Bedfellows: Insomnia and Depression
Sleep disturbances are a hallmark of depression, but insomnia can actually unleash the mood disorder. Treating sleep disturbances might help prevent depressive episodes.
By July 1, 2003 - last reviewed on June 9, 2016published
Sleep disturbances and unipolar depression are such intransigent bedfellows that troubled sleep is considered a hallmark of the mood disorder. At least 80% of depressed people experience insomnia—difficulty falling asleep or, most often, staying asleep. Indeed, early morning awakening is a virtual giveaway of depression. Another 15% of the depressed sleep excessively.
But it may be that insomnia is more than just a symptom of depression. It may in fact unleash the mood disorder. If sleep researcher Michael Perlis, Ph.D., is right, insomnia may be an early harbinger of depression. His longitudinal studies show that it appears to precede episodes of depression by about five weeks. And sleep disorder intensifies over the course of a new depressive episode or relapse, says Perlis, associate professor of psychiatry and psychology at the University of Rochester and director of the behavioral sleep medicine service.
In a complex mix of chemistry and behavior, disordered sleep may actually bring on depression, setting in motion an array of forces in the nervous system that result, ultimately, in a frank depressive episode. Most intriguing, treating the insomnia may forestall a first episode of depression or recurrent disorder, or at least keep it from becoming chronic.
It isn't just that depression sufferers wake up early and get less sleep. The makeup of their sleep is shattered. Normal sleep has a well-defined architecture. Four or five times a night we cycle through periods of deepening, relaxing sleep, marked by slow waves if the brain is monitored electronically. Then we burst into dream sleep, marked by dramatic brain activity and rapid eye movements.
Depressed people lapse quickly into REM sleep, as if they were in a hurry to get to the highly emotionally charged activity. "For some reason, there is a lot of pressure to get into it," says Perlis. And it's unusual both in duration and intensity, more dense, intense and longer-lasting.
But exactly what it is is not quite clear. "It certainly looks like REM sleep represents an abnormality in the neurobiologic machinery of dreaming," says Perlis. "But there is still something wrong with the way that the depressed dream; the function of dreaming is undermined."
One of the functions of sleep is to facilitate the consolidation of memory. REM sleep in particular is involved with affective, or emotional, memory. "There's something wrong with the memories depressed people are consolidating and the way that the REM system is mood-regulating," says Perlis.
The intense activation of REM sleep in the depressed may lead to the overconsolidation of negative memory, rendering the depressed overly biased to remember bad things. They do not discharge negative feelings over time.
Disordered REM sleep is a deep marker of depression. REM sleep remains disordered even in persons whose depression has remitted, and it is disordered among first-degree relatives of the depressed. It seems to be related to depression vulnerability. Long-term monitoring of remitted patients shows that their sleep disturbance becomes progressively worse before they relapse into the full clinical syndrome of depression. Still, it is the reduction in slow wave sleep, brought about by the rush to REM sleep, that correlates most strongly with severity of current depression, along with the density and duration of REM sleep.
The insomnia that occurs in major depression typically leaves patients with six or more hours of sleep per night. That, however, is enough to interfere with one of the primary functions of sleep—consolidation of learning and memory.
The loss of slow-wave sleep and the rush to REM sleep have a significant effect on information and memory processing. They enhance it, and the revved-up ability to recall information appears to get in the way of perceiving what is actually going on around the time of falling sleep. As a result, patients with insomnia overestimate the time it takes them to fall asleep and underestimate the amount of time they actually spend sleeping.
It's entirely possible that the disturbed sleep that so typifies depression is the body's own attempt to correct itself. Researchers have evidence that in a certain proportion of sufferers insomnia has an antidepressant effect. Evidence has long existed that extended wakefulness improves the functioning of the serotonin neurotransmitter system, one of the brain-chemical systems that goes awry in depression. It may also beef up the release of dopamine, another neurotransmitter linked to depression.
In fact, sleep deprivation has been used as a depression treatment. Awakening patients early improves mood in 30% to 60% of cases. The problem is, the effect is short-lived. Once patients sleep again, they wake up depressed the next day. A variation of sleep deprivation called phase advancing, is now used as treatment in some circumstances.
The sleep loss of insomnia may begin, says Perlis, as a compensatory mechanism, a valiant attempt to enhance serotonin production. It may also have other antidepressant effects not related to serotonin. For example, the stress system of depressed people appears to be in a chronically activated mode, and insomnia may dampen the hyperarousal of body and brain created by the stress response.
But the insomnia doesn't work well enough to counteract depression. Its effect on serotonin is not huge. In failing to fully offset the serotonin deficiency and nervous system fallout from the extended stress response, insomnia precipitates the other depressive symptoms.
Once a bout of insomnia occurs, most people experience a great deal of frustration and anxiety about falling asleep and staying asleep. They take behavioral steps to compensate for the sleep loss, napping during the day or early evening. They go to bed early the next night. They stay in bed later the next morning. Or they drink as a way to relax themselves into sleep.
But these behaviors alter the sleep mechanism and wind up perpetuating insomnia. And now the insomnia exists as a result of behavioral contingencies. As a short term insomnia gets transformed into a persisting state by behaviors intended to counteract it but that backfire, the sleep loss builds.
Disordered sleep sets off a cascade of symptoms. It leads to fatigue, irritability, memory and concentration problems, loss of interest in social and other activities and the inability to draw pleasure from them. The fatigue strips away libido. Weight loss could follow extended sleep loss. Insomnia, in short, becomes depression.
The depression is actually secondary to the insomnia. And in disrupting the brain, and serving as a stressor itself, sleep loss renders people even more neurobiologically vulnerable to depression and precipitates onset of episodes.
Further, insomnia can wreak havoc with a person's capacity to cope with stressors at home, on the job, or in social life. The sense of feeling "out of control" can generate feelings of helplessness. And these negative feelings may spread, dredging up negative memories and amplifying negative thoughts, creating the cloud of pessimism that the depressed typically dwell under.
Perlis believes that behavioral treatment specifically aimed at curbing the insomnia of depression may rout the entire disorder. Behavioral treatment during periods of remission may keep full-blown depression at bay. But even in frank depressive episodes, behavioral treatment targeted specifically at the insomnia may hasten recovery. And cognitive-behavioral therapy of insomnia may be a way to augment standard treatments of depression
"Maybe we can protect people by paying attention to their insomnia," says Perlis. "If it is an unleashing factor, perhaps if we get rid of the insomnia we can get rid of the depression risk."