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The Impact of Stress on Insomnia and Treatment Considerations
Abstract
The role of stressors in the genesis of chronic insomnia has been documented in a number of studies. In a retrospective assessment of good vs poor sleepers, those with insomnia reported significantly more negative life events, such as losses and illnesses, during the year prior to the onset of insomnia, and many specifically attributed their insomnia to a major life event.(1) In a prospective study of young adults assessed over a 7-year period, those who experienced more frequent negative life events and interpersonal conflicts were more likely to have occasional insomnia or repeated bouts of brief insomnia.(2) In addition, a Finnish study found that psychosocial stressors were more likely to be associated with insomnia than were health problems,(3) indicating the strong link between stressors and sleep problems. Although major stressful events can trigger insomnia, chronic exposure to minor stress may also contribute to an increased risk for insomnia and may be particularly important in the genesis of chronic sleep disturbance. In a population-based study in Japan, insomnia was significantly correlated with daily stress levels, whereas regular exercise was negatively correlated with sleep problems.(4) A recent study of over 3400 male civil servants in Japan assessed the relationships of a variety of stressors on 3 aspects of insomnia: difficulty initiating sleep, difficulty maintaining sleep, and poor-quality sleep.(5) Higher perceived stress, the consideration of life as not meaningful/worth living, and a variety of job-related stressors showed the strongest independent associations with all 3 types of insomnia complaints. Recent work has begun to look more closely at the effects of specific stressors on insomnia. Some of these studies have demonstrated relationships between family conflict and insomnia in children, adolescents, and young adults, consistent with the idea that early and chronic stress may contribute to lifelong sleep problems. In a study of French adolescents, those who had insomnia symptoms came from families with higher divorce rates, had poorer relationships with their families, and reported higher rates of medical and psychological illness or death in parents.(6) A prospective study of undergraduate college students assessed the impact of family, academic, and social events on insomnia;
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To estimate the direct and indirect cost burden of untreated insomnia among younger adults (age 18-64), and to estimate the direct costs of untreated insomnia for elderly patients (age 65 and over).
A retrospective, observational study comparing insomnia patients to matched samples without insomnia.
Self-insured, employer sponsored health insurance plans in the U.S.
138,820 younger adults and 75,558 elderly patients with insomnia, plus equal-sized, matched comparison groups.
NA.
Direct costs included inpatient, outpatient, pharmacy, and emergency room costs for all diseases, for six months before an index date. The index date for insomnia patients was the date of diagnosis with or the onset of prescription treatment for insomnia, some-time during July 1, 1999-June 30, 2003. Non-insomnia patients were assigned the same index dates as the insomnia patients to whom they were matched. Indirect costs included costs related to absenteeism from work and the use of short-term disability programs. Propensity score matching was used to find insomnia and non-insomnia patients who had similar demographics, location, health plan type, comorbidities, and drug use patterns. Regression analyses controlled for factors that were different even after matching was completed. We found that average direct and indirect costs for younger adults with insomnia were about $1,253 greater than for patients without insomnia. Among the elderly, direct costs were about $1,143 greater for insomnia patients.
Insomnia is associated with a significant economic burden for younger and older patients.
Groups of 10 objectively defined insomniacs and age-, sex- and weight-matched normal sleepers were evaluated on sleep, performance, mood, personality and metabolic measures over a 36-hour sleep laboratory stay. Insomniacs were defined to have increased wake time during the night but also had decreased stage 2 and rapid eye movement sleep. As expected insomniacs reported increased confusion, tension and depression and decreased vigor on the profile of mood states mood scale throughout the evaluation period as compared to the normals. Insomniacs also had decreased memory ability on the short-term memory test and the MAST. These performance and mood differences were not secondary to sleepiness because the insomniacs also had significantly increased multiple sleep latency test (MSLT) values throughout the evaluation period. In conjunction with the consistent mood, performance and MSLT differences during the day and the sleep differences at night, whole body VO2, measured at intervals across the day and throughout one night of sleep, was consistently elevated at all measurement points in the insomniacs as compared to the normals. The nocturnal increase in metabolic rate remained even after metabolic values from periods during the night containing wake time or arousals were eliminated from the data set. It was concluded that patients who report chronic insomnia may suffer from a more general disorder of hyperarousal (as measured here by a 24-hour increase in metabolic rate) that may be responsible for both the daytime symptoms and the nocturnal poor sleep. Future studies need to explore 24-hour insomnia treatment strategies that decrease hyperarousal.
