Can’t sleep? Tips on how to sleep better and faster

Can't sleep pips on how to sleep better and faster

The prevalence of insomnia is skyrocketing. Population based estimates indicate that about 30% of adults complain they can’t sleep. Sleep medicine has developed strategies and tips on how to sleep better and faster. There are a number of alternative, effective nonpharmacologic therapies that can help patients who can’t sleep at night.

Common insomnia symptoms include:

  • difficulty falling asleep
  • trouble staying asleep, waking up in the middle of the night and having difficulty going back to sleep
  • waking up too early with the inability to return to sleep
  • interrupted or broken sleep

Psychological factors, such as worry about not being able to sleep can influence and even perpetuate sleep problems.

What is insomnia and why you can’t sleep

Insomnia is a symptom with numerous possible causes but it can also be a syndrome or a disease. This is the case of primary insomnia, which is unrelated to any physical or mental comorbidity, but is characterized by a set of symptoms, a defined disease course, and a predictable response to treatment.

Chronic insomnia is present for at least a month, as opposed to acute or transient insomnia, which may last days to weeks.

Insomnia symptoms are a feature of other sleep disorders such as:

  • sleep-related breathing disorders
  • circadian rhythm disorders
  • sleep-related movement disorders (restless legs or periodic limb movements during sleep)
  • parasomnias (nightmare disorder and sleep-related breathing disorder)

Risk factors for insomnia:

  • increasing age
  • female sex
  • comorbid (medical, psychiatric, sleep, and substance use) disorders
  • shift work
  • possibly unemployment and lower socioeconomic status

The course of insomnia is often chronic, with studies showing persistence in 50% to 85% of individuals over follow-up intervals of one to several years.

The classification of sleep disorders includes insomnia:

Insomnias
Sleep Related Breathing Disorders
Hypersomnias of Central Origin
Circadian Rhythm Disorders
Parasomnias
Sleep Related Movement Disorders

Different types of insomnia are also described below:

I. Primary insomnia:

1.Psychophysiological insomnia- characterized by:

  • heightened arousal (physiological, cognitive, or emotional, characterized by muscle tension, “racing thoughts,” or heightened awareness of the environment)
  • learned sleep-preventing associations (increased concern about sleep difficulties and their consequences, leading to a “vicious cycle” of arousal, poor sleep, and frustration)
  • maladaptive conditioned response in which the patient learns to associate the bed environment with heightened arousal rather than sleep;
  • onset often associated with an event causing acute insomnia, with the sleep disturbance persisting despite resolution of the precipitating factor

2. Paradoxical insomnia- characterized by a marked mismatch between the patient’s description of sleep duration and objective polysomnographic findings

3. Idiopathic insomnia: onset in infancy or early childhood and no or few extended periods of sustained remission; it is not associated with specific precipitating or perpetuating factors.

II. Secondary insomnia

  1. Behavioral insomnia of childhood: the result of inappropriate sleep associations or inadequate limit setting
  2. Adjustment (acute) insomnia: associated with a specific stressor (psychosocial, physical, or environmental disturbances). The sleep disturbance has a relatively short duration (days-weeks) and is expected to resolve when the stressor resolves.
  3. Inadequate sleep hygiene: associated with lifestyle habits that are inconsistent with good sleep quality. These activities produce increased arousal or directly interfere with sleep
  4. Insomnia due to mental disorder: an active psychiatric disorder, such as anxiety or depression
  5. Insomnia due to medical condition such as restless legs syndrome, chronic pain, nocturnal cough or dyspnea, or hot flashes
  6. Insomnia due to drug or substance: the direct effects of over-the-counter and prescription medications and substances, and their effects upon withdrawal may impact sleep and even cause insomnia. When the substance is stopped, and after discontinuation effects subside, the insomnia is expected to resolve.

Common Contributing Substances:
Antidepressants: SSRIs (fluoxetine, paroxetine, sertraline, citalopram, escitalopram, fluvoxamine), venlafaxine, duloxetine, monoamine oxidase inhibitors
Stimulants: caffeine, methylphenidate, amphetamine derivatives, ephedrine and derivatives, cocaine
Decongestants: pseudoephedrine, phenylephrine, phenylpropanolamine
Narcotic analgesics: oxycodone, codeine, propoxyphene
Cardiovascular: β-Blockers, α-receptor agonists and antagonists, diuretics, lipid-lowering agents
Pulmonary: theophylline, albuterol
Alcohol

The most important is to recognize and treat comorbid conditions that commonly occur with insomnia, and to identify and modify behaviors and substances that impair sleep.

The etiology of insomnia is typically multifactorial.

The fundamental issue is whether there is any indication of other primary sleep disorders or comorbid medical, neurologic, or psychiatric conditions that might contribute to the insomnia complaint. The majority of chronic insomnia is comorbid with another medical, substance, or psychiatric problem. Consideration should be given to commonly undiagnosed disorders such as depression, anxiety disorders, or occult medical problems (thyroid disease).

1. Medical Conditions Commonly Comorbid with Insomnia

  • Comorbid sleep disorders: circadian rhythm sleep disorders, parasomnias, sleep apnea, restless legs syndrome, periodic limb movement.
  • Neurologic: peripheral neuropathy, headache, stroke, seizure disorders, traumatic brain injury, dementia, Parkinson’s disease, chronic pain disorders, neuromuscular disorders.
  • Cardiovascular: angina, congestive heart failure, dyspnea, dysrhythmias
  • Reproductive: pregnancy, menopause, menstrual cycle variations
  • Pulmonary: asthma, emphysema, laryngospasm, chronic obstructive pulmonary disease
  • Digestive: irritable bowel syndrome, peptic ulcer, reflux, cholelithiasis, colitis.
  • Genitourinary: nocturia, incontinence,enuresis, benign prostatic hypertrophy, interstitial cystitis
  • Arthritis and other musculoskeletal disorders (fibromyalgia, Sjögren syndrome, kyphosis)
  • Endocrine disorders: diabetes mellitus, hypothyroidism, hyperthyroidism. Thyroid disease occurs when the thyroid gland either produces too much (hyperthyroidism) or too little (hypothyroidism) thyroid hormone. If left untreated, this health problem can lead to severe sleep disturbances. The most commonly used methods for diagnosing a thyroid condition are blood tests along with radiologic screening. Blood tests: Thyroid Stimulating Hormone (THS) – plays a key role in regulating thyroid hormone production and helps determine how well your thyroid gland is functioning and Free Thyroxine (T4) concentration
  • Other: allergies, rhinitis, sinusitis, bruxism, alcohol and other substance use/withdrawal

2. Psychiatric Conditions Commonly Comorbid with Insomnia

  • Mood disorders: Major depressive disorder, Dysthymic disorder, Bipolar disorder, Seasonal affective disorder
  • Anxiety disorders: Generalized anxiety disorder, Posttraumatic stress disorder (nightmares and flashbacks of the trauma while trying to sleep), panic disorder, obsessive compulsive disorder
  • Psychotic disorders: schizophrenia, schizoaffective disorder
  • Attention-deficit/hyperactivity disorder
  • Eating disorders: Bulimia nervosa, Anorexia nervosa
  • Adjustment disorder
  • Personality disorder
  • Bereavement, stress
  • Amnestic disorders: alzheimer disease, other dementias

Insomnia is an important mechanism in the multifactorial cause and maintenance of psychiatric disorders. When present, should always be targeted in treatment. The combined approach is superior to monotherapy, having better outcomes for both depression and insomnia. Patients who are treated for both the depression (with an antidepressant) and the insomnia (with either a hypnotic or cognitive behavior therapy for insomnia) have better outcomes than patients treated only for depression.

