:54, 4 December 2016 (UTC)[reply]
Apologies, I certainly didn't mean to imply that it isn't a hormone, but that like norepinephrine it is both. I'm definitely not an expert, but I'm assuming its activity with Melatonin receptors in the suprachiasmatic nuclei of the hypothalamus means that it is also a neurotransmitter. I'm quite willing to be educated that it is not, but if that's the case it should be removed from the neurotransmitter page and the neurotransmitter list.--Whilom Chime (talk) 20:14, 4 December 2016 (UTC)[reply]
No problem. I am not an expert either. The sources that I have read invariably describe melatonin as a (neuro)hormone that is synthesized in the pineal gland. For melatonin to be classified as a neurotransmitter, it would also need to be released from presynaptic neurons and I can find no support for that in the literature. Hence as you suggest, I think melatonin should be removed from the {{Neurotransmitters}} navbox and neurotransmitter article. Boghog (talk) 06:12, 5 December 2016 (UTC)[reply]

Review article saying that melatonin is effective for treating primary insomnia

Here's the article: https://www.ncbi.nlm.nih.gov/pubmed/28648359 I don't want to edit the part of the article which says that there's not enough evidence for this myself owing to my very limited knowledge of such subjects, but perhaps that should be done if that review article is right. Dakane2 (talk) 19:37, 23 January 2018 (UTC)[reply]

medical uses and side effects categories overlap

There are quite a few side effects listed under medical uses. Perhaps these categories should simoly be combined into "Medical uses and side effects". Dig deeper talk 04:11, 1 March 2018 (UTC)[reply]

Proofreading

@Emh975: Can you proofread what you added? There's grammar mistakes and omissions (e.g., the bioavailability statement says "is between to and 50%" and doesn't specify a route of administration). Also, can you move the content you added in Melatonin#Pharmacodynamics to Melatonin#Biosynthesis and Melatonin#Regulation? Also, keep in mind that some of what you added is already covered there. Seppi333 (Insert 2¢) 20:13, 29 January 2019 (UTC)[reply]

First sentence

IMO this is better "Melatonin is a hormone, produced primarily by the pineal gland, which regulates wakefulness"

Than "Melatonin is a hormone and free radical scavenger that regulates sleep-wake cycles and functions as a mitochondrial antioxidant"

The ref is not very definitive says "targeted to the mitochondria where it seems to function as an apex antioxidant"[1]

And this ref "Evidence has emerged to show that both mitochondria and chloroplasts may have the capacity to synthesize and metabolize melatonin."[2]

Hardly definitive and as such IMO belongs lower in the body. Doc James (talk · contribs · email) 02:38, 1 February 2019 (UTC)[reply]

Seems fair. The only reason I edited the lead is because of the phrase "primarily by the pineal gland" - will cut that. Also, melatonin doesn't regulate wakefulness; it regulates sleep-wake cycles. They're not the same thing. Seppi333 (Insert 2¢) 05:17, 1 February 2019 (UTC)[reply]
What is wrong with "primarily by the pineal gland"? Yes it may be produced by other locations but it is primarily by the pineal no? Doc James (talk · contribs · email) 05:52, 1 February 2019 (UTC)[reply]
Based upon the references I've read, I think the only thing that can be said for certain is that melatonin which circulates in plasma (i.e, secreted/hormonal melatonin) is primarily synthesized in the pineal gland. Pinealectomy appears to increase its concentration in some fluid compartments. Seppi333 (Insert 2¢) 06:02, 1 February 2019 (UTC)[reply]
This ref says it is primarily made by the pineal gland.[3] Yes it might be made by other locations aswell.
But we have lots of refs that say that [4] Doc James (talk · contribs · email) 06:04, 1 February 2019 (UTC)[reply]
Then just clarify that melatonin which circulates in the blood stream is produced in the pineal gland. That's the only gland that produces and secretes it as a hormone. Seppi333 (Insert 2¢) 06:06, 1 February 2019 (UTC)[reply]
Okay so at least the hormone version is primarily from the pineal than. Have clarified. Doc James (talk · contribs · email) 06:14, 1 February 2019 (UTC)[reply]
That seems fine. Seppi333 (Insert 2¢) 06:22, 1 February 2019 (UTC)[reply]

Out of place

This article is not about have sleep disorder are or are not a "grave public health crisis"...

There are also concerns that Frontiers is a predatory publisher.

