These days, five to 10 percent of adults are chronic insomniacs. And According to the NIH, at least a third of us have battled the can’t-sleep disease at some point in our lives. While accounts of insomnia date back to ancient civilization, the history of the disorder as a codified disease, treated with patented drugs and studied through controlled experiments, starts in the 19th century. In general, our understanding and treatment of clinical-grade sleeplessness has come a long way in the past 150 years. But, in some ways, we’re still hashing out the same debates, and hitting the same research roadblocks that we were in the 1800s. Here's how what we knew then aligns with what we know now.
In the 1890s, scientists conducted the first controlled experiments to explore the impact of sleep deprivation on regional brain function. In a 1894 study, a Russian doctor named Marie de Manaceine reported that puppies who’d been kept active and deprived of sleep died and developed severe brain lesions within a few days. In two other studies, scientists similarly found that dogs who’d been kept awake died within two weeks or less, and exhibited degenerative changes in several areas of the brain.
We no longer reserve space in the New England Journal of Medicine for puppy-killers. But we do perform experiments on genetically modified rodents to understand the neurobiological impact of insomnia. We also recruit participants for studies involving short-term sleep deprivation to assess the impact of sleep loss on cognitive performance, and invite insomniacs to try out drugs and behavioral therapy in a hell of alot of clinical trials.
Yet, we still don’t know the neurobiological basis of insomnia.
In 1811, a physician classified seven sleep disturbances including insomnia. He further categorized it as being either symptomatic (of another disease) or idiopathic (a disease that arises spontaneously and without obvious roots.)
Alexander William Macfarlane emphasized the same symptom-disease tension in his book Insomnia and its Therapeutics, in which he defined insomnia as both “loss of sleep” and “want of sleep.” Like most experts then, however, Macfarlane primarily saw insomnia as a symptom of “many diseases differing widely in their nature and complexity as well as gravity.”
While the medical definition of insomnia has changed, it still remains more general than technical. Per the International Classification of Sleep Disorders it’s defined as “a complaint of sleep onset, sleep maintenance, waking too early, or un-restorative sleep…” (There’s a lot more to the definition, but that’s the gist.)
When it comes to characterizing insomnia, we’re still in “ontological limbo.” Meaning we still consider it both a symptom and a disease. Thankfully, we’ve become more comfortable accepting that.
The tail-end of the century saw a move away from broad theorizing about insomnia towards more concrete efforts to explain its origins. Macfarlane used his own medical case reports to identify eight causes of insomnia, the two most common being neurasthenia (a vague, catch-all nervous system condition) and worry.
We still diagnose insomnia based on subjective complaints from patients. Now, however, we might also stick them in clinic beds and strap sensors to their heads to assess just how poorly they’re sleeping and hunt for other sleep disorders that may hinder all that sheep-counting.
Sleep doctors can use brain activity recordings to understand sleep patterns and problems. But we still can’t look at the brain of an insomniac and identify it as such. For now, we look to the International Classification of Sleep Disorders, which provides criteria for diagnosing “the insomnias”, which include primary, psychophysiological and pill-related.
The first prescription drugs marketed and sold specifically as sleep aids arrived during the industrial revolution. They included the barbiturate chloral hydrate and hypnotic remedies, most famously Laudanum, a mixture of opium and wine (or water) that was prescribed to poor infants and elders alike. (Unfortunately, Laudanum, “the aspirin of the 19th century” was also implicated in a fair amount of death.)
Marijuana was a widely available sleep aid in the 19th century, though it had a reputation as being more dangerous than Laudanum. Perceptions changed when word spread that Queen Victoria’s personal doctor, J.R. Reynolds, prescribed her highness pot to help her sleep through menstrual cramps.
Opium is illegal. Barbiturates are mainly used as surgical anesthetics. Pot is slowly and incrementally re-claiming its spot among regulated legal drugs, though the FDA hasn’t approved it to treat insomnia — yet.
The past 15 years have really been about Z-drugs, including Ambien and Sonata. Z-drugs work on the same neurotransmitter, GABA, as xanax and other anti-anxiety benzodiazepines, but they target neuron receptors more precisely. As a result, they have stronger sedative effects without inducing broader anxiety relief. 2015 saw the emergence of a new prescription sleep aid, called Belsomra, the first (and only) sleep drug to target the neurotransmitter orexin. So far, Belsomra hasn’t done much to hurt the popularity of Z-drugs or Benzos.
The most significant change in insomnia drugs, however, might be the move away from them. In 2005, the National Institute of Health decided that behavior change is the most effective treatment for insomnia.
According to Professor Eluned Summers-Bremner’ 2009 book Insomnia: A Cultural History, nineteenth-century doctors commonly blamed “the stimulations of the industrial age,” for what they perceived as an uptick in insomnia.
Different stimulations, snazzier industrial age, similar perceptions. In today’s age of anxiety, we’re like Oliver Twist, if Oliver were less interested in filling his belly with porridge than feverishly searching for a wi-fi connection so he could send snaps. We say our blue-lit gizmos are ruining our circadian rhythms, our retinas and our rest cycles. And we write self-loathing tirades about late-night work emails and generally treating our phones like morphine drips.
Research backs up a lot of our griping. When people live like Thoreau for a week their body clocks recalibrate to match light-and-dark cycles. And anxiety is a big part of poor sleep for many people.
“Modern nervousness was understood to affect men and women differently,” wrote Summers-Bremner, explaining that medical experts commonly held that women needed more sleep because they had more nervous excitability. In the late 1800s, doctors began to prescribe the “rest cure” for modernity-addled women with the means and time to spend 10 days in bed. (Remember the Yellow Wallpaper? Rest cure sounds fun and not at all counter-productive.)
We no longer put women on bed rest for their nervous excitability, but anxiety-based insomnia is still a gendered issue in some ways. We’ve moved away from the notion that women are nervous insomniacs because they have nervous brains, and now look at underlying causes for disproportionate rates of anxiety across the gender spectrum.