Insomnia is a clinical condition characterized by persistent difficulty initiating sleep, maintaining sleep, or early-morning awakening with associated daytime impairment, occurring despite adequate opportunity for sleep. In the presented context, the phrase “can’t sleep” maps most directly to insomnia, a syndrome with multifactorial neurobiological drivers that can be intensified by stress, cognitive arousal, and irregular circadian demands.
Insomnia can be categorized as transient (days to weeks), short-term (up to ~3 months), or chronic (≥3 nights per week for ≥3 months) and may coexist with anxiety, depression, post-traumatic stress disorder, substance use disorders, or medical comorbidities such as hyperthyroidism, pain syndromes, and sleep-related breathing disorders. Clinically, the hallmark is the downstream impairment: fatigue, reduced attention and executive function, mood lability, decreased reaction time, and impaired emotional regulation. Chronic insomnia is also associated with increased cardiometabolic risk and dysregulation of stress physiology.
Mechanistically, insomnia involves hyperarousal of the central nervous system and dysregulation across sleep-wake circuitry. At the neurochemical level, elevated cortical and limbic activation can increase cortical thickness/heightened sensory processing and perpetuate a state of vigilance. The hypothalamic-pituitary-adrenal (HPA) axis may be overactive, leading to higher cortisol rhythms or flattened diurnal variation, which can interfere with sleep onset and maintenance. Circadian misalignment—whether from shift work, late-night cognitive tasks, or stress-induced circadian delay—impairs melatonin secretion and sleep pressure accumulation.
Cognitive mechanisms are particularly relevant when insomnia is driven by rumination or perceived responsibility. Cognitive arousal and maladaptive beliefs about sleep can create a self-perpetuating cycle: poor sleep increases anxiety about further sleep loss; this anxiety elevates sympathetic activation, which in turn worsens sleep. Behavioral conditioning also matters: spending extended time awake in bed can condition the bed to become a cue for wakefulness rather than sleep. This is commonly conceptualized in the cognitive-behavioral model of insomnia (CBT-I), which integrates stimulus control and cognitive restructuring.
Risk factors include high psychosocial stress, irregular schedule, evening screen exposure, caffeine or nicotine use, and alcohol use (which may reduce sleep onset latency but fragments sleep later). Medical causes must be considered, including restless legs syndrome, sleep apnea, pain, gastroesophageal reflux, medication effects (e.g., corticosteroids, stimulants, some antidepressants), and neurologic conditions. A careful history should assess onset pattern, sleep duration, awakenings, napping, daytime consequences, and any circadian preference changes.
Diagnosis is clinical and based on symptoms and their impact. Tools such as sleep diaries and actigraphy can support the assessment and track treatment response. Screening instruments like the Insomnia Severity Index quantify symptom burden. Polysomnography is not routinely required but is indicated when there is suspicion of comorbid sleep apnea, periodic limb movement disorder, or complex treatment-resistant cases.
Evidence-based management centers on CBT-I as first-line therapy. CBT-I typically includes stimulus control (using bed only for sleep and sex; getting out of bed if unable to sleep), sleep restriction therapy (limiting time in bed to consolidate sleep while monitoring for daytime impairment), sleep hygiene (reducing caffeine late in the day, consistent wake time, light management), cognitive therapy targeting maladaptive beliefs, and relaxation training. Pharmacologic options may be considered short-term for severe insomnia or while CBT-I is initiated. These include non-benzodiazepine hypnotics (“Z-drugs”), orexin receptor antagonists, and—depending on patient factors—selected sedating antidepressants or antihistamines. Clinicians aim to minimize adverse effects such as next-day sedation, falls risk, dependence, tolerance, and complex sleep behaviors.
Orexin biology offers mechanistic insight: orexin/hypocretin promotes wakefulness, and antagonism can facilitate stable sleep without the same degree of GABAergic dependence risk as some traditional sedatives. Nevertheless, medication selection should account for comorbidities, drug interactions, and safety concerns such as impaired driving performance.
Long-term success requires addressing perpetuating factors: treating underlying anxiety or depression, managing pain, and correcting circadian rhythm disruptions. Emerging adjuncts include mindfulness-based interventions, light therapy for circadian delay, and structured behavioral interventions for stress-related hyperarousal.
When insomnia is present in high-stress settings, the clinician should also evaluate for burnout and chronic stress-related psychiatric conditions. Escalation criteria include suicidal ideation, severe functional impairment, or the emergence of parasomnias or red-flag medical symptoms.
In summary, insomnia is a common but complex disorder driven by hyperarousal, cognitive-behavioral conditioning, stress physiology, and circadian dysregulation. CBT-I remains the most supported first-line treatment, with pharmacotherapy reserved for targeted, time-limited use. A comprehensive assessment for medical sleep disorders and substance/medication contributors is essential for durable recovery. Source: [Joel Pollak/X]
Joel Pollak: Jake Sullivan can’t sleep, he says. Not because of his role in the Russia collusion hoax, but because he thinks Biden could have done more to restrain Netanyahu. No such thoughts, apparently, about how Biden enabled Hamas by restoring aid Trump had ended.. #breaking
— @joelpollak May 1, 2026
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