And we already discuss sleep disorders with better references. Why a 2004 review when 2015 AHRQ reviews are avaliable? Doc James (talk · contribs · email) 11:47, 24 January 2020 (UTC)[reply]

Secondary sleep disorders

Somnipathy, or sleep disorders, are a familiar yet grave public health crisis that can be addressed with timely and effective pharmacological and/or non-pharmacological – and sometimes a combination of the two – treatments.[1] With the disadvantage of poor compliance to traditional pharmacological therapy coupled with the increasing complexity of multifaceted non-drug sleep therapies to suit individual needs, the exogenous administration of melatonin – an endogenous, naturally-produced hormone in the human body involved in sleep regulation – is looked at as a potential solution to secondary somnipathy, sleep disorders caused by another existing medical or psychological condition.[1] Melatonin has long been used to treat various insomnias (problems with falling and/or staying asleep) and delayed sleep phase disorder.[2] In 2004, a review of 30 randomized-controlled trial studies revealed that specifically to secondary sleep disorders, melatonin did not significantly have any effect neither on sleep onset latency (SOL), on wake after sleep onset (WASO), nor on the percentage of time spent in REM sleep.[3] However, melatonin did significantly increase sleep efficiency and total sleep time (TST) in people with secondary sleep disorders.[3]

References

  1. ^ a b Li T, Jiang S, Han M, Yang Z, Lv J, Deng C, et al. (January 2019). "Exogenous melatonin as a treatment for secondary sleep disorders: A systematic review and meta-analysis". Frontiers in Neuroendocrinology. 52: 22–28. doi:10.1016/j.yfrne.2018.06.004. PMID 29908879.
  2. ^ van Geijlswijk IM, Korzilius HP, Smits MG (December 2010). "The use of exogenous melatonin in delayed sleep phase disorder: a meta-analysis". Sleep. 33 (12): 1605–14. doi:10.1093/sleep/33.12.1605. PMC 2982730. PMID 21120122.
  3. ^ a b Buscemi N, Vandermeer B, Pandya R, Hooton N, Tjosvold L, Hartling L, et al. (November 2004). "Melatonin for treatment of sleep disorders". Evidence Report/Technology Assessment (108): 1–7. doi:10.1037/e439412005-001. PMID 15635761.

We already have a section on this

And we provide a better summary of the evidence. Doc James (talk · contribs · email) 11:47, 24 January 2020 (UTC)[reply]

Alzheimer's disease

Hypothalamic nuclei, such as the suprachiasmatic nuclei and the lateral hypothalamic area, that are affected by β-amyloid plaques and neurofilament tangles in brains with Alzheimer's diseases are also involved in the severe disruption of the circadian rhythm and consequently, the occurrence of sleep disorders.[1] Sleep disturbances as well as poor sleep quality may contribute to the development of Alzheimer's disease, to some degree through the facilitation of β-amyloid buildup (a risk factor for Alzheimer's disease) in the human brain.[2][3] Research shows that in the pre-onset stages of Alzheimer's disease, melatonin levels in the CSF are significantly lower.[1] Furthermore, there is evidence in transgenic animal models of Alzheimer's disease that the exogenous administration of melatonin not only decreases the production and/or deposition of β-amyloid peptide but also increases its clearance through the glymphatic system.[4] Recent research concluded that exogenous melatonin administered in the preclinical phase of dementia demonstrates a significant increase in sleep quality and efficiency.[1]

  1. ^ a b c Spinedi, Eduardo; Cardinali, Daniel P. (2019). "Neuroendocrine-Metabolic Dysfunction and Sleep Disturbances in Neurodegenerative Disorders: Focus on Alzheimer's Disease and Melatonin". Neuroendocrinology. 108 (4): 354–364. doi:10.1159/000494889. ISSN 0028-3835.
  2. ^ Spira, Adam P.; Gottesman, Rebecca F. (April 2017). "Sleep disturbance: an emerging opportunity for Alzheimer's disease prevention?". International Psychogeriatrics. 29 (4): 529–531. doi:10.1017/S1041610216002131. ISSN 1041-6102. PMC 5493989. PMID 27938445.
  3. ^ Brown, Belinda M.; Rainey-Smith, Stephanie R.; Villemagne, Victor L.; Weinborn, Michael; Bucks, Romola S.; Sohrabi, Hamid R.; Laws, Simon M.; Taddei, Kevin; Macaulay, S. Lance; Ames, David; Fowler, Christopher (2016-05-01). "The Relationship between Sleep Quality and Brain Amyloid Burden". Sleep. 39 (5): 1063–1068. doi:10.5665/sleep.5756. ISSN 0161-8105. PMC 4835305. PMID 27091528.
  4. ^ Shukla, Mayuri; Govitrapong, Piyarat; Boontem, Parichart; Reiter, Russel J.; Satayavivad, Jutamaad (2017-08-28). "Mechanisms of Melatonin in Alleviating Alzheimer's Disease". Current Neuropharmacology. 15 (7). doi:10.2174/1570159X15666170313123454. PMC 5652010. PMID 28294066.
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