In comorbid insomnias, treatment begins by addressing the comorbid condition. It was widely assumed that treatment of these comorbid disorders would eliminate the insomnia. However, it has become increasingly apparent that over the course of these disorders, numerous psychological and behavioral factors develop which perpetuate the insomnia problem.

Excessive time spent awake in bed is one of the most common perpetuating factors. This behavior is often associated with “trying hard” to fall asleep and growing frustration and tension in the face of wakefulness. Thus, the bed becomes associated with a state of waking arousal.

The 3P behavioral model of insomnia is based on the interaction of three factors: predisposing, precipitating and perpetuating factors. It is the first fully articulated model of insomnia and delineates how insomnia occurs acutely and how acute insomnia becomes chronic and self-perpetuating.

The predisposing factors or basic sleep drive, represent a constant vulnerability for insomnia. Predisposing factors can be:

  • biological (regularly elevated cortisol, altered neurotransmission, trait arousal, genetic susceptibility),
  • psychological (tendency to worry, ruminative personality, perfectionistic personality traits; Perfectionism is a personality profile comprising doubt, extremely high standards and fear of making mistakes)
  • social (work schedule incompatible with sleep schedule).

Some individuals may have a strong sleep drive and are always far from the sleeplessness threshold. Other people have a weak sleep drive and are close to the sleeplessness threshold even under the best circumstances. Any small event can trigger their insomnia, and sometimes they will be sleepless for no apparent reason. Unfortunately, this is a lifelong problem arising from a weak homeostatic drive or an overreactive autonomic nervous system. Among the predisposing factors, the familial component seems to play a significant role.

Precipitating factors, such as stressful life events (occupational stress, health problems, a grief reaction) trigger the acute onset of insomnia. Under normal circumstances, the influence of these factors diminishes over time. Therefore, insomnia should be only transient or short-term. Sometimes, even though the precipitating event has long gone, the insomnia remains. If insomnia persists long after the stressful life event has gone, there is something perpetuating the insomnia.

The perpetuating factor serve to maintain the insomnia caused by precipitating factors. This perpetuation factor can be:

  • a grief reaction turned to depression
  • maladaptive sleep practices, which interact with experienced insomnia symptoms and are aimed at coping with the consequences of poor sleep during the day (drinking coffee to improve alertness), or directly trying to increase the probability of “achieving” sleep (extending time in bed)
  • dependence on alcohol to fall asleep

The brain acquires habits through frequent repetition. Therefore, the sooner the perpetuating factor is eliminated, the faster the sleep system will bring the sleep–wake pattern back to normal. The perpetuating factors are typically the targets of treatment.

The identification of predisposing, precipitating, and perpetuating factors of insomnia helps establish a valid diagnosis and creates a comprehensive treatment approach that improves sleep for the long term. Effective clinical management of insomnia must address perpetuating factors that contribute to persistent insomnia such as sleep scheduling factors, conditioning, hyperarousal, and misconceptions about sleep. Addressing the perpetuating factors produces rapid improvement.

Numerous questionnaires related to insomnia and comorbid conditions are available. Here are several of the most widely used and well-validated instruments:

  1. The Insomnia Severity Index (a seven-item, patient completed questionnaire that is applied as a measure of subjective severity)
  2. The Pittsburgh Sleep Quality Index (a 24-item patient-reported measure of global sleep quality and disturbance)
  3. The Dysfunctional Beliefs and Attitudes Scale (identifies maladaptive beliefs that serve to maintain insomnia)
  4. The Epworth Sleepiness Scale (screens for pathologic sleepiness, the presence of which may suggest other sleep related disorders as comorbid factors in the insomnia presentation)
  5. Beck Depression Inventory (for comorbid psychopathology)
  6. State-Trait Anxiety Inventory (for comorbid psychopathology)

Quality-of-life assessments for evaluating the degree of dysfunction and impairment associated with the insomnia condition:

  1. Medical Outcomes Study
  2. Fatigue Severity Scale

At minimum, the patient should complete:

  1. A general medical/psychiatric/medication questionnaire (to identify comorbid disorders and medication use)
  2. The Epworth Sleepiness Scale or other sleepiness assessment (to identify sleepy patients)

Patients with insomnia may develop behaviors that have the unintended consequence of perpetuating their sleep problem:

  • strategies to combat the sleep problem, such as spending more time in bed in an effort to “catch up” on sleep.
  • behaviors in bed or in the bedroom that are incompatible with sleep: talking on the telephone, watching television, computer use, exercising, eating, smoking, or “clock watching.”

Insomnia patients report sensations of being more aware of the environment than are other individuals and may report anticipating a poor sleep hours before bedtime, and become more alert and anxious as bedtime approaches.

Common complaints for insomnia patients are:

  • an average sleep latency >30 minutes
  • wake after sleep onset >30 minutes
  • total sleep time <6.5 hours

Physical sensations and emotions associated with wakefulness (such as pain, restlessness, anxiety, frustration, sadness) may contribute to insomnia.

Sleep and waking problems may lead to restriction of daytime activities, including social events, exercise, or work. Lack of regular daytime activities and exercise may in turn contribute to insomnia.

How to sleep better using psychological and behavioral therapies

Treatment options for insomnia can be divided in three classes of interventions including:

  1. sleeping pills (short-term hypnotic treatment should be supplemented with behavioral and cognitive therapies when possible)
  2. psychological and behavioral therapies
  3. complementary and alternative therapies

Significant advances have been made in the development and validation of nonpharmacologic therapies for insomnia.

Most patients who initiate treatment for insomnia do so without professional consultation and often resort to alternative remedies (herbal supplements) that have unknown risks and benefits.

When insomnia is brought to professional attention (typically to a primary care physician), treatment is often limited to medication. Although hypnotic medications are clinically indicated in selected situations, psychological and behavioral factors are almost always involved in perpetuating sleep disturbances.

Effective management of persistent insomnia must address these perpetuating factors, which can involve:

  • sleep scheduling factors
  • poor sleep habits
  • conditioning (the association of bed with arousal states)
  • hyperarousal
  • faulty beliefs and excessive worrying about sleep
  • inadequate sleep hygiene practices

With solid evidence supporting their efficacy, as well as their relative lack of adverse effects, psychological and behavioral therapies are often the treatments of choice for persistent insomnia being recognized as valid therapeutic approaches.

Specific indications for psychological and behavioral interventions include:

  1. primary insomnia
  2. insomnia occurring in the context of another medical or psychiatric disorder
  3. insomnia in older adults
  4. insomnia associated with chronic hypnotic usage

Psychological and behavioral therapies that have been validated in controlled clinical trials for persistent insomnia include:

  1. sleep restriction
  2. stimulus control therapy
  3. relaxation training
  4. cognitive therapy
  5. sleep hygiene education
  6. cognitive behavior therapy (CBT) which is a combination of those methods

Psychological and behavioral therapies should be the first-line therapy for persistent insomnia. Studies show that 80% of patients with persistent insomnia respond to treatment, and approximately half of them achieve clinical remission.

