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A new study claims the 'sleep hormone' melatonin may give relief to patients with multiple sclerosis...Read more - http://www.ms-uk.org/MSnews

the following from the link is a little confusing.

They saw that during fall and winter, patients’ relapse rates were 32% lower than the rest of the year, when melatonin levels naturally dip.

Huh? The only explanation I could think of is that the "dip" in melatonin being measured in vivo was due to its utilization? whiuch I would say is a baaaaad guess. anyone else understand it better?

CureOrBust wrote:the following from the link is a little confusing.

They saw that during fall and winter, patients’ relapse rates were 32% lower than the rest of the year, when melatonin levels naturally dip.

Huh? The only explanation I could think of is that the "dip" in melatonin being measured in vivo was due to its utilization? whiuch I would say is a baaaaad guess. anyone else understand it better?

I think this is an error, as it doesn't make sense with the rest of the article. Earlier in the article it states that melatonin levels are at their highest during fall and winter. This makes more sense with why they think it could help treat MS, if they have seen that relapse rates are lower when melatonin levels are higher. Other studies have investigated the use of melatonin as a treatment for MS or potential links between the two, we have published some articles about these on our site, which you can find via the following links:

http://www.mstranslate.com.au/melatonin ... del-of-ms/

http://www.mstranslate.com.au/fatigue-m ... sclerosis/

Hope this helps!

Brett (MS researcher, science communicator and co-founder of MStranslate)

Perhaps poorly worded, but they're stating that the "rest of the year" is when melatonin levels dip.

MStranslate wrote:I think this is an error, as it doesn't make sense with the rest of the article.

OK, thanks, I did mean to find the original article for clarity.

But the team’s main concern doesn’t have to do with experimental setup. It has to do instead with the knock-on effects of publishing such research. Melatonin is widely available as an over-the-counter sleep aid, and they worry that some MS patients might use the hormone as a supplemental treatment. 'We don’t want patients to see the study and misinterpret our results,' Farez says. “It’s a neat study and great data, but we still need to do a lot of work.”

What they're saying... "No, don't take the stuff. It's cheap and it might be good for you, but we need to publish some more papers, tweak its chemical structure so it does the same thing, but doesn't kill people and then patent it."

Multiple sclerosis: the role of melatonin and N-acetylserotonin.
Mult Scler Relat Disord. 2015 Mar;4(2):112-23.

• Multiple sclerosis (MS) is an immune mediated disorder that is under intensive investigation in an attempt to improve on available treatments. Many of the changes occurring in MS, including increased mitochondrial dysfunction, pain reporting and depression may be partly mediated by increased indoleamine 2,3-dioxygenase, which drives tryptophan to the production of neuroregulatory tryptophan catabolites and away from serotonin, N-acetylserotonin and melatonin production. The consequences of decreased melatonin have classically been attributed to circadian changes following its release from the pineal gland. However, recent data shows that melatonin may be produced by all mitochondria containing cells to some degree, including astrocytes and immune cells, thereby providing another important MS treatment target. As well as being a powerful antioxidant, anti-inflammatory and antinociceptive, melatonin improves mitochondrial functioning, partly via increased oxidative phosphorylation. Melatonin also inhibits demyelination and increases remyelination, suggesting that its local regulation in white matter astrocytes by serotonin availability and apolipoprotein E4, among other potential factors, will be important in the etiology, course and treatment of MS. Here we review the role of local melatonin and its precursors, N-acetylserotonin and serotonin, in MS. Free full text.

Protective role of melatonin in mitochondrial dysfunction and related disorders.
Arch Toxicol. 2015 Jun;89(6):923-39.

• Mitochondria are the powerhouse of the eukaryotic cell through their use of oxidative phosphorylation to generate ATP. Mitochondrial dysfunction is considered an important contributing factor in a variety of physiopathological situations such as aging, heart ischemia/reperfusion injury, diabetes and several neurodegenerative and cardiovascular diseases, as well as in cell death. Increased formation of reactive oxygen species, altered respiratory chain complexes activity and opening of the mitochondrial permeability transition pore have been suggested as possible factors responsible for impaired mitochondrial function. Therefore, preventing mitochondrial dysfunction could be an effective therapeutic strategy against cellular degenerative processes. Cardiolipin is a unique phospholipid located at the level of inner mitochondrial membrane where it plays an important role in mitochondrial bioenergetics, as well as in cell death. Cardiolipin abnormalities have been associated with mitochondrial dysfunction in a variety of pathological conditions and aging. Melatonin, the major secretory product of the pineal gland, is a well-known antioxidant agent and thus an effective protector of mitochondrial bioenergetic function. Melatonin was reported to prevent mitochondrial dysfunction from oxidative damage by preserving cardiolipin integrity, and this may explain, at least in part, the beneficial effect of this compound in mitochondrial physiopathology. In this article, mechanisms through which melatonin exerts its protective role in mitochondrial dysfunction and related disorders are reviewed.

Melatonin prevents cell death and mitochondrial dysfunction via a SIRT1-dependent mechanism during ischemic-stroke in mice.
Arch Toxicol. 2015 Jun;89(6):923-39.

• Silent information regulator 1 (SIRT1), a type of histone deacetylase, is a highly effective therapeutic target for protection against ischemia reperfusion (IR) injury (IRI). Previous studies showed that melatonin preserves SIRT1 expression in neuronal cells of newborn rats after hypoxia-ischemia. However, the definite role of SIRT1 in the protective effect of melatonin against cerebral IRI in adult has not been explored. In this study, the brain of adult mice was subjected to IRI. Prior to this procedure, the mice were given intraperitoneal with or without the SIRT1 inhibitor, EX527. Melatonin conferred a cerebral-protective effect, as shown by reduced infarct volume, lowered brain edema, and increased neurological scores. The melatonin-induced upregulation of SIRT1 was also associated with an increase in the anti-apoptotic factor, Bcl2, and a reduction in the pro-apoptotic factor Bax. Moreover, melatonin resulted in a well-preserved mitochondrial membrane potential, mitochondrial Complex I activity, and mitochondrial cytochrome c level while it reduced cytosolic cytochrome c level. However, the melatonin-elevated mitochondrial function was reversed by EX527 treatment. In summary, our results demonstrate that melatonin treatment attenuates cerebral IRI by reducing IR-induced mitochondrial dysfunction through the activation of SIRT1 signaling.