However, almonds also contain two chemicals that are good for sleep: magnesium and tryptophan. Magnesium acts as a muscle relaxant, which is why many athletes use it for post-workout recovery. Furthermore, it can calm nerves, helping you to release stress from your day.

Tryptophan is an amino acid that your brain converts into 5-HTP, a compound that is then metabolized into serotonin. Serotonin is a neurotransmitter that has a relaxing effect on the mind and body.

Chamomile has long been prized for its relaxing and calming properties, and science can explain why. Chamomile contains the antioxidant apigenin, which binds to certain receptors in the brain.

This process may promote sleepiness and reduce insomnia. Drinking a cup of hot chamomile tea before bed helps you relax.

Kiwis are rich in serotonin, as well as antioxidants like vitamin C and E. These antioxidant vitamins also have stress-reducing qualities. A defect shared among short-sleeping fruit fly mutants suggests that sleep supports antioxidant processes CREDIT: pbio.

Understanding sleep has become increasingly important in modern society, where chronic loss of sleep has become rampant and pervasive. As evidence mounts for a correlation between lack of sleep and negative health effects, the core function of sleep remains a mystery.

But in a new study published July 12 in the open access journal PLOS Biology , Vanessa Hill, Mimi Shirasu-Hiza and colleagues at Columbia University, New York, found that short-sleeping fruit fly mutants shared the common defect of sensitivity to acute oxidative stress, and thus that sleep supports antioxidant processes.

Understanding this ancient bi-directional relationship between sleep and oxidative stress in the humble fruit fly could provide much-needed insight into modern human diseases such as sleep disorders and neurodegenerative diseases.

Why do we sleep? During sleep, animals are vulnerable, immobile, and less responsive to their environments; they are unable to forage for food, mate, or run from predators. Despite the cost of sleep behavior, almost all animals sleep, suggesting that sleep fulfills an essential and evolutionarily conserved function from humans to fruit flies.

The researchers reasoned that if sleep is required for a core function of health, animals that sleep significantly less than usual should all share a defect in that core function. Clinical Psychology Review, 8 1 , 77— Bishop, T. Sleep, suicide behaviors, and the protective role of sleep medicine.

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Of these, our study is most comparable to Kim et al. Main differences between this study and ours, includes Kim's use of actigraphy-based sleep measures, adjustment for diabetes and depression, and investigation of moderation by sex. Our analysis accounts for a diverse range of age, demographic, and ethnic groups while investigating diabetes-related outcomes, building upon previous analyses by our group that included sex-stratified results While it is not clear why the contributions may be stronger in women, sleep disturbance induced psychological stress and physiological changes may provide a partial explanation Indeed, age, sex, smoking history, alcohol consumption, physical activity, and comorbidities are known confounders of the multiple linear relationships evaluated in the present mediation analysis 8 , 28 — For instance, moderate intensity and lifestyle-related physical activity have been found to be large mediators of the sleep—fasting insulin concentration relationship It is well known that physical activity plays an important roles in glycemic control due to its acute blunting effect on insulin levels 33 , and that muscular contraction stimulates insulin sensitivity by increasing AMPK activity, deactivating TCB1D1 and promoting GLUT4 translocation to the cell membrane, which increases cellular glucose uptake Therefore, future attempts to quantify, and de-couple the direct and indirect paths between sleep and metabolic health would benefit from causal modeling that considers a more comprehensive set of factors as covariates.

confounders, mediators, and moderators. Finally, in exploring mediators of the relationship between sleep, insulin sensitivity, and glycemic control, we are attempting to understand factors which underlie the pathway as possible mechanistic links.

It therefore bears repeating that although we used Preacher and Hayes's SAS procedure to estimate the indirect effects path ab , the negative ab does not indicate a negative mediation, but rather that one of the paths is negative while the other is positive For example, since the association between sleep duration and CRP path a is negative, and the relationship between CRP and fasting insulin concentration path b is positive 35 , the resulting ab is negative.

Similarly, since the association between sleep quality and CRP is positive i. Our finding of a much weaker mediation by CRP, bilirubin, and vitamins C and D to the sleep—glycosylated hemoglobin relationship as compared to insulin sensitivity also warrants discussion, and may be explained by the use of the bootstrap method—a non-parametric test that assumes linear relationships between paths—which likely produced conservative estimates of the indirect effect sizes 25 , or a narrower homeostatic range of glycosylated hemoglobin in the non-diabetic and medicated diabetic populations There are several limitations associated with our study.

First, though mediation analysis is a causal path analysis, given the cross-sectional nature of the design, causal inference may not be made from our findings alone, and future longitudinal studies are needed to confirm the directionality and importance of these findings.

Second, in applying our study exclusion criteria, our final analytic sample was only a fraction of the initial adult sample; however, all analyses were bootstrapped with replacement, which provided conservative, bias-corrected indirect effect estimates.

Given that our study considered multiple mediators, the use of a lower p -value for significance testing and estimating a narrower confidence interval—a common practice in the genetics literature 23 —may be a reasonable alternative for evaluating the indirect effects. Further, mediators and outcomes were objectively measured, but sleep measures were self-reported and susceptible to recall and response bias.

CRP, GGT, bilirubin, carotenoids, uric acid, and vitamins C and D made large, significant contributions to the observed relationships between sleep and fasting insulin concentration, but explained less of the relationship with glycosylated hemoglobin.

Publicly available datasets were analyzed in this study. TK designed the study, conducted the analyses, and drafted the manuscript. MR and CA consulted on the study design, analysis, interpretation of findings, and revised the drafted manuscript.

All authors reviewed and approve of the final manuscript version. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

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Toxic free radicals, or reactive oxygen species, build up in cells from normal metabolism and environmental damage. If the function of sleep is to defend against oxidative stress, then increasing sleep should increase resistance to oxidative stress. Hill and co-workers used both pharmacological and genetic methods to show that this is true.

Finally, the authors proposed, if sleep has antioxidant effects, then surely oxidative stress might regulate sleep itself. Consistent with this hypothesis, they found that reducing oxidative stress in the brain by overexpressing antioxidant genes also reduced the amount of sleep.

Taken together, these results point to a bi-directional relationship between sleep and oxidative stress—that is, sleep functions to defend the body against oxidative stress and oxidative stress in turn helps to induce sleep.

This work is relevant to human health because sleep disorders are correlated with many diseases that are also associated with oxidative stress, such as Alzheimer's, Parkinson's, and Huntington's diseases.

Sleep loss could make individuals more sensitive to oxidative stress and subsequent disease; conversely, pathological disruption of the antioxidant response could also lead to loss of sleep and associated disease pathologies.

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