Treatment produces significant improvements of:

  • sleep quality
  • sleep efficiency
  • sleep-onset latency
  • wake after sleep onset

Sleep hygiene education, although useful, is often insufficient to treat chronic insomnia. It must be distinguished from more formal cognitive behavioral therapies.

Psychological and behavioral therapies remain under utilized by health care practitioners despite the strong evidence supporting their effectiveness.

Sleep hygiene may be described as practicing behaviors that facilitate sleep and avoiding behaviors that interfere with sleep (Riedel, 2000).
Inadequate sleep hygiene is defined in the International Classification of Sleep Disorders (American Sleep Disorders Association,1990) as a “sleep disorder due to the performance of daily living activities that are inconsistent with the maintenance of good quality sleep and full daytime alertness”.
Sleep hygiene education is intended to provide information about health practices (diet, exercise, substance use) and environmental factors (light, noise, temperature) that might either interfere with or promote better sleep. This may also include:

  • basic information about normal sleep, individual differences in sleep needs and changes in sleep patterns with aging; this is useful to help some patients distinguish clinical insomnia from normal (age-related) sleep disturbances
  • general sleep-facilitating recommendations, such as allowing enough time to relax before bedtime, avoiding clock watching, and maintaining a regular sleep schedule.

Some of these instructions overlap with other behavioral procedures.

Instructions for patients:

  1. Avoid stimulants (caffeine, nicotine) for several hours before bedtime. Coffee, different sort of tea, soft drinks and chocolate contain caffeine which is a stimulant that may make it harder for you to sleep well at night. Caffeine stays in your system for several hours (approx. 8 hours) after you consume it. It is recommended to limit caffeine consuption to the equivalent of no more than 3 cups of coffee per day. You should not consume caffeine in the late afternoon or evening hours.
  2. Avoid alcohol around bedtime, because it fragments sleep. Alcoholic beverages may make you fall asleep more easily but they also make sleep to be much more broken and far less refreshing than normal. Therefore, it is not recommended to use much alcohol in the evening or to use alcohol as a sleep aid.
  3.  Exercise regularly (especially in late afternoon or early evening). Try some regular moderate exercise such as walking, swimming, or bike riding. Generally, such exercise performed in the late afternoon or early evening leads to deeper sleep at night. Also, improving your fitness level will likely improve the quality of your sleep. However, avoid exercise right before bed because it may make it harder to get to sleep quickly.
  4. Allow at least a 1-hour period to unwind before bedtime.
  5. Keep the temperature in your bedroom comfortable. Temperatures above 75 degrees Fahrenheit usually cause unwanted awakenings from sleep.
  6. Keep the bedroom environment quiet, dark, and comfortable. Noise and even dim light may interrupt or shorten your sleep.
  7. Try a light bedtime snack that includes cheese, milk, or nuts. These foods contain chemicals that your body uses to produce sleep and may help bring on drowsiness.
  8. Maintain a regular sleep schedule.

Although inadequate sleep hygiene is rarely the primary cause of insomnia, it can potentiate sleep difficulties caused by other factors or can interfere with treatment progress.

Poor sleep hygiene has a detrimental impact and it is very important to directly address these factors in therapy.

Although sleep-hygiene education may be helpful for mild insomnia, it is rarely sufficient for more severe insomnia, which requires more directive and potent behavioral interventions.

Perpetuating Factors that are the main target of sleep hygiene education:

1. Behavioral

Practices intended to improve sleep

  • Going to bed early
  • Staying in bed late
  • Increasing time in bed
  • Falling asleep with TV or radio left on
  • Staying in bed during awakenings
  • Getting extra sleep during the weekends

Practices intended to counter fatigue

  • Napping
  • Increasing caffeine ingestion
  • Lying down to rest
  • Decreasing physical activity

2. Cognitive

Anxiety

  • Worry about consequences of insomnia
  • Worry about sleeplessness (“I’ll never get to sleep tonight”)
  • Worry about the self ( “My sleep is out of control, just like my life”)

False beliefs

  • Misconceptions about sleep (“Everybody sleeps 8 hours,” “I can’t function on less than 7 hours of sleep”)
  • Catastrophizing (“Insomnia is ruining my life”)
  • Requirements for sleep (“I cannot sleep without sleeping pills,” “I must sleep alone”)

Other

  • Alcohol
  • Noise
  • Pets sleeping in the same bed
  • Clock watching during the night
  • Getting home late without enough time to wind down

Cognitive Behavior Therapy is becoming the preferred approach to treating insomnia. It is a multicomponent intervention that combines effectively some of the cognitive and behavioral procedures (stimulus control, sleep restriction, relaxation).
This approach is appealing because it addresses different insomnia features with different therapeutic recommendations, which is consistent the multidimensional etiologic model of insomnia.

Complementary and Alternative Therapies

Several complementary and alternative therapies, within the nondrug domain, have been used in the treatment of chronic insomnia.

These include:

  • exercise
  • acupuncture
  • tai chi
  • hypnosis
  • electrosleep therapy

Although potentially useful in clinical practice, those methods have not been evaluated as extensively in controlled studies as the other interventions.

Efficacy of cognitive behavioral therapy

Evidence from clinical trials evaluating the efficacy of psychological and behavioral therapies for insomnia shows that treatment produces reliable changes in several sleep parameters including:

  • sleep latency (large effect size)
  • wake after sleep onset (large effect size)
  • number of awakenings
  • total sleep time
  • sleep quality (large effect size)

Approximately 70% to 80% of patients with insomnia benefit from treatment.

The effect sizes are similar to those obtained for benzodiazepine-receptor agonists with a slight advantage for cognitive behavioral therapy on measures of sleep onset latency and sleep quality and for pharmacotherapy on total sleep time.

In terms of absolute changes the treatment produces:

  • a reduction in subjective sleep latency and time awake after sleep onset from an average of 60 to 70 minutes at baseline to about 35 minutes after treatment.
  • an increase in total sleep time by an average of 30 minutes, from 6 to 6.5 hours after treatment, with additional gains made after treatment is completed.

For patients with persistent insomnia (sometimes exceeding 10 years in duration), cognitive behavioral treatment may be expected to:

  • reduce sleep latency and wake after sleep onset by an average of about 50%
  • bring the absolute values of those sleep parameters below or near the 30-minute cutoff criterion initially used to define sleep-onset or sleep-maintenance insomnia.

Although the majority of patients benefit from treatment, only about half of them achieve full remission. Unfortunately a significant number continue to experience residual sleep disturbances.

Except for a modest increase in stages 3 and 4 after sleep restriction, there are few changes in sleep stages with cognitive behavioral therapy.

Insomnia is often a recurrent or persistent problem.

A robust finding across clinical trials is that sleep improvements achieved with cognitive behavioral therapy are well sustained after treatment is completed .

Long-term outcome must be interpreted cautiously because few studies report long-term follow-up and, among those that do, attrition rates increase substantially over time.

In addition, patients with chronic insomnia, even those who benefit from short-term therapy, might remain vulnerable to recurrent episodes of insomnia in the long term.

Maintenance therapy in the form of booster therapy sessions might contribute to improved long-term outcome because it facilitates better integration of newly learned self-management skills.

Multimodal cognitive behavioral therapy is becoming the standard approach in the field.

