Insomnia: What It Is, What Causes It, and How It Is Treated

Almost everyone sleeps badly on occasion. A stressful day, a noisy environment, an anxious night before an important event — these produce acute sleep disruption that resolves when the trigger passes. Insomnia becomes a clinical condition when sleep difficulty becomes persistent, causes distress or impaired daytime functioning, and occurs despite adequate opportunity and circumstances for sleep.

The defining feature of insomnia is not just poor sleep — it is poor sleep that the person could not control even if the external circumstances were ideal.

Defining Insomnia

Clinical insomnia disorder, as defined in the Diagnostic and Statistical Manual (DSM-5) and the International Classification of Sleep Disorders (ICSD-3), requires:

• Difficulty initiating sleep, maintaining sleep, or waking too early, with inability to return to sleep
• The sleep problem causes clinically meaningful distress or impairment in daytime functioning
• Occurs at least three nights per week
• Has been present for at least three months (for chronic insomnia; acute insomnia can be shorter)
• Occurs despite adequate opportunity and circumstances for sleep
• Is not better explained by another sleep disorder, substance use, or medical condition

That last criterion — adequate opportunity for sleep — is important. Someone who works a schedule that only permits four hours in bed is not insomniac; they are sleep-deprived. Insomnia specifically involves the inability to sleep when the conditions are appropriate.

Types of Insomnia

The Hyperarousal Model: Why Chronic Insomnia Persists

The most widely supported scientific model of chronic insomnia is the hyperarousal model, developed and refined through the work of researchers including Arthur Spielman, Colin Espie, and Allison Harvey. It explains insomnia not as a problem of insufficient sleep drive, but as a problem of excessive arousal at the times when sleep is attempted.

People with chronic insomnia show elevated physiological arousal compared to good sleepers — higher core body temperature, higher cortisol, higher heart rate and metabolic rate during sleep, more high-frequency EEG activity (which suppresses slow-wave sleep), and higher overnight levels of norepinephrine. This is not just anxiety about sleep; it is a measurable physiological state.

The three-factor model (also called the Spielman model or "3-P model") explains how this develops:

• Predisposing factors: Biological or psychological traits that increase vulnerability — high trait anxiety, tendency toward hyperarousal, genetic variants affecting sleep regulation.
• Precipitating factors: The initial trigger — a stressful event, illness, life change, shift in schedule.
• Perpetuating factors: The behaviors and thought patterns that keep insomnia going after the precipitant has passed — spending too much time in bed, napping to compensate, sleep-related worry, monitoring the clock, avoiding activities for fear of tiredness.

The therapeutic implication is important: CBT-I targets the perpetuating factors, not the original trigger — which is usually irrelevant to the ongoing insomnia by the time treatment occurs.

The Role of Thought Patterns

Cognitive factors are central to chronic insomnia. Allison Harvey's cognitive model identifies several processes that perpetuate wakefulness:

Excessive worry about sleep: Ruminating about sleep quality, sleep's importance, and the consequences of poor sleep increases arousal and makes sleep harder. This creates a self-fulfilling cycle — the harder you try to sleep, the less you can.

Selective attention to sleep-related threat: People with insomnia become hypervigilant to internal and external signals that might mean sleep is at risk — clock-watching, body-scanning for signs of arousal, monitoring for intrusive thoughts.

Misperception of sleep: Many people with insomnia significantly underestimate how much they actually slept. EEG studies routinely find that people who report sleeping only four hours actually slept six. This does not mean the distress is not real — subjective sleep quality matters — but it does mean that sleep misperception itself becomes a problem to address.

Safety behaviors: Behaviors adopted to protect sleep that actually maintain hyperarousal — going to bed earlier, canceling evening plans to "save energy," napping aggressively, avoiding exercise in case it causes wakefulness. These behaviors signal to the nervous system that sleep is something to be managed with great effort, which increases arousal.

CBT-I: The Gold Standard Treatment

Cognitive behavioral therapy for insomnia (CBT-I) is recommended as the first-line treatment for chronic insomnia by clinical guidelines in the United States, United Kingdom, and Europe — ahead of medication. Multiple meta-analyses demonstrate that CBT-I produces larger and more durable improvements than sleeping pills, with no rebound insomnia when treatment ends.

CBT-I typically involves five to eight sessions with a trained therapist and combines several components:

Sleep Medications: What They Do and Don't Do

Sleep medications are widely prescribed, but they do not address the perpetuating factors that sustain chronic insomnia. They can be appropriate for short-term acute insomnia or as a bridge during CBT-I, but long-term use involves trade-offs that are worth understanding.

Benzodiazepines and Z-drugs (zolpidem, zaleplon, eszopiclone): These are GABA-A receptor modulators that produce sedation. They reduce time to fall asleep and improve some measures of sleep continuity. However, they suppress deep sleep (N3), create tolerance over weeks, carry dependence risk, and produce rebound insomnia when discontinued. They also have cognitive side effects — next-day grogginess and, with longer use, impacts on memory — that are more serious than often acknowledged, particularly in older adults.

Orexin receptor antagonists (suvorexant, lemborexant): A newer class of sleep medication that works by blocking the wake-promoting orexin system rather than broadly suppressing the nervous system. Generally considered to have a better side-effect profile than benzodiazepines, with less next-day impairment and lower dependence risk — though long-term data are still accumulating.

Low-dose doxepin: FDA-approved for sleep maintenance insomnia. At very low doses (3–6mg), it selectively blocks histamine receptors, prolonging sleep without the dependence concerns of benzodiazepines.

Antihistamines (diphenhydramine — the active ingredient in most over-the-counter sleep aids): Widely available but poorly suited to ongoing use. Tolerance develops within a few nights, and the anticholinergic effects — dry mouth, constipation, next-day cognitive impairment — are more significant than many people realize, particularly in older adults where anticholinergic burden is associated with cognitive decline.

A Practical Path Forward

If you have struggled with sleep for more than three months and it is affecting your daytime functioning, the most evidence-supported path is:

1. See a clinician to rule out an underlying sleep disorder (particularly sleep apnea, which often presents with insomnia-like complaints) or contributing medical condition.
2. Pursue CBT-I — either with a therapist trained in CBT-I or through a validated digital program.
3. If using medication short-term, choose one with a lower dependence profile and discuss a clear plan for discontinuation with your prescribing clinician.
4. Approach sleep as a biological function rather than a performance. The effort to sleep is counterproductive. The goal of CBT-I is largely to stop trying so hard.