Why We Sleep

At age six, I remember my first-grade teacher telling us that 9-11 hours of sleep each night was the biological requirement for our unique life stage, childhood. That night, I laid awake watching the minutes turn to hours on my Sony Dream Machine clock radio … wondering what terrible fate befell kids who sleep less because they’re worried about sleeping enough!

What we know is that sleep and lack of sleep affects our whole bodies, not just our central nervous system as previously thought. In the nutrition office, we can’t possibly talk about hunger and fullness, nor even expect nutrition education to be effective, when such basic a need as adequate rest is denied. This readily became clear to me, nearly three decades later, while reading Matthew Walker’s Why We Sleep.

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Sleep, it turns out, is an intensely metabolically active state for brain and body alike.

Walker writes from more than 20 years of experience studying sleep, first at Harvard Medical School and now as the director of the Center for Human Sleep Science at UC Berkeley. Below, a couple fascinating research findings presented in his book:

  • Sleep deprivation can significantly impact release of hormones affecting appetite.1 Study participants whose sleep was limited to 4 hours/night for two nights had significantly higher levels of ghrelin, a hormone responsible for hunger and drive to eat, and reduced levels of leptin, a hormone which suppresses appetite, than participants allowed up to 10 hours of sleep. Sleep-deprived participants reported an increase in hunger which strongly correlated with increased ghrelin-to-leptin ratio. (Neat fact; this randomized study used a within-subject crossover design, meaning that the same participants experienced both study conditions --six weeks apart-- thus serving as their own baseline control.)

  • Sleep-deprived study participants consumed more when given unlimited access to food (buffet meals and snacks) than their well-rested counterparts.2

  • Sleep curtailment may play a role in the development of insulin resistance, which may int turn increase diabetes risk independent of a person’s weight or body size. Using a similar crossover design, participants were subjected to either 4.5 hours or 8.5 hours of sleep per night for four nights. Cells of sleep-deprived participants were found to be less receptive to insulin, i.e., repelling instead of absorbing glucose (energy!) from the blood.3

  • Sleep deprivation may negatively impact our gut microbiome. One mechanism is thought to be via elevated production of the stress hormone, cortisol. It’s no surprise that when we rest, so too does the part of our nervous system responsible for activating our “fight or flight” response.4,5

  • (Walker outlines so many more facts and findings, including how caffeine “works”, but for brevity’s sake, will stop here.)

Of course, t’s important to note that the studies mentioned above had limitations including small sample sizes, and lack of gender, age, and size diversity to name a few. Larger, longer, and more diverse studies are needed.

While we’ve so much yet to understand (I’m particularly intrigued by the sleep-microbiome connection!), here’s an important ‘for now’ takeaway: As we sleep, our brains release hormones that support a normally functioning metabolism. When we sleep well and enough, we get our normal amounts of these hormones, allowing our hunger and fullness signals to function properly. Adequate rest is fundamental to our self-care and directly impacts how we nourish our bodies. 

To this point, Walker urges that we maintain a regular sleep-wake schedule to the best of our abilities. But how, when everything in our lives pull us away from getting to bed? He writes, “Set an alarm for bedtime. Often we set an alarm for when to wake up but fail to do so for when it’s time to sleep. If there is one piece of advice you take, this should be it.” (And the next time someone tells you sleep is overrated, give them this book!)

References

  1. Spiegel, Karine & Tasali, E & Penev, P & Van Cauter, Eve. (2004). Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Ann Intern Med, 141, 451-846.

  2. Broussard, J. L., Kilkus, J. M., Delebecque, F., Abraham, V., Day, A., Whitmore, H. R., & Tasali, E. (2016). Elevated ghrelin predicts food intake during experimental sleep restriction. Obesity (Silver Spring, Md.), 24(1), 132–138. doi:10.1002/oby.21321

  3. Broussard, J. L., Ehrmann, D. A., Van Cauter, E., Tasali, E., & Brady, M. J. (2012). Impaired insulin signaling in human adipocytes after experimental sleep restriction: a randomized, crossover study. Ann Intern Med, 157(8), 549–557. doi:10.7326/0003-4819-157-8-201210160-00005

  4. Benedict, C., Vogel, H., Jonas, W., Woting, A., Blaut, M., Schürmann, A., & Cedernaes, J. (2016). Gut microbiota and glucometabolic alterations in response to recurrent partial sleep deprivation in normal-weight young individuals, Mol Metab, 5(12), 1175-1186.

  5. Van Cauter, E., Spiegel, K., Tasali, E., & Leproult, R. (2008). Metabolic consequences of sleep and sleep loss. Sleep Medicine, 9(1), S23–S28. doi:10.1016/S1389-9457(08)70013-3

  6. Walker, M. P. (2017). Why we sleep: Unlocking the power of sleep and dreams. New York, NY: Scribner, an imprint of Simon & Schuster, Inc.