Insomnia is characterized by difficulty with initiating or maintaining sleep, or awakening too early.[1] It is the most common sleep disorder in the United States, affecting about 1/3 of adults at some point in their lives. Approximately 10% of those with symptoms experience persistent insomnia.[2]

Affected individuals may experience daytime fatigue, inability to concentrate, irritability, anxiety, depression, and forgetfulness and may have an increased risk of automobile accidents.[3] Further, these patients often have associated psychosomatic symptoms, such as nonspecific aches and pains, as well as increased risk of suffering from hypertension and cardiovascular diseases.[4]

The International Classification of Sleep Disorders, 3rd Edition (ICSD-3), classifies insomnia as short-term (also called stress-related or transient), which signifies a duration of less than 3 months; chronic, with episodes occurring at least 3 times per week for longer than 3 months; and “other” for patients who do not meet the criteria for the other two.[1]

Sleep impairment lasting only a few days to a few weeks may result from lifestyle changes, such as jet lag, change in work shift, acute illness, and stressful life events. Taking medications with stimulant properties and use of or withdrawal from drugs or alcohol may also contribute to impaired sleep. Insomnia lasting more than a few weeks may be associated with chronic drug or alcohol abuse, medical disorders, or psychiatric disorders, or it may result from primary sleep disorders, such as restless legs syndrome and sleep apnea.

Risk Factors

Insomnia occurs disproportionately in women and in people who have disruptions in interpersonal relationships.[2] Previous episodes and family history of insomnia are also associated with an increased risk. Additional risk factors include:

Age. Prevalence increases with age.

Psychiatric comorbidities. Sleep disturbances are more common in patients with mood disorders, such as major depression, dysthymia, and bipolar affective disorder, as well as in those with anxiety disorders, schizophrenia, and acute stress.[2] Additionally, a predisposition to easy arousal, sleep reactivity trait (exaggerated sleep disruption as a result of stressful events), or maladaptive behaviors and attitudes regarding sleep may contribute to insomnia.

Drugs and alcohol. Use of even small quantities and/or withdrawal may be associated with impaired sleep.

Stimulants. Use of medications and other substances with stimulant properties is a common cause of insomnia. These include caffeine, theophylline, thyroxine, corticosteroids, bronchodilators, antidepressants, and methylphenidate.[5]

Nicotine use and withdrawal are associated with sleep fragmentation. Insomnia is also a frequent side effect of nicotine patches and of bupropion, an antidepressant often used for smoking cessation.[6][7]

Diagnosis

History and physical examination, including a sleep history and psychiatric history, should include evaluation of sleep habits, sleep environment, drug and alcohol use, medical and medication history, and family medical history. It is often helpful to interview the patient’s bed partner and to ask the patient to keep a sleep log.

According to the ICSD-3, the diagnosis can be established when the following 4 criteria are met: Patient has trouble initiating sleep, difficulty maintaining sleep, or a tendency to awaken early; it occurs despite having adequate opportunity and time to sleep; patient complains of difficulty with daily functioning due to lack of sleep; and the sleep problems are not due to other sleep disorders.[1]

Laboratory testing may identify medical disorders (such as endocrinopathies) that can contribute to sleep difficulties.

Sleep testing is used in some patients. Polysomnography can identify sleep-related breathing disorders.[8] Multiple sleep latency testing evaluates for inappropriate daytime sleepiness due to narcolepsy. Actigraphy measures motion during sleep.

Treatment

Underlying medical, surgical, or psychiatric disorders should be treated as appropriate.

Proper sleep hygiene is an often-overlooked high-yield, low-risk means of helping patients with insomnia. The essentials of this are to keep a regular sleep schedule, avoid excess use of light-emitting screens shortly before bed, exercise regularly, avoid caffeine, and limit alcohol and cigarettes, particularly near bedtime.[6]

Exercise has been shown to improve total sleep duration, sleep onset latency, and global sleep quality.[9] However, timing is important. Physical activity early in the day is generally not associated with improved sleep, and exercise taken shortly before bedtime can delay sleep onset.[6]