Studies comparing the relative efficacy of single therapies have found that:

  • stimulus control and sleep restriction therapies are more effective than relaxation alone
  • relaxation is more effective than sleep hygiene education
  • sleep restriction produces better outcomes than stimulus control in terms of sleep efficiency and continuity, but it also decreases sleep time during initial treatment
  • relaxation methods focusing on cognitive arousal (e.g., reducing intrusive thoughts) yield slightly greater improvements than those targeting somatic arousal
  • sleep hygiene education, when used alone, produces little effect on sleep and insomnia symptoms; this didactic approach should be seen as a minimal intervention.

Based on criteria set forth by the American Psychological Association, there are currently five interventions that have sufficient evidence to meet criteria for well-established psychological treatment for insomnia:

  • cognitive behavioral therapy
  • sleep restriction
  • stimulus control
  • relaxation
  • paradoxical intention

When these approaches are evaluated with older adults, only the following interventions meet similar efficacy standards:

  1. cognitive behavioral therapy
  2. sleep restriction
  3. stimulus control

As studies suggested, the most critical approaches associated with long-term improvements were stimulus control and sleep restriction, followed by cognitive restructuring.

Relaxation is the most commonly endorsed component (79% of respondents). Unfortunately it does not predict improvement in any of the sleep variables.
Studies have also examined the association between changes in sleep beliefs and sleep improvements. The results show that reductions of dysfunctional sleep cognitions during treatment are correlated with sleep improvements after treatment. Fewer dysfunctional cognitions after treatment are associated with better maintenance of sleep changes over time.

Within the medication, the addition of cognitive behavior therapy plays a complementary role in the management of insomnia. Medication produces fast symptomatic relief and cognitive behavior therapy yields durable benefits over time.

Principally, combined approaches should optimize outcome by capitalizing on the more immediate and potent effects of medication and the more sustained effects of cognitive behavior therapy.

Studies indicate that both treatment modalities, when used singly, are effective in the short term. Medication produces rapid improvements, but these benefits are quickly lost after the drug is discontinued.

Cognitive behavior therapy does not improve sleep as rapid as medication, the process takes longer but the improvements are well sustained even after treatment.

There is an additive effect of combined approaches relative to medication alone, but not necessarily relative to cognitive behavior therapy alone.

A combined intervention (e.g., benzodiazepine plus relaxation) produces more sustained benefits than medication alone.

Treatment responses vary across individual patients: some patients retain their initial sleep improvements, but others return to their baseline values.

Psychological factors have an important role in chronic insomnia. Therefore, behavioral and attitudinal changes are essential to sustain improvements in sleep patterns.

Patients’ attributions of the initial benefits of the combined behavioral and drug therapies is critical in determining long-term outcomes. Without integration of self-management skills, attribution of therapeutic benefits to the medication alone can place a patient at greater risk for insomnia recurrence after the drug is discontinued.

There is a risk that the availability of medications might undermine the patient’s motivation to implement behavioral changes in sleep habits.

Rather than initiating and discontinuing treatment simultaneously, it may be preferable to introduce treatment sequentially in order to optimize outcome.

Studies that examined the impact of different treatment sequences combining cognitive behavior therapy with medication show that the optimal sequence is when cognitive behavior terapy is introduced early on in treatment, either before or concurrently with medication.

The best long-term improvement is achieved when a combined approach is followed by cognitive behavior therapy alone during drug tapering.

The success of cognitive behavior therapy depends on the patient’s willingness to comply with the self-management procedures.
Due to the multifactorial nature of insomnia, to achieve clinical remission it is necessary to combine different clinical procedures rather than to rely on a single treatment modality.

The use of sleep restriction procedure early in therapy is likely to produce rapid therapeutic benefits.

Stimulus control procedures (getting out of bed when unable to sleep) might not be necessary when the initial sleep window is restricted to 5 to 6 hours per night. These procedures become relevant as the sleep window is increased.

Relaxation is helpful for persons with elevated tension or anxiety. There are cases when some patients have a paradoxical response and become more anxious.

Cognitive therapy is particularly helpful because:

  • challenges some misconceptions about sleep and daytime impairments
  • alleviates emotional distress
  • minimizes recurrence of sleep disturbances over time.

For milder forms of insomnia, basic sleep hygiene education may be sufficient.

More-severe insomnia often requires multimodal interventions and more frequent follow-up visits.

Cognitive behavior therapy is a valid therapeutic approach. Often it is the treatment of choice for persistent insomnia and sleep improvements are well sustained over time.

The gains derived from these treatments have been shown to be durable in follow-up studies of up to 24 months. Therefore, these aproaches should be used for managing chronic primary and comorbid insomnia, including in older adults and in persons who chronically use hypnotics.

How to fall asleep quickly using sleep restriction therapy

There is a natural tendency among persons with insomnia to increase the amount of time they spend in bed simply to rest or provide more opportunity for sleep. Although this strategy may be effective in the short term, in the long run it is more likely to result in fragmented and poor-quality sleep.

Sleep restriction primarily aims to improve sleep efficiency. Because sleep efficiency is the ratio of time asleep to time in bed, it can be improved either by increasing the numerator (time spent asleep) or by reducing the denominator (time spent in bed)
Sleep restriction therapy consists of curtailing the amount of time spent in bed as close as possible to the actual sleep time. This sleep time is then gradually increased over a period of a few days or weeks until optimal sleep duration is achieved. If a person reports sleeping an average of 6 hours per night out of 8 hours spent in bed, the initial prescribed sleep window (from initial bedtime to final arising time) would be 6 hours. To prevent excessive daytime sleepiness, time in bed should not be reduced to less than 5 hours per night, regardless of the number of hours of sleep reported by the patient.

Sleep restriction improves sleep continuity through two mechanisms:

  • leads to an increased homeostatic sleep drive through a mild sleep deprivation
  • alleviates some of the sleep anticipatory anxiety by changing the patient’s focus of attention

Sleep restriction therapy is indicated for the treatment of insomnia, including trouble sleeping during the beginning, middle or end of the time spent in bed.

Individuals who fall asleep quickly and have short, compact sleep prior to a terminal early morning awakening are unlikely to benefit from sleep restriction therapy. In these cases restricting time in bed will not increase the duration of sleep.

There are cases when patients report that they stay in bed completely awake just to rest. The ability to perceive sleep sometimes is imperfect. Some individuals may be unaware that they are getting some sleep after the major sleep period. Sleep restriction therapy may be of benefit also in cases where some unappreciated sleep does occur at the end of the night.

Sleep restriction also redresses indicators of poor sleep:

  • elevated amounts of light stage N1 sleep
  • prolonged sleep latencies
  • excessive wakefulness after sleep onset

Rapid sleep onset and a well-consolidated night of quality sleep are achieved rapidly and reliably at the start of sleep restriction therapy.

According to the 3P model of insomnia, behavioral practices and cognitive tendencies that perpetuate sleep disturbance are often the most promising targets for intervention. Sleep restriction therapy addresses many of these perpetuating factors, such as:

  • spending too much time in bed
  • anticipatory anxiety about the prospects for sleep
  • excessive concern about daytime performance deficits.

Sleep restriction therapy replaces sleep that has been haphazard and light with deeper, more consolidated sleep.

Patients can rest assured that their sleep problem is being addressed, and this translates into less worry about what the night will bring.

Hyperarousal is directly dampened by sleep loss.

