Long Nights and Open Eyes: A Short History of Insomnia (part 1)

I dread the night. I sit in the living room with my family, drinking camomile tea, until 10pm or so. Then I retreat to my room, and look at my bed with a kind of revulsed horror — a sense of oncoming battle. I lie in bed, and try to quieten my mind. I try relaxation strategies. I see myself walking into the Abbotsford Convent, into one of the workshop rooms, crawling under the table and lying there. Breathing in, breathing out. This is the “safe place” I chose from the Melbourne University counselling website’s “safe place exercise”. I become marginally calmer for a little while, and then an alien, familiar thought collapses into my skull: What if this doesn’t work? I tense up, and a torrent of frustration, hatred, and helplessness will swiftly follow the thought. I’m in for a long night.

Insomnia is prevalent. Chronic insomnia is present in around nine percent of the population, and around 30 percept of people have short periods of insomnia. It’s more common in older people, and more common in women. It’s incredibly common in people with other psychological disorders — over 75% of psychiatric patients have sleep difficulties during the acute phase of their illness (Sweetwood, Grant, Kripke, Gerst, & Yager, 1980; found in Morin, 1993). If insomnia affects so many people, why isn’t everyone aware of treatments they can use?

I had insomnia for a few months in 2012. When I went to the doctor after a few weeks of not sleeping, I was prescribed temazepam and a script to see a psychologist. I also received a pamphlet about sleep hygiene. Don’t look at blue light close to bedtime, no exercise less than three hours before bed, get out into the sun as much as possible, no caffeine late in the afternoon. However, when applied on its own, sleep hygiene information is one of the least effective sleep interventions. None of the medical practitioners mentioned the most effective psychological form of treatment: cognitive behavioural therapy for insomnia.

Like many insomniacs, I was desperate for a solution, but I also thought that the solution would come from my own ruminations. If I thought enough about my past, about the issues that may have caused the insomnia in the first place, I could figure everything out, and my insomnia would be fixed. In a kind of folk-Freudian perspective, I imagined that the answer lay deep inside my subconscious. Unfortunately, this attempt at self-understanding only increased the number of thoughts and the strength of my emotion directed towards sleep. Instead, what helped me was a book and a state of mind. More on that later.

This article is in two parts because it has grown so large it has overgrown my garden, crept up the side of my house and is spreading into neighbouring villages. In this first part, I discuss the potential aetiology of insomnia and summarise some key theories by leading researchers. In the second part, I will outline modern therapies that have been developed over the past 50 years, and the evidence supporting these therapies.

I need to emphasise that if you yourself have insomnia, there is a possibility that this could be due to a huge number of factors — sleep apnoea, restless legs syndrome, periodic limb movements, circadian rhythm disorders, parasomnias, and more. These have very different aetiologies and treatment plans than sleeplessness due to primary insomnia, so any information here might not be relevant. Please, consult your doctor! I am not a professional in sleep research or treatment, and all I can do is assess and distribute the research to the best of my ability, and share some of my own experiences.

“Why do we get insomnia?”

No one can be 100% sure.

In most areas of psychological research, certainty is hard to come by, and insomnia is no exception. Insomnia is not a disease with a clear cause. Insomnia cannot be grasped with two hands; cannot be examined under a microscope. And because we’re all unique snowflakes, individual differences in aetiology are inevitable.

However, there are themes that do reappear in the research with a regularity that merits attention. These won’t apply to everyone, but they will to some. I’m going to focus on a series of related theories that were written about in the 1920s, then mainly forgotten until the 1980s, and still today are not really known by a general audience. To summarise these theories in a semi-obscure way that might become clear upon a second reading: it’s a sharp shock followed by a self-fulfilling prophecy.

In 1929, in Brooklyn, New York, there lived a physician called Robert Kingman. As Kenton Kroker documents in his book The Sleep of Others and the Transformation of Sleep Research, Kingman saw patients who presented with significant trouble sleeping, and he developed a particular opinion about what was causing sleeplessness in these patients. This opinion would be paralleled more than sixty years later in modern theories of insomnia. The following is an excerpt from The Sleep of Others.

[Kingman] observed that ‘the dangers of insomnia have been so widely and generally exaggerated that the average person becomes little short of panic stricken when sleeplessness attacks him.’ … Insomnia had become such a well-publicised phenomenon, he argued, that the fear of insomnia had itself become a cause of insomnia…Kingman presented a picture of the insomniac as someone who suffered from a sort of circular madness, in which modern media had so exaggerated the problem of insomnia that, for many people, the normal rhythms of sleep and wakefulness had become distorted by excessive emotion.

Recognising the physiological need for sleep, people experienced an overstated desire for it, which was counterbalanced by a pathological fear of continued wakefulness. This battle between two ‘complexes’ ultimately left its victims lying in bed, hopelessly awake.