It was hypothesized that psychophysiological insomniacs, who have been shown to have elevated heart rate, body temperature, and whole body metabolic rate, would also have increased low frequency and decreased high frequency power in the spectral analysis of their heart period data.
Groups of 12 objectively defined insomniacs and age-, sex-, and weight-matched controls with normal sleep were evaluated on sleep and EKG measures over a 36-hour sleep laboratory stay.
Heart period was decreased (ie, heart rate was increased) and its SD was decreased in all stages of sleep in the insomniacs compared with the controls. Spectral analysis revealed significantly increased low frequency power and decreased high frequency power in insomniacs compared with controls across all stages of sleep.
Because increased low frequency spectral power is an indicator of increased sympathetic nervous system activity, these data imply that chronic insomniacs could be at increased risk for the development of disorders, such as coronary artery disease, that are related to increased sympathetic nervous system activity.
We reviewed the literature on sleep in psychiatric disorders and evaluated the data by meta-analysis, a statistical method designed to combine data from different studies. A total of 177 studies with data from 7151 patients and controls were reviewed. Most psychiatric groups showed significantly reduced sleep efficiency and total sleep time, accounted for by decrements in non-rapid eye movement sleep. Rapid eye movement sleep time was relatively preserved in all groups, and percentage of rapid eye movement sleep was increased in affective disorders. Reduction in rapid eye movement sleep latency was seen in affective disorders but occurred in other categories as well. Although no single sleep variable appeared to have absolute specificity for any particular psychiatric disorder, patterns of sleep disturbances associated with categories of psychiatric illnesses were observed. Overall, findings for patients with affective disorders differed most frequently and significantly from those for normal controls.
The association of three subtypes of insomnia with psychic and functional syndromes, and the course of insomnia over 7 years were examined in a Swiss cohort of young adults interviewed three times. Specific associations were found between repeated brief insomnia (RBI) and recurrent brief depression (RBD). Continued insomnia (CI) was associated with major depression. All three subtypes of insomnia were associated with anxiety disorders; 52% of insomniacs were free of concurrent anxiety and depression. Insomnia--especially RBI and CI--was also associated with a number of functional complaints, but not with the consumption of alcohol, medicine, or illegal drugs. Insomniacs with RBI and occasional insomnia (OI) experienced more life events and interpersonal conflicts than controls. These findings support the subdivision of insomnia into different subtypes. The longitudinal analysis showed that insomnia tends to reoccur. For subjects with insomnia either at age 21 or 23 years, there was a higher risk of further insomnia at follow-ups. The specific subtype of insomnia at the first occurrence was not predictive for the outcome: all subtypes of insomnia enhance the risk of relapses in a similar way. Insomnia at age 21 is no precursor of the first onset of a depressive or anxiety disorder within a 2-year follow-up. With respect to the course of insomnia over 7 years, the subtypes did not differentiate.
During the year their insomnia began, chronic insomniacs experienced a greater number of stressful life events compared with previous or subsequent years and compared with good sleepers. In addition, among the life event categories assessed, insomniacs reported a greater number of undesirable events, particularly events related to losses and to ill health. They also had lifelong histories of more illnesses and somatic complaints, beginning with more childhood illnesses and more childhood problems related to eating and sleeping. During childhood, insomniacs reported more frequent discontent with their families, and prior to the onset of insomnia, they had less satisfying relationships with their parents as well as problems in other interpersonal relations and in their self-concepts. Currently, insomniacs felt considerably less satisfied with their lives, had lower self-concepts, and had greater difficulty with interpersonal relationships. Thus, stressful life events, mediated by certain predisposing factors of personal vulnerability, were found to be closely related to the onset of chronic insomnia.