Sleep restriction therapy tightens regulatory control of sleep by the endogenous circadian pacemaker. Patients with chronic insomnia often display widely varying times of retiring to and rising from bed, with consequent variability in the timing of light exposure, physical activity, social interaction, and other stimuli that entrain the circadian system. Therefore, the output of the endogenous oscillator is weakened as it continually responds to these shifting patterns, leading in turn to increased variability in the propensity to fall asleep and wake up.

Sleep restriction therapy gradually returns sleep regulation to effective circadian control by regulating the time of “lights on” and “lights out”, resulting in more reliably timed phases of sleep and wakefulness.

Instructions for patients:

  • restrict the time you spend in bed to the actual amount of sleep you get (e.g. if you sleep 6 hours per night out of 8 hours spent in bed, you should curtail the time you spend in bed to these 6 hours)
  • there is no reason for staying in bed any longer than that, since the remaining time is spent awake anyway
  • spending excessive amounts of time lying down attempting to relax, rest, or nap fragments rather than consolidates sleep and contributes to maintaining the sleep problem currently

As sleep becomes more efficient, patients will gradually be allowed to spend more time in bed.

It is very important for patients to understand the treatment rationale. Reducing time spent in bed seems counterintuitive and often contradicts strategies they have tried on their own to manage insomnia.

Precautions and contraindications

Some individuals experience difficulties falling asleep when they are overtired. Usually, when you get less sleep on consecutive nights, you begin to accrue a sleep debt.  As sleep debt increases your body experiences a stress response and begins to release adrenaline, which is a stimulating hormone. Therefore, a vicious cycle has been created: you experience the feeling of being more and more tired, but your body is increasingly stimulated.

Sleep restriction is contraindicated in:

  • individuals who need to maintain optimal vigilance to avoid serious accidents (long-haul truck drivers, long-distance bus drivers, air traffic controllers, operators of heavy machinery, and some assembly-line workers)
  • individuals with conditions that are exacerbated by sleepiness or deep sleep, such as epilepsy, parasomnias (e.g. sleepwalking), and sleep disordered breathing.
  • bipolar illness

Sleep restriction can lower the threshold for a seizure or sleepwalking episode and might exacerbate a manic episode.

Sleep restriction should also be used cautiously with:

  • patients whose jobs require operating motor vehicles
  • patients who have duties in which drowsiness may be a danger to the patient or others
  • patients who operate heavy equipment
  • patients who might otherwise be at increased risk for falling asleep during the day.

Stimulus control, paradoxical intention, and cognitive therapy show you what to do when you can’t sleep

A set of five instructions also known as stimulus control therapy are designed to reinforce the association between the bed and bedroom with rapid sleep onset. They also aim to re-establish a regular circadian sleep–wake rhythm and to recreate a positive association between the presleep rituals and the bedroom environment.

Persons with insomnia often develop apprehension around bedtime and the bedroom. They come to associate this particular time of the day and environment with the frustration of being unable to sleep. Over time, the presleep rituals usually associated with relaxation and sleep become cues for worrying and wakefulness. This conditioning process can take place over several weeks or months. Many insomniac patients display poor sleep habits that initially emerge as a means of coping with sleep disturbances. Poor sleep at night can lead to daytime napping or sleeping late on weekends in an effort to catch up on lost sleep. Such patients might lie in bed for prolonged periods trying to force sleep, only to find themselves becoming more awake.

Instructions for patients:

  1. Lie down intending to go to sleep only when you are sleepy- not just fatigued, but sleepy.
  2. Do not use your bed or bedroom for anything except sleep (no reading, eating, watching television, listening to the radio, or planning or problem solving in bed). Sexual activity is the only exception to this rule. The activities associated with arousal must occur elsewhere. The goal is to break up patterns that are associated with disturbed sleep. If bedtime is the only time patients have for thinking about the day’s events and planning the next day, they should spend some quiet time doing that in another room before they go to bed. People who do not have insomnia read or listen to music in bed without problem. This is not the case for insomniacs, however. Those who have sleep problems must establish new routines to facilitate sleep onset.
  3. Get out of bed when unable to fall asleep (e.g. after 20 minutes) and go into another room. Stay up as long as you wish and then return to bedroom only when sleep is imminent. You must avoid clock-watching. The goal is to disassociate the bedroom from the arousal and frustration of not being able to sleep and to associate your bed with falling asleep quickly. If you still cannot fall asleep, repeat this step as often as is necessary throughout the night.
  4. You must try to get up at the same time every morning irrespective of how much sleep you got during the night. This will help your body acquire a consistent sleep rhythm. Insomniacs have irregular sleep rhythms because they try to make up for poor sleep by sleeping late or napping the next day. Keeping consistent wake times helps patients develop consistent sleep rhythms. The set wake times mean that the patients will be sleep-deprived after a night of insomnia. This will make it more likely that they will fall asleep quickly the following night, strengthening the cues of the bed and bedroom for sleep. It is important to have as consistent a schedule as possible, seven nights a week. A deviation of no more than one hour in the wake time on days off does not produce problems in establishing a consistent rhythm.
  5. Avoid daytime napping. Insomniacs should not disrupt their sleep patterns by irregular napping. The goal of this instruction is to prevent patients losing the advantage of the sleep loss of the previous night for increasing the likelihood of faster sleep onset the following night. A nap that takes place seven days a week at the same time would be permissible. For those elderly insomniacs who feel that they need to nap, a short daily afternoon nap of 30 to 45 minutes or the use of 20 to 30 minutes of relaxation as a nap substitute is recommended.

Paradoxical intention is a method designed for those patients with an intense preoccupation about sleep loss, and its consequences. It is a procedure designed to eliminate performance anxiety. Because sleep is an involuntary physiologic process, any attempt to control or induce sleep voluntarily generates performance anxiety which delays sleep onset.

The main instruction of this procedure is to allow sleep to occur naturally. Good sleepers do not make any effort to fall asleep. Insomnia patients should remain passively awake and give up any effort to fall asleep. Paradoxical intention works by reducing anxiety and the associated sleep worry and sleep preoccupation.

The rationale underlying this procedure is to consider “How does a good sleeper do it?” Good sleepers are good sleepers precisely because they just do not really think about it, nor do they do anything in particular. Their perspective simply supports sleep coming automatically and naturally. If the insomnia patient wants to become a good sleeper, one of the biggest challenges will be to develop the mindset of the good sleeper, who is relatively “care-less” about sleep.
First method is a “giving up trying” (acceptance and mindfulness) method. This approach helps reduce anxiety and effort around sleep.

The idea of accepting situations, rather than fighting them all the time, has its roots in a number of ancient philosophies. Acceptance leads to a problem having a less dominating position and influence. A more mellow perspective about sleep is an adaptive outlook, and one that can lead to improved sleep.

Instructions for patients:

  1. Take every opportunity to be carefree about your insomnia
  2. Relish opportunities to get out of bed whenever you can.
  3. Try to imagine as many catastrophes as you can that will happen, just because you are awake at night. See them as exaggerated and absurd.
  4. Accept the fact that you have insomnia. Even tell others about it.
  5. Think of wakefulness as an opportunity. Use the time when you are up, to do something useful or something you enjoy.

