Research ArticlePHYSIOLOGY

Acute sleep loss results in tissue-specific alterations in genome-wide DNA methylation state and metabolic fuel utilization in humans

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Science Advances  22 Aug 2018:
Vol. 4, no. 8, eaar8590
DOI: 10.1126/sciadv.aar8590

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  • RE: Sleep Loss Reduces DHEA which Increases DNA Methylation and Inflammation

    I suggest the basis of Cedernaes, et al., may be explained by reduced dehydroepiandrosterone (DHEA).

    Very briefly, it is my hypothesis that the function of sleep is to produce dehydroepiandrosterone (DHEA) which stimulates consciousness (http://anthropogeny.com/Sleep%20and%20SIDS.htm ). My mechanism suggests that the light-dark cycle is involved in stimulating DHEA. This requires melatonin production during the dark phase which then results in the production of DHEA. Melatonin triggers prolactin production which is a direct and specific stimulator of DHEA. As DHEA is literally used during the day, melatonin increases at sleep. During sleep the melatonin - prolactin cycle increases until sufficient levels of DHEA are produced to induce awakening and consciousness during the day. The function of sleep / circadian rhythm is production of DHEA. "Sleep deprivation" is caused by low / insufficient DHEA.

    Regarding DNA methylation and reduced DHEA caused by reduced / disrupted sleep, I suggest DNA methylation is an evolutionary consequence of reduced levels of DHEA and is involved in cancer initiation (http://anthropogeny.com/DNAmethDHEAcancer.html). DHEA has been found to exert anti-inflammatory effects. I submit the findings of increased DNA methylation and inflammation in Cedernaes, et al., may be explained by reduced DHEA....

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    Competing Interests: None declared.

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