Because of the role of psychological factors in insomnia, the shortcomings of hypnotic medications, and patients' greater acceptance of nonpharmacological treatments for insomnia, the authors conducted a meta-analysis to examine the efficacy and durability of psychological treatments for the clinical management of chronic insomnia.
A total of 59 treatment outcome studies, involving 2,102 patients, were selected for review on the basis of the following criteria: 1) the primary target problem was sleep-onset, maintenance, or mixed insomnia, 2) the treatment was nonpharmacological, 3) the study used a group design, and 4) the outcome measures included sleep-onset latency, time awake after sleep onset, number of nighttime awakenings, or total sleep time.
Psychological interventions, averaging 5.0 hours of therapy time, produced reliable changes in two of the four sleep measures examined. The average effect sizes (i.e., z scores) were 0.88 for sleep latency and 0.65 for time awake after sleep onset. These results indicate that patients with insomnia were better off after treatment than 81% and 74% of untreated control subjects in terms of sleep induction and sleep maintenance, respectively. Stimulus control and sleep restriction were the most effective single therapy procedures, whereas sleep hygiene education was not effective when used alone. Clinical improvements seen at treatment completion were well maintained at follow-ups averaging 6 months in duration.
The findings indicate that nonpharmacological interventions produce reliable and durable changes in the sleep patterns of patients with chronic insomnia.
Investigated the treatment of bedtime problems and its generalization to night wakings. Six children (M age = 35 months) and their parents participated in this study. A multiple-baseline design across subjects was employed and found that treatment instituted at bedtime was successful in relieving both bedtime disturbances and night wakings. Furthermore, significant positive changes in parental sleep and family satisfaction occurred following amelioration of the children's sleep problems. Data support recent work suggesting that chronic sleep problems in children are amenable to behavioral interventions. In addition, this method appears to be more cost-effective and less stressful for parents to implement than behavioral interventions that directly target night wakings.
The purpose of the study was to assess the prevalence and correlates of sleep problems in adolescents.
A total of 763 students chosen at random among the 15 secondary schools of a French département were given a self-report questionnaire.
As much as 40.8% reported at least one of the five sleep disturbances we studied including difficulties falling asleep and staying asleep, a need for more sleep, early awakenings, and chronic sleeping pill intake. These sleep problems were highly related to various personal and family disorders. Discriminant analysis for categorical data pointed to a consistent but not significant descriptive profile accounting for sleep problems in these students. Suicide, weight concerns, and stimulant abuse were the most informative personal correlates as parts of this profile.
These findings suggest that the complaint of poor sleep should be regarded with special care in adolescents as a possibly meaningful and sensitive sign of severe family or personal disruption.
The aim of this study was to assess whether there is an association between chronic insomnia and the activity of the stress system. Fifteen young adult insomniacs (<40 years) were studied. After an adaptation night, each subject was recorded in the sleep laboratory for three consecutive nights. During this period, 24-hour urine specimens were collected for measurements of urinary free cortisol (UFC), catecholamines, and growth hormone (GH). The 24-hour UFC levels were positively correlated with total wake time (p=0.05). In addition, 24-hour urinary levels of catecholamine metabolites, DHPG, and DOPAC were positively correlated with percent stage 1 sleep (p<0.05) and wake time after sleep onset (WTASO) (p<0.05). Norepinephrine tended to correlate positively with percent stage 1 sleep (p=0.063) and WTASO (p=0.074), and negatively with percent slow-wave sleep (p=0.059). Twenty-four-hour urinary GH excretion was detectable in only three insomniacs, two of whom had low indices of sleep disturbance. We conclude that, in chronic insomnia, the activity of both limbs of the stress system (i.e., the HPA axis and the sympathetic system) relates positively to the degree of objective sleep disturbance.