The second method is more explicitly paradoxical in a manner that is encouraging the patient to stay awake, instead of getting to sleep. By deciding to stay awake, the patient is completely giving up trying to sleep. This fact leads to a strong possibility that the patient will find himself falling asleep, in spite of efforts to remain awake. It can be enormously reassuring for the patient to be overtaken by sleep.

Instructions for patients:

  1. go to bed at a normal time when you feel sleepy and put the lights off but keep eyes open; give up any effort to fall asleep and concern about still being awake;
  2. this is a passive approach rather than an active one; you should not deliberately try to keep yourself aroused by thinking about something stimulating, moving your arms and legs, or staying physically active to remain awake; rather, you are to resist the tendency for your eyelids to close; you should encourage yourself to remain awake until sleep comes naturally; if you shift the focus off attempting to fall asleep, you will find that sleep comes naturally.

Patients should follow the same instructions if they waken during the night and do not quickly return to sleep.

Cognitive therapy uses socratic questioning and behavioral experiments to reduce excessive self-monitoring and worrying about sleep, and to reframe faulty beliefs about insomnia and its daytime consequences.

Paradoxical intention technique is an additional cognitive strategy.

The basic premise of paradoxical intention is that appraisal of a given situation (sleeplessness) can trigger negative thoughts and emotions (fear, anxiety) that are incompatible with sleep.

When a person is unable to sleep at night and worries about the possible consequences of sleep loss, a spiral reaction is set off that feeds into a vicious cycle of emotional distress, increased arousal, and more sleep disturbance.

Upon night waking, a person may watch the clock to check how many hours are left in the night or engage in safety activities (trying to stop thinking), which can prolong the nocturnal awakenings.
This technique is designed to stop the self-fulfilling nature of this vicious cycle.

Some therapeutic targets for cognitive restructuring include:

  • unrealistic expectations (“I must get my 8 hours of sleep every night”)
  • faulty causal attributions (“My insomnia is entirely caused by a biochemical imbalance”),
  • amplification of the consequences of insomnia (“After a poor night’s sleep, I am unable to function the next day”).

If you are predisposed to insomnia, it is likely that you will remain vulnerable to sleep disturbances even after treatment.

Patients should:

  • keep realistic expectations with regard to sleep requirements and daytime energy
  • not blame insomnia for all daytime impairments because there may be other explanations for these deficits
  • never try to sleep, because it is likely to exacerbate sleep difficulties
  • give less importance to sleep; although sleep should be a priority, it should not become the central point of life.
  • not catastrophize after a poor night’s sleep; insomnia is very unpleasant, but it is not necessarily dangerous to health, at least not in the short term
  • develop some tolerance to the effects of insomnia

Can’t sleep because your mind is racing?

Relaxation training might be the solution.

This technique comprises clinical procedures such as progressive muscle relaxation, meditation, guided imagery, or abdominal breathing. The goal of this treatment is to reduce arousal at bedtime or on nighttime awakening, muscle tension and intrusive thoughts interfering with sleep.

Biofeedback and progressive relaxation techniques have the most solid evidence base for individual component use.

Most relaxation procedures require professional guidance initially and daily practice over a period of a few weeks.

Specific techniques are widely available in written and audio form.

Relaxation is probably the most commonly used intervention for insomnia. Stress, tension, and anxiety are contributing factors to sleep disturbances.

There are different relaxation interventions:

  • progressive muscle relaxation focus primarily on reducing somatic arousal (muscle tension); this procedure involves methodical tensing and relaxing different muscle groups throughout the body
  • attention-focusing procedures (imagery training, meditation, thought stopping) target mental arousal in the form of worries, intrusive thoughts, or a racing mind.

Mindfulness therapy is another form of relaxation that has been evaluated in the management of insomnia.

Most relaxation procedures are equally effective for treating insomnia.

Relaxation technique usually combines aspects of muscle tension release, breathing control, and imagery to create a progressive relaxation program.

The context in which relaxation is carried out is essential to the process: patients are instructed to wind down prior to going to bed and cease stimulating activities 1 to 2 hours before retiring for sleep.

Once in bed, the patient is guided through a series of exercises, directed at making them aware of muscle tension increase and release, as well as the impact of breathing exercises in promoting relaxation.

Selection of a particular method (progressive muscle relaxation versus meditation) should be based on the subtype of arousal (somatic or mental) interfering with sleep, although these often overlap.

Some patients (those who tend to be perfectionists) might have a paradoxical response and actually become more anxious when trying to relax.

The most critical issue is to ensure daily practice of the selected method for at least 2 to 4 weeks. The aim of this method is to reduce arousal rather than induce sleep.

Biofeedback refers to a broad category of techniques that involve the monitoring of participants’ physiologic signals through an electronic/computerized interface.

Sometimes, it is necessary to implement a more comprehensive stress-management program involving relaxation and other therapeutic components, such as time management and problem-solving training.

To minimize worrying and mental activity interfering with sleep, it is also helpful to instruct patients to set aside a time and a place (other than bedtime and the bedroom) to write down thoughts or worries of the day and plans for the next day. Imagery techniques can also be useful to block out such unwanted presleep thoughts.
Tools that can help implement this therapy:

1. Structured Problem-Solving

Worry or problem-solving in the presleep period is one of the strongest predictors of delayed sleep onset latency.

One of the original problem-solving cognitive strategies is a presleep writing procedure developed by Espie and colleagues; this technique is similar to a procedure called constructive worry.

In constructive worry, patients are asked to set aside some time several hours before bedtime to complete a homework assignment using a worksheet that is divided into two columns. The first column is labeled “Concerns” and the second column is labeled “Solutions.” In the Concerns column, patients list worries that have the greatest likelihood of keeping them awake at night. In the Solutions column, patients generate the next, immediate step they can take toward the ultimate goal of solving the problem. Patients are instructed not to write down the ultimate end solution, as they may view this solution as out of reach or difficult to implement. They are refocused on the most immediate step in the sequence. When there are no apparent solutions to solve a problem, patients are encouraged to write down an acceptance-based or self-care strategy.

Worry management techniques are likely most helpful to reduce presleep cognitive arousal. Management of emotional complaints is a worthwhile endeavor because patients identify it as one of the most common contributors to insomnia.

2. Thought records- a cognitive therapy tool for modifying negative thinking

Maladaptive thinking styles have been involved in a variety of disorders including insomnia.

The negative sleep-related thoughts and beliefs in insomnia do not appear to be simply attributable to the high rate of comorbid disorders with a similarly unhelpful cognitive style. Negative thoughts and moods can exert reciprocal negative influences on each other, and both can perpetuate insomnia.

The purpose of the thought record is to observe the connections between negative thoughts and distress and to interrupt this process.

The observation is achieved via prospective monitoring using a specially designed worksheet divided into columns. Several versions of thought records are available, including a version specifically designed for use with insomnia patients. The first three columns of a typical thought record are labeled Situations, Mood and Mood Intensity Rating (0% to 100%), and Thoughts. Observing which situations (column 1) tend to give rise to distress (column 2), and subsequent negative thoughts (column 3) can provide insight into a seemingly automatic cognitive-emotional process. Although observing these connections can be helpful in initiating cognitive change, the main use of the thought record is to actively challenge unhelpful thoughts.

People with insomnia:

  • have been shown to have beliefs that overestimate the negative effects of insomnia
  • focus on the belief that sleep is out of one’s control
  • are rigid or have unrealistic expectations about how much sleep is needed for functioning
  • have misconceptions about the causes of insomnia

Whereas some of these beliefs may be true to varying degrees, the cognitive inflexibility or degree to which people with insomnia adhere to such thoughts perpetuate insomnia and are thus unhelpful.

