This past March, Graham Mitchell, a 48-year-old British psychiatric nurse, hanged himself in his garden. During the subsequent inquest, family members expressed surprise at Mitchell’s decision to commit suicide, as reported by the Macclesfield Express. They knew Mitchell’s mental health had deteriorated, as he’d become noticeably depressed in the wake of a few personal setbacks. During the weeks before his death, Mitchell’s sister said he seemed shell-shocked.
But the inquest revealed issues of which Mitchell’s family was unaware, including his longtime struggle with chronic insomnia. In recent years, his shift-work schedule had apparently amplified his battle with rest.
The story mentioned Mitchell’s insomnia several times, but didn’t flesh out the dialectical relationship between disturbed sleep, mental disorders and suicide, perhaps understandably.
For more than a hundred years, experts have recognized interrelated connections between sleep, depression and suicide: At least three-quarters of clinically depressed people struggle with sleep, and insomnia is a well-proven risk factor for suicide across different cultures and age groups. Moreover, sleep disturbances increase the likelihood of non-depressed people becoming depressed. We don’t yet have any tidy divine theory to tie these pieces together, but researchers are working hard to get us there.
Doctors have treated poor sleep as a hallmark symptom of mental disorders for the better part of the last century. The Diagnostic Statistic Manual (DSM), first introduced in 1952 and now in its fifth edition, is used to diagnose all mental disorders. Since 1994, the DSM has explicitly instructed doctors and therapists to ask about irregular sleeping patterns in diagnosing depression.
An emerging school of thought, however, frames the relationship between sleep and depression differently. Non-depressed people who sleep poorly for a long period of time have an increased risk of developing clinical-grade blues. This progression suggests that not sleeping may contribute to the onset of mood disorders that might otherwise lay dormant.
Depression rarely boils down to any single factor. Instead, the abstruse disease rears its head thanks to some combination of genes, environmental factors and personal experiences. Increasingly, experts are seeing disrupted sleep as part of the recipe.
“In many cases, we often see insomnia and then later on, depression follows,” said Dr. Peter Meerlo, a behavioral physiologist at the University of Groningen who focuses on the relationship between the brain and sleep. “This doesn’t in itself yet prove that there’s a causal relationship. It still may be that disrupted sleep and mood disturbances are both a result of some third underlying process, but [the observed relationship] has at least put the issue on the map.”
Meerlo uses rodents to study the sleep-depression relationship. He’s seen changes in the brains of chronically sleep-deprived mice analogous to those in depressed human patients. Among other changes, Meerlo has observed the generation of new neurons — a process called neurogenesis — in specific brain regions critical to cognitive processes and emotion regulation. He’s also seen reduced volume in the hippocampus, a change observed in depressed patients that’s considered an important signifier of clinical depression.
The theory underlying Meerlo’s research depicts depression as a disease of plasticity rather than biochemistry. The current biochemistry model identifies low serotonin levels as the neural basis of depression. A plasticity-based explanation, however, focuses on the way nerve cells are wired, which informs how brain regions communicate with one another. Attempts to clarify the function of sleep — still an enormous mystery — have also increasingly focused on plasticity. The most popular modern theory, explained Meerlo, says sleep functions to strengthen connections between nerve cells (plasticity).
“Depression theory and sleep theory are meeting now,” said Meerlo, “so the way disrupted sleep affects depression is by impairing plasticity and the connections between brain regions.”
Yes, discussion of neurogenesis is the sort of inside baseball neuroscience that makes most people’s eyes glaze over. But, the implications of these brain changes are fairly concrete.
“It could change our view on treatment,” said Meerlo, “because many drugs now used to treat depression aren’t really helping you sleep better. In fact, some make it worse. So, we want to see the development of drugs that not only target aspects of mood disorders, but also target and improve sleep.”
But it’s not all about drugs. Understanding the sleep-mood relationship can also help us fine-tune non-pharmaceutical treatment methods, including Cognitive Behavioral Therapy (CBT), an increasingly popular, seemingly effective and low-cost path to better rest.
Presumably, Mitchell was severely depressed when he hanged himself. And, in some way, insomnia played a role in his despondence — perhaps as a symptom, an exacerbating factor, a cause, or some combination of the three.
His tragic situation is hardly unique. Experts have called attention to the troubling insomnia-suicide link since at least 1914, when opthalmic surgeon Ernest Pronger penned an editorial in the Lancet lamenting the frequent mention of insomnia in news reports of suicide. “Probably if all the cases in all the papers were collected,” he wrote, “we should find that annually very great wastage of human life from this cause alone goes on which might to a great extent be prevented.”
Now consider what Meerlo describes as the ultimate paradox: While long-term insomnia and depression go hand-in-hand, short-term sleep deprivation is used as a last-ditch effort to revive suicidal patients.
“While evidence is accumulating that chronically insufficient sleep may be a causal factor that increases the risk for depression,” wrote Meerlo in the preface to his new book on sleep and neuronal plasticity, “once people are depressed, many of them respond positively to a night of sleep deprivation. Although this phenomenon seems contradictory, it clearly underscores the importance of sleep-related processes in the regulation and dysregulation of mood.”
How could short-term sleep deprivation curb anguish if long-term deprivation might both cause and exacerbate it? We don’t really know.
“It’s a rather acute effect,” said Meerlo. “Most of the drugs now being used to treat depression only become effective after weeks, and sleep deprivation can work after a single night.”
The confusing remedy isn’t a new discovery, but decades of research haven’t done much to clear the fog.
“The downside of treatment is that it works very fast but it’s also short-lasting, so in most cases, when people go to sleep again the next night, there’s an immediate relapse in depression.”
But here’s one theory: Sleep-deprived people get hyper-emotional. Severely depressed people, however, tend to be hypo-emotional — they fall into a state of steady, rudderless sadness. Sleep-deprivation therapy may work, at least in part, by temporarily restoring emotional reactivity stolen by depression.
“In healthy people,” Meerlo said, “sleep deprivation causes hyper activity in the amygdala, making us emotionally unstable and disinhibited, but in depressed patients who have hypoemotionality, sleep deprivation simply has the same effect, just starting at a lower level.”
As more research takes place and the fog continues to lift on the tangled relationship between sleep, mental illness and suicide, scientists and doctors will hopefully be able to make sense of tragedies like Michell’s before it’s too late.
By Theresa Fisher