Nonpharmacologic Therapy

Maladaptive behaviors or thought patterns can sustain insomnia symptoms, independent of the initial underlying cause. Cognitive-behavioral therapy for insomnia addresses these problems and has proven more effective over the long term than pharmacologic therapy.[10] Although additional evidence from controlled trials is needed, cognitive-behavioral therapy was also found effective for insomnia related to a spectrum of medical and psychiatric conditions (e.g., cancer, chronic pain, human immunodeficiency virus [HIV], depression, posttraumatic stress disorder, alcoholism, bipolar disorder, eating disorders, generalized anxiety, and obsessive compulsive disorder).[11]

Disruptions of circadian rhythm can be treated with phototherapy (bright lights used at bedtime for those who become sleepy too early in the evening or on awakening for those who stay up too late) or chronotherapy (a stepwise advance of the bedtime and waking time later and later).

Warm-bath immersion to the mid-thorax, with water temperature at 40-41ºC, for 30 minutes in the evening was shown to increase slow-wave sleep (deep sleep) in healthy elderly women with insomnia.[12]

Pharmacologic Therapy

Drug classes often used in the treatment of insomnia include benzodiazepines (e.g., temazepam, lorazepam, flurazepam). Currently, these medications are rarely used to treat insomnia because they cause rebound insomnia and suppress stage 3-4 deep sleep, which are the restorative stages. More commonly used drugs include the nonbenzodiazepine “z drugs” (e.g., zolpidem, zaleplon, and eszopiclone), antihistamines (e.g., diphenhydramine), antidepressants (e.g., amitriptyline, trazodone), and melatonin agonists. There are no reliable predictors of response to any insomnia therapy, and drugs often do not improve the quality of sleep. In fact, many can cause next-morning sleepiness and impairment.

Among the warnings for zolpidem are abnormal thinking, behavioral changes, and complex behaviors: These may include “sleep-driving” and hallucinations. Patients may walk, eat, or do other things while under the influence of the medication, with no subsequent memory of the event. Additionally, long-term use of some of these medication classes has been associated with an increased risk of dementia and all-cause mortality.[13]

Low-dose doxepin is the only antidepressant approved by the Food and Drug Administration (FDA) for insomnia. Ramelteon, a melatonin-receptor agonist, has been approved by the FDA for insomnia treatment, but evidence of efficacy is weak.
Benzodiazepines are relatively contraindicated in women who are pregnant or breastfeeding and in patients with renal, hepatic, or pulmonary disease. They should be used with caution in patients who consume alcohol or who are prescribed other sedating medications, including any opioid or opioid derivative. In general, they are poor choices for chronic use. Long-term use has been associated with increased risk of falls, motor vehicle accidents, and dementia.

Orexin receptor antagonists (e.g., suvorexant) are a new class of drugs developed for treatment of insomnia, but their clinical utility is yet to be determined.[14]

Nutritional Considerations

Healthy natural sleep should follow as a consequence of the normal physical and mental fatigue people typically experience during an active life. However, sleep deprivation is increasingly common, and it may be attributed to poor lifestyle choices. Chief among these are excesses of screen time, caffeine and alcohol, and inadequate physical activity. Steps to be considered are discussed below.

Avoiding alcohol. Small amounts of alcohol (e.g., 1 standard drink per evening) may not have negative effects on sleep for most people, but tolerance to its sedative effects can develop quickly, making it less useful for inducing sleep.[15] Alcohol may increase the risk of insomnia by several mechanisms. Excess or chronic alcohol intake (i.e., alcohol abuse or dependence) can decrease REM-phase sleep in a dose-dependent manner.[16] Alcohol consumption in the amount of 0.5 or 1.0 g/kg (3-6 standard drinks) also causes disruption of normal circadian rhythms, probably through inhibiting melatonin secretion by more than 40%.[17][18][19] Alcohol may cause rebound excitation through an increase in the number or sensitivity of receptors for glutamate, an excitatory neurotransmitter.[18] As alcohol is metabolized, it produces aldehydes, which can have stimulating effects several hours after ingestion.[20] Alcohol hangover, an excitatory state despite its reputation as one involving malaise, may be related to acetaldehyde.18 Alcohol may also increase the level of histamine, a known excitatory neurotransmitter, in the central nervous system.[21]