To modify these beliefs, patients are asked to challenge unhelpful thoughts using a series of questions. For example, after a poor night’s sleep patients may struggle with the negative thought, “I’ll never be able to make it through the day.” These questions underlie other point of view and may be helpful for patients dealing with this situation:

Have you ever had any experiences that show this thought has not been true 100% of the time?
Is it guaranteed that a poor night’s sleep will prevent you from functioning?
Will you be able to function but perhaps it will be more difficult?
Are there times when you had a good day even after a poor night or a poor day after a good night’s sleep?
Are there strategies you have used in the past to be able to cope with the negative effects of insomnia?
This line of questioning is aimed at modifying thoughts and thus improving the patient’s mood. The level of mood disturbance would be expected to improve if the thought mentioned is modified to, “I don’t feel well now, but I’ve always made it through, and things tend to get better as the day goes on anyway.”

Clinical trials have shown that cognitive behavior therapy produces declines in the belief of unhelpful sleep-related thoughts. The described cognitive restructuring is viewed as a useful component of the overall insomnia treatment process.

How to get to sleep when you have comorbid insomnia

Comorbid insomnia refers to insomnia coexistent with other medical or psychiatric disorers. In these cases insomnia is merely a symptom, such forms of insomnia being more common than primary insomnia.

Treating the suspected “primary” condition of insomnia is traditionally the management of such forms of insomnia. It is generally assumed that the sleep disturbance will remit once the associated comorbid condition is resolved.

In some cases insomnia can persist as a clinically significant residual symptom after remission from the “primary” disorder and is even a risk factor for future relapse of major depression. The presence of residual symptoms suggests that the disorder is not completely cured. Therefore, the antidepressant treatment should be continued until the symptoms disappear completely.

Insomnia often becomes either partially or totally independent from the comorbid psychiatric condition and persists as a separate disorder.

In addition, insomnia can be a predictor of poorer response to treatment of the coexisting condition. Insomnia should be regarded as a comorbid disorder when observed in patients with concurrent conditions such as the major psychiatric disorders.

Some studies suggest that patients with medical and psychiatric conditions can also benefit from insomnia-specific treatment. The outcome with those patients is more modest compared to patients with primary insomnia. However, these sleep improvements obtained after treatment were paralleled by reductions of depressive and fatigue symptoms. Moreover, cognitive behavioral treatment has an augmentation effect when used in combination with antidepressant medication in the treatment of insomnia comorbid with major depression. Studies show that the addition of cognitive behavioral therapy for insomnia, relative to antidepressant therapy alone, resulted in higher remission rates of depression (61% versus 33%) and insomnia (50% versus 8%) and larger improvements in measures of sleep continuity.

The addition of a pharmacologic treatment of insomnia to the treatment of the comorbid psychiatric disorders produces better results than treating the comorbid disorder alone.

Drawbacks to some pharmacologic approaches:

  • possible dependence
  • shorter durability of posttreatment effects (relative to psychological treatments such as cognitive behavior therapy)
  • unknown polypharmacy effects in patients with complex disorders.

Because the psychological or behavioral insomnia therapies have comparable short-term efficacy, better durability, and fewer safety concerns than do the pharmacologic approaches, they are attractive alternative (or augmenting) strategies for insomnia management.

Sometimes patients with comorbid insomnia have the same insomnia-maintaining factors targeted by the psychological or behavioral insomnia therapies as do patients with primary insomnia.

For example, patients with insomnia and comorbid depression exhibit similar levels of sleep-disruptive beliefs as patients with primary insomnia. Moreover, patients with depression and insomnia display sleep-disruptive activities and similarly elevated sleep effort as do patients with primary insomnia alone.

Stress can be an endogenous event (e.g., a change in neurochemical activity) or a life event (e.g., the birth of a baby). Whether the stressor is an external life event or a physiologic event, it can directly cause either sleep disruption or the comorbid disorder.

Alternatively, the stressor might operate through a shared vulnerability trait of insomnia and the comorbid condition such as ruminative tendency or specific maladaptive beliefs.

Once sleep disruption occurs, attempts at coping or compensating for the sleep loss result in behaviors such as:

  • increasing time in bed
  • using alcohol or sleep aids
  • avoiding obligations or socializing

Such actions have been posited as perpetuating factors in insomnia and lead to:

  • circadian or homeostatic disruption
  • increased arousal
  • reinforcement of beliefs that one is helpless to cope with sleep loss.

Insomnia exerts negative influence on the comorbid disorder, and in some cases it could cause the disorder.

Even in cases where a comorbid disorder might have initially caused the sleep disruption, cognitive and behavioral factors are perpetuating factors for an insomnia that remains after the comorbid condition remits.

The vast majority of people with depression also have sleep complaints. So common is this association that there is a well-documented tendency in physicians to presume that an insomnia complaint is diagnostic of a major depressive episode even in the absence of other major depressive disorder diagnostic criteria. Insomnia can predate and predict initial major depressive disorder onset. It also can persist as a clinically significant condition long after the associated depressive episode remits.

Insomnia also predicts poorer response to depression treatment. In most cases, the treatment of insomnia enhances response of depression symptoms to treatment.

Studies have revealed that cognitive behavior therapy is effective for improving both sleep and mood in patients with comorbid insomnia and major depressive disorder.

Studies show that augmentation of antidepressant medication with cognitive behavior therapy produces a far greater remission rate (depression remission rate, 62%) than antidepressant therapy and a sham behavioral control therapy (depression remission rate, 33%).

Cognitive behavior therapy has also been used effectively in persons with posttraumatic stress disorder and in persons in recovery from alcohol abuse. Elements of cognitive behavior therapy have also been incorporated into an effective nocturnal panic disorder treatment protocol.

Recent studies have also shown that cognitive behavioral therapy is effective for treating insomnia associated with fibromyalgia, chronic pain, cancer, and various medical conditions in older adults.

How to improve sleep using light therapy

Light therapy is effective for sleep problems in general, particularly for:

  • circadian rhythm sleep disorders
  • insomnia symptoms.

However, most effect sizes are small to medium.

In order to pursue optimal adaptation to the imposed light–dark cycle, light influences alertness, pupillary constriction, hormonal secretion, heart rate, body temperature, sleep propensity, and gene expression.

Light has an important influence on sleep and wakefulness. It acts through:

  • influencing the suprachiasmatic nucleus (SCN), a bilateral cluster of neurons in the anterior hypothalamus that controls circadian rhythms, through the eye and the retinohypothalamic tract. The response of the central circadian pacemaker to light pulses plays a crucial role in the synchronization to the environmental light–dark cycles. Light pulses (usually presented during the day) induce expression of the immediate early gene c-fos and the clock gene Per1 within the SCN, resulting in phase shifts of behavioral circadian rhythms. Thus, the Per genes are not only light-responsive components of the circadian oscillator but also are involved in resetting of the circadian clock. Usually, exposure to light in the dusk leads to a delay in human sleep onset, while exposure to light early in the dawn advances activity onset. Not enough light, or light of an inappropriate wavelength (light at longer wavelengths, > 600 nm) and light at inappropriate times (during the night) can lead to improper entrainment between internal circadian time and external 24-h earth rotation time.
  • inhibiting the secretion of melatonin. Acute melatonin suppression may be a cause for the acute alerting effects of light. Increased melatonin suppression is associated with greater arousal and attenuation of the endogenous circadian drive for alertness.
  • indirect projections on the ascending arousal system, which facilitates thalamic and cortical connections; therefore it has alerting effects. Even nighttime exposure to typical room light can exert an alerting effect in humans, as indexed by less theta and alpha waking EEG activity.

