Why Sleep?

It was a sad day in December when I read the obituary of Allan Rechtschaffen, who died at 93 earlier that month after a half century of trying to answer the question, Why do we sleep? Imagine a whole career in the Department of Psychology at the University of Chicago devoted to one question and dying without knowing the answer. Though I never met Dr Rechtschaffen, it was a sad day for me because if he had only come to me sooner—I who have never conducted a single sleep study in my life—I could have told him the answer to his question. My answer may not have prolonged his already long life, but I might have helped him rest in peace.

“Because it feels soooo good,” I would have said. “And because no sleep feels so bad, so fast.”

And like a good scientist, Dr R. would have smiled at me, and said, “And why does sleep feel so good?”

“Because evolution has selected for this strict reward and punishment system. Only those who sleep regularly survive to procreate,” I would have said, knowing he’d not have taken the night train from Chicago to Cincinnati just to roll over and sigh.

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“Ah, but nature, or evolution as you call it, is quite loose about other essentials such as when and how we eat, how we procreate, how we fight, and how we raise our young. The function of sleep is such a tough nut to crack. Why is she so strict about how we sleep, why eight hours each night for almost everyone?”

Now it would be my turn to smile. “Ah yes, Dr R. That is the question! And the answer, my friend, is that the function of sleep is to regulate the stress response system.”  He might not have considered me his friend at this point, but it would be my way of showing him I had secured the upper hand by then, and I was ready to go on to arguing about the proper definitions of “regulate” and “the stress response system,” and we could arm wrestle over how those terms could be reliably measured in animals and humans.

In 1983 Dr Rechtschaffen published a report in Science showing that lab rats could not survive more than three weeks without sleep. He had developed an ingenious setup that tilted the disk the rat stood on as soon has its brains waves started to drift into sleep, making the rat slide toward the edge over a pool of water. Rats hate water even more than sleeplessness, so they stayed awake day after day until they died within two to three weeks. Some died by weight loss, others by loss of temperature regulation, others by skin lesions and infection, but none fell in the water. Twenty years later Dr Rechtschaffen was still disappointed by this ground-breaking study, and wrote: “…since we did not find an unambiguous cause of death, that dramatic symptom [death] did not tell us much about why sleep was necessary… The function of sleep has been such a tough nut to crack.”

Since Dr R. made that statement about twenty years ago, I felt sure that someone else would have cracked that nut by now and that Google would quickly identify the squirrel who had cracked it. So when my Google scholar search failed to come up with any good recent studies of stress and sleep and death, I tried PubMed, the inside track for academics like me. And when I came up with nothing there, I felt sure I had the wrong search terms, so I wrote my friend and colleague, Jim Herman, PhD, who is chair of our Department of Pharmacology and Systems Physiology, and the editor of the academic journal Stress for as long as I’ve known him. Listen to what he said:

“Yes, the gap in the literature is real and likely because of a silo thing. ‘Sleep’ is a silo, ‘stress’ is not. I served on the Neuroendocrinology (i.e., stress) Neuroimmunology, Rhythms and Sleep study section [for NIH] for over 6 years, 2 as Chair. Despite being the primary place one would see proposals on stress and sleep, we reviewed exactly zero grants on the topic. We publish very few stress-sleep papers in Stress, though the topic is picking up a bit.”  

If you’re a fly on the wall in any primary care clinic, you hear every day about insomnia, and in most conversations about insomnia, “stress” is the common thief of sleep. But so far, sleep science has overlooked stress and the stress response system. Amazing but true.

One way of understanding this paradox about how the stress response system may be hidden in plain sight is that the stress response system is complex and defies the silos of medical science. Most sleep researchers work in one silo or another. To recognize the stress response system as one coherent system that manages all the demands, big and small, physical, psychological, and social, across the range of responses from “fight or flight” to “rest and restore”—that requires thinking of the macrosystem of at least nine organ systems, each of which appears to have its own internal structure and rhythms and self-regulation mechanisms. The heart has evolved to regulate the frequency of its beats and can’t function for long outside of the range of 30-200 beats per minute. The lungs can’t function for long outside the range of 4-40 respirations per minute. Similar ranges of normal functioning can be drawn for the immune system, the endocrine system, and the others. Dysregulation in one organ system can be compensated by overactivation in another, but that only works for a limited time (days, maybe weeks?) before the second system loses its capacity to self-regulate, and the cascade of multi-system organ failure begins. 

Sleep is one way we reset our stress response systems. It’s a measure of the complexity of this system and its delicacy that it requires 8 hours every night to restore optimal functioning in each of the organ systems and the macrosystem too. In many studies, too much sleep is as much of a risk factor for early death as too little. And it’s a measure of how young sleep science is that relatively recently (2014) one of the lead sleep researchers, Dan Buysse, called on his colleagues to help define “sleep health.”

Before Dr. Rechtschaffen would get back on the train to Chicago, he would surely challenge me to describe the study that could answer this question about why we sleep, or at least advance our understanding. I would ask him to repeat his 1983 sleep-deprivation in rats study, this time while monitoring a measure of coherence for each of five or six organ systems, or nine if he could manage them all. And then study the process by which each organ system shifts from coherence to chaos or some state of dysregulation as the sleep-deprivation works its lethal ways. It does not matter what the final “cause of death” appears to be, or which organ is the last to collapse. But the pattern of collapse should reveal the pathways for how sleep deprivation kills and why the process works so fast, at least in rats. That study could put the stress response system on the map.

How to study lethal sleep deprivation in humans will be a tougher nut to crack. They might have trouble recruiting volunteers for that one.

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