Limiting caffeine.[20] Caffeine produces varying effects in individuals. In middle-aged persons drinking up to 7 cups of coffee per day (600 mg) and in subjects to whom caffeine was acutely administered, few or no effects on sleep were noted.[6][22] However, some persons are affected by caffeine unknowingly when it is consumed in over-the-counter medications.[23] Individual differences in caffeine effects appear to be related to differences in clearance from the bloodstream.[24] In persons with caffeine-related insomnia, caffeine from all sources, including cola beverages, tea, chocolate, and medications, must be considered.[25]

Avoiding milk if intolerant. Infants with cow’s milk allergy have been found to have frequent arousals during sleep, shorter sleep cycles, and larger amounts of non-rapid eye movement (NREM) sleep with easy awakening. After elimination of cow’s milk for several weeks, a significant decrease in the number of arousals occurred, while total sleep time and time spent in NREM2 and NREM3 sleep all increased significantly.[26] Further study by the same researchers using double-blind, crossover methodology also found normalization of sleep in a group of children < 5 years of age.[27]

Carbohydrates. Tryptophan and 5-hydroxytryptophan are precursors of melatonin through the serotonin pathway and have some efficacy in the treatment of insomnia.[20] Neither can be recommended, however, due to previous findings of contamination with a compound that has caused eosinophilia-myalgia syndrome.[28] The passage of tryptophan across the blood-brain barrier depends on the extent to which it must compete with other amino acids. In this context, carbohydrate-rich foods may prove helpful. Over the short run, they stimulate the release of insulin, which reduces blood concentrations of competing amino acids, fostering tryptophan’s passage across the blood-brain barrier.[29]

Avoiding over-the-counter weight loss products. Products that contain ephedra alkaloids (e.g., Ma huang) in combination with caffeine have been increasingly used for weight loss, but they have been found to cause insomnia when compared with a placebo.[30]

Rectifying poor iron status. Insomnia is a frequent problem in patients with restless legs syndrome. Iron deficiency, even at levels insufficient to cause anemia, has been associated with this syndrome, and iron-deficiency anemia is also associated with insomnia in pregnancy.[31] Although more research is needed, available evidence implicates low brain iron concentration caused by the inadequate transportation of iron from the blood to the central nervous system as a cause of dopaminergic dysfunction in these patients.[32] Iron supplementation was found effective for improving insomnia in teens with low iron stores.[33]

The following supplements are under investigation for their roles in treating insomnia:

Melatonin. Disturbances in circadian rhythm and melatonin production are more common among shift workers and elderly individuals, and evidence suggests that these disturbances can be partly ameliorated by supplemental melatonin. Although melatonin supplementation appears to be safe and effective for treating delayed sleep phase syndrome, most evidence does not support its effectiveness for the majority of primary and secondary sleep disorders.[34] Melatonin is found in some plant foods (e.g., tomatoes, olives, barley, rice, walnuts), and increased vegetable consumption raises serum levels though the clinical significance has not been fully evaluated.[35][36]

Valerian. Valerian’s sedative and hypnotic effects probably result from increases in the secretion of the neurotransmitter γ-aminobutyric acid (GABA) and inhibition of its uptake. Valerian binds to the same receptors as benzodiazepines but with less efficiency and milder effects; this difference may account for the lack of residual morning sedation that is a common side effect of hypnotics.[37] Doses of 400-500 mg/day have been found to significantly decrease sleep latency and improve subjective sleep quality. However, not all studies have found valerian to be effective.[38][39] In addition, caution is warranted to avoid side effects, which may include headache, hangover, paradoxical stimulation, restlessness, and cardiac disturbances, as well as potentially dangerous interactions with barbiturates, benzodiazepines, opiates, and alcohol.[38]

Orders

See Basic Diet Orders chapter.

What to Tell the Family

Acute or chronic insomnia can be caused by several factors, the most common involving caffeine, alcohol or stimulating substance intake, lack of exercise, psychosocial stressors, and poor sleep hygiene. Family members can often help the patient alter habits relating to these contributors. Chronic insomnia can adversely affect quality of life and should be discussed with a physician to rule out underlying medical or psychiatric etiologies.

References