The explanation for light’s effects relies on human circadian rhythms. When isolated from external time cues, humans continue to present rest/activity cycles that are different than the 24-h day. A wide variety of physiological and behavioral functions, (neurohormone secretion, rhythms of body temperature, sleep propensity and structure, vigilance, and mood), continue to oscillate with an approximately 24-h rhythmicity.

Each day, biological rhythms must be adjusted to their geophysical environment via external time-cues. Otherwise, these rhythms would shift by a small amount each day, and over several consecutive weeks, this would lead to a substantial desynchrony between endogenous daily rhythms and the environment.

The suprachiasmatic nucleus (SCN) is the locus of the brain’s internal time keeper, or ‘master clock.’ The light/dark cycle is the most powerful environmental cue that transmits information about the time of day to the organism. Such synchronization is important to allow the central circadian clock to properly coordinate internal physiology with the external environment.

Photic information from the environment is transmitted to the brain’s time-keeping system via a direct monosynaptic pathway linking the retina to the SCN, called the retino-hypothalamic tract. A specialized class of nonimage-forming, blue-light-sensitive photopigments called melanopsin, found in the retina, is thought to mediate the effects of light on the central circadian pacemaker, although participation of cones is also involved. The circadian system is most sensitive to shorter wavelength light. Thus, blue visible light range can more efficiently induce larger phase shifts in biological rhythms.
Because light is such an important factor in the regulation of sleep and wakefulness, light has been applied therapeutically as a treatment for sleep disorders.

The interaction between the sleep–wake cycle and the circadian system is implicated in the regulation of mood across the 24-h day and the pathogenesis of certain affective disorders. Relatively minor changes in the timing of sleep can have deleterious effects on alertness levels, sleep quality, and mood the following day. Appropriately timed bright light exposure can have many practical and useful applications for the well-being of individuals experiencing sleep or mood disturbances associated with altered circadian rhythms.

Although light therapy is nowadays applied to different types of sleep disorders, it was originally applied to circadian rhythm sleep disorders (advanced sleep phase disorder and delayed sleep phase disorder). The core problem of circadian rhythm sleep disorder is the misalignment between the endogenous rhythm and the environment, or the lack of an endogenous rhythm.
Appropriately timed bright light exposure can be used to alleviate symptoms associated with each.

Bright light exposure late at night, before the minimum limit of circadian core body temperature, causes delays of the circadian system, whereas exposure in the early morning, after the minimum limit of circadian core body temperature results in advances of the circadian system.

Advanced sleep phase disorder is characterized by:

  • a sleep–wake schedules that occur earlier than desired
  • evening sleepiness and early morning awakening
  • typically initiation of sleep between 6.00 and 9.00 p.m., with awakening occurring between 2.00 and 5.00 a.m.
  • higher prevalence in the elderly, being less reported in younger individuals

For these patients, bright light exposure after awakening in the morning should be avoided in order to minimize the potential for unwanted phase advances of the circadian system. Evening bright light exposure before bedtime has been used to induce adaptive phase delays in sleep timing and in circadian rhythms of melatonin and core body temperature.

Delayed sleep phase disorder is characterized by:

  • a sleep–wake schedule that occurs later than desired
  • an extreme difficulty in advancing the sleep schedule to earlier hours
  • typically initiation of sleep between 2.00 and 6.00 a.m., with awakening occurring between 10.00 a.m. and 1.00 p.m
  • higher prevalence in adolescents and young adults, but does occur in other age groups.

For these patients, light exposure in the evening before the sleep episode should be minimized to avoid an exacerbation of the phase-delayed sleep–wake schedule. Even normal room light levels can induce and maintain circadian rhythm phase delays.

Once awake on their delayed schedule, most patients exhibit normal alertness and energy, but others report difficulties for several hours after awakening and spurts of energy after midnight. Often these patients show comorbid mood and personality disorders.

The circadian rhythm of core body temperature and the sleep-wake rhythm of patients with delayed sleep phase disorder could be shifted by 2 h of bright light exposure in the morning and restriction of light in the evening.

Light therapy in the morning should occur as early as possible but without forcing individuals to wake up too early, in order to prevent sleepiness during the day.

At the start of therapy, light exposure should be scheduled to begin after the time of habitual awakening, and should be progressively advanced each day until the target time interval is reached.

A dysregulation of sleep–wake or circadian rhythms was also observed in patients with mood disorders, including seasonal affective disorder, major depressive disorder, premenstrual dysphoric disorder, and bipolar disorder.

Light therapy, that targets and aims to correct circadian rhythm abnormalities, exerts its action via a realignment of biological rhythms with the sleep–wake cycle.
There is recent evidence that light per se may directly impinge on sleep, alertness, cognitive performance, and even mood levels probably even without its action via the central circadian pacemaker.

Light may have a direct action on brain mechanisms underlying emotion and mood processing, in a mechanism independent of the circadian system.

The direct mood-stabilizing effects of bright light were studied in a group of women with subclinical winter depression who underwent acute tryptophan depletion (a neurotransmitter involved in serotonin formation). Although mood was significantly worsened in tryptophan-depleted participants in dim light, mood showed no decrement when participants were kept in bright light. This result implies an interaction between the bright light exposure and the serotoninergic system in mood regulation.

Bright light per se, in addition to its phase-shifting effects, is beneficial for patients with affective disorders, highlighting the acute mood-elevating effects of bright light.
Disturbances in the sleep–wake cycle are common in major depressive disorder. Patients report insomnia symptoms which are mainly caused by disruptions in circadian and homeostatic factors involved in sleep regulation.

The endogenous circadian system is altered in major depressive disorder, with reports of rhythms being abnormally phase-advanced and diminished in amplitude.

A desynchronization of physiological rhythms with the light–dark and sleep–wake cycles could be exacerbated by a misalignment between clock gene expression centrally at the SCN, non-SCN brain oscillators, and oscillators in the periphery. Thus, because bright light exposure can shift circadian rhythms and increase circadian amplitude, it may be an effective treatment for major depressive disorder. A therapeutic effect of bright light is found in approximately 50% of patients with major depressive disorder.
Exposure of the eyes to light of appropriate intensity and duration, at an appropriate time of day, can have marked effects on the timing and duration of sleep and on the affective and physical symptoms of depressive illness.

Clinical studies of phase shifting and antidepressant effect with blue light have shown no advantage over broad-spectrum white light, which remains the standard. White light, of course, includes a blue component, though in lower relative proportion than from narrow-band or blue-supplemented sources.
Adverse Effects of Bright-Light Exposure

If evening light is timed too late, the patient can develop insomnia and hyperactivity.

If morning light is timed too early, the patient can awaken prematurely, well before light onset, and be unable to resume sleep.

These problems are responsive to timing and dose (duration and intensity) adjustments during treatment.

 

One thought on “Can’t sleep? Tips on how to sleep better and faster

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