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We’ve all experienced a sleepless night or two, and for some people that’s actually the norm. But why do we experience insomnia at all? What is going on in our minds and bodies, to cause this awful condition? Here’s what scientists know so far.
The prevalence of insomnia in adults varies widely, depending on how the condition is defined. Most broadly, someone has insomnia if he or she simply suffers from difficulty falling asleep, waking up over and over during the night, or nonrestorative sleep — and according to that definition, up to 50 percent of adults experience insomnia. But only around 20 percent of the population deals with insomnia, if we’re going by the 4th edition of the Diagnostic and Statistical Manual of Mental Disorders, where insomnia is considered a sleeping disorder (pdf) that lasts at least a month and causes daytime distress.
In any case, our understanding of insomnia is constantly evolving. For many years, insomnia was considered just a symptom of other issues, including depression, anxiety and schizophrenia. The prevailing thought was that if you treated the dominant condition, insomnia would subside as well. Insomnia is now known to be a syndrome in its own right, one that occurs alongside (is comorbid with) other disorders. So if you suffer from depression and insomnia, both issues should be treated at the same time — rather than just treating your depression alone.
To doctors, this type of insomnia, which is not caused by other medical issues or medicines, is called primary insomnia (as opposed to its sibling, secondary insomnia). They further describe the condition by how long it lasts — acute insomnia occurs for days or weeks, while chronic insomnia goes on for a month or more.
The basic models
In the past few decades, scientists have proposed a number of models to describe how chronic primary insomnia arises. One of the foundational paradigms was the ” 3-P model,” referring to the supposed Predisposing, Precipitating and Perpetuating factors of the condition.
The model says that certain attributes, including being highly anxious or a perfectionist, may first make you more susceptible to insomnia. Then, some precipitating event, such as a death in the family or a new job, throws your sleep out of balance, causing acute insomnia. Finally, poor attitudes and perceptions perpetuate insomnia — these can include heightened uneasiness and tension regarding sleep, or poor sleep hygiene.
Over the years, other models have come along, some of which adapted concepts of the 3-P model. For example, the cognitive model, proposed a little over a decade ago, explains that insomniacs are overly worried about sleep and about what happens if they don’t get enough of it. These negative thoughts trigger arousal and emotional distress, which essentially plunges people into an anxious state, causing them to actively monitor themselves and the environment for sleep-related threats (noises, body sensations and the like). Of course, this only exacerbates sleeplessness.
But insomnia (and the models to explain it) isn’t limited to the psychological realm. The neurocognitive model explains that people with insomnia show more high-frequency electrical activity in the brain (EEG) when they’re going to sleep compared with normal sleepers. This cortical arousal suggests that insomniacs have enhanced sensory or information processing and long-term memory formation during a time when normal sleepers do not, which could ultimately affect sleep. For example, the enhanced sensory processing may make insomniacs more sensitive to and aware of what’s going on in the environment.
A common theme in these models and others is this idea of arousal. In fact, many researchers now consider insomnia to be a state of 24-hour hyperarousal, brought on by the interplay between psychological and physiological factors.