Sleep came only when the insomniac resigned himself or herself to fate, declaring ‘What’s the use of trying any longer; there’s no time for a decent sleep now anyway.’ At this point (which Kingman thought usually occurred around five o’clock in the morning), sleep would finally come.

Kingman could not provide a solution to this dilemma, merely advising his patients not to stay in bed after the sun rises, or for any longer than eight or nine hours. Still, it is uncanny how similar this passage is to a highly influential model of insomnia, the diathesis-stress-response model.

This model was developed by sleep researcher Arthur Spielman in 1986, almost 60 years after Kingman’s initial comments. Spielman proposed that there are a number of barriers which interfere with the ability to sleep.

Initially, there are predisposing factors. This includes anything that makes you initially more likely to develop insomnia, such as biological and genetic traits, personality traits, a tendency toward anxiety, and social/environmental history.

Next come precipitating factors, which are the “trigger” for initial insomnia. These could include a stressful working environment, a death in the family, or a mental illness.

Finally you have  perpetuating factors, which are developed as coping mechanisms but actually act to maintain insomnia. These include spending huge amounts of time in bed, irregular sleep and wake times, drinking lots of caffeine and/or alcohol, rumination, anxiety over the potential inability to function the next day and expectation of a bad night’s sleep. As you can see in the figure above, precipitating factors decline over time, but perpetuating factors actually grow over time, thus maintaining the insomnia. Spielman and his colleague Paul Glovinsky write in 1991:

As events fade, or stress is adapted to, the insomnia wanes; however, in some individuals the self attribution “I am an insomniac,” the expectation of a bad night, the anticipation of the discomfort of a sleepless night, or the dread of daytime deficits is in and of it self arousing. The subsequent sleep disturbance completes the vicious cycle: anxious worry —> sleep disturbance —> anxious worry —> sleep disturbance —> anxious worry —> sleep disturbance… Effective treatments of any type will help interrupt this cycle. 

Sound familiar? Perpetuating factors are clearly what Kingman claimed to see in his patients back in 1929.

Kingman’s comments, Spielman’s model, and the quote by Spielman and Glovinsky, all have one thing in common: they all explicitly or implicitly refer to the effect of hyperarousal on sleeplessness.

In the book Insomnia: Psychological Assessment and Management, Doctor Charles Morin reviews the evidence for the effect of physiological, cognitive, and emotional arousal on insomnia. In terms of physiological arousal, studies have indicated that insomniacs, compared to good sleepers, have a faster heart rate, and have a higher body temperature both during the day and at night. Incredibly, insomniacs are also rated as no more sleepy during the day than normal sleepers, despite having much more disrupted sleeping patterns at night.

However, individuals with insomnia blame cognitive arousal ten times more frequently than physiological arousal as the cause of their sleeplessness. Experimental manipulations have also hinted that cognitive activity (i.e., thoughts) may be related to time taken to get to sleep. For example, participants who were good sleepers were informed that they would have to present a speech after taking a nap. This group took significantly longer to fall asleep than a second group who had not been told to give a speech. Additionally, another study gave good sleepers and insomniacs an arithmetic task to do before bed, which resulted in a delayed sleep onset in good sleepers, but a much quicker sleep time in insomniacs. The implication here is that for the insomniacs, a non-sleep-related cognitive task might direct attention away from sleep-related cognitions and thus reduce intrusive thoughts.

Research has also been published on the effect of emotional arousal on sleeplessness. The content of insomniacs’ cognitions have been found to be more negatively toned than for good sleepers. And thoughts that are negative (e.g., dreading a bad night’s sleep) are associated with more severe difficulties. Finally, insomniacs tend to have elevated rates of neuroticism, a measure which indexes anxiety, worry, and general low emotional stability. Individuals higher on neuroticism may have a stronger emotional response to poor sleep.

Of course, all of these types of arousal can influence one another in a bidirectional fashion. In Morin’s own model of insomnia, the perpetuating factors (physiological, cognitive and emotional arousal, maladaptive sleep habits, excessive caffeine, fatigue, performance impairments) all influence each other to maintain and heighten insomnia. It’s like some obscene symphony.

As I researched this information, I have to admit that I found something comforting about Morin’s theory of arousal. Here was a sign that the issue wasn’t a deep-seated experience from my childhood, or an unconscious desire that I had to untangle. It was simply my thoughts, my emotions, my hyperarousal. In a sense, I was safe, and the terror I had felt was nothing but the boogeyman of my own mind.

And this understanding is, essentially, how my own insomnia ended, although with less analytical searching of Pubmed and PsycInfo and more wandering through my local library. There was a book that made me feel safe. This book. I felt safe, and I started to sleep.

Sleep cannot be produced by force of will. All we can do is position ourselves to let it overtake us, like a surfer waiting for a wave.

— Spielman and Glovinsky in Hauri (1991), Case Studies in Insomnia

Part 2 (Psychological Treatments for Insomnia) will be coming soon!