A community-based study of insomnia in Hong Kong Chinese children: Prevalence, risk factors and familial aggregation.
ABSTRACT There has been limited data on familial aggregation of insomnia. We aimed to explore the prevalence, risk factors and familial aggregation of childhood insomnia with a large community-based sample.
A community-based epidemiologic study of sleep disorders was conducted among primary school children. Those children with at least one reported biological parent were recruited. A total of 5695 children (mean age 9.2; SD 1.8), 4939 of their reported biological mothers (mean age 38.9; SD 4.6) and 4289 of their reported biological fathers (mean age 43.3; SD 5.5) were studied.
The rates of insomnia 3 times/week in the past 12 months were 4.0%, 12.8% and 9.7% for children, mothers and fathers, respectively. A robust familial aggregation of insomnia was found even after adjustment of the shared environmental and socio-demographic factors. There was a significant dose-response relationship among the children across their parental status from neither, fathers, mothers to both parents with insomnia [3.0%, 7.1%, 9.5% and 11.9%; with ORs (95% CIs)=2.48 (1.82-4.37) for fathers, 3.42 (2.55-4.59) for mothers and 4.42 (2.42-8.10) for both parents, respectively]. In addition, the frequency of insomniac symptoms of the parents also had a dose-response effect on the rate of insomnia of their children.
Insomnia is a common problem in both children and their parents. A significant familial aggregation of childhood onset insomnia was seen in this study even after adjustment of the co-risk factors. There was a dose-response effect of parental insomnia on the rate of insomnia of their children with a slight predilection of maternal influences.
- SourceAvailable from: Julio Fernandez-Mendoza[Show abstract] [Hide abstract]
ABSTRACT: Cognitive-emotional hyperarousal is believed to be a predisposing factor for insomnia; however, there is limited information on the association of familial vulnerability to insomnia and cognitive-emotional hyperarousal. The aim of this study was to estimate the heritability of stress-related insomnia and examine whether parental vulnerability to stress-related insomnia is associated with cognitive-emotional hyperarousal in their offspring. We studied a volunteer sample of 135 nuclear families comprised of 270 middle-aged (51.5 ± 5.4 years) fathers and mothers and one of their biological offspring (n = 135, 20.2 ± 1.1 years). We measured vulnerability to stress-related insomnia (i.e. Ford Insomnia Response to Stress Test: FIRST), perceived stress, depression and anxiety in all participants, and arousability, presleep cognitive and somatic arousal, coping and personality in the offspring. We found a heritability estimate of 29% for FIRST scores. High FIRST parents had three to seven times the odds of having offspring highly vulnerable to stress-related insomnia. Offspring of high FIRST parents showed higher arousability, presleep cognitive arousal and emotion-oriented coping. Furthermore, high FIRST mothers contributed to offspring's higher anxiety and lower task-oriented coping, while high FIRST fathers contributed to offspring's higher presleep somatic arousal and conscientiousness. Vulnerability to stress-related insomnia is significantly heritable. Parents vulnerable to stress-related insomnia have offspring with cognitive-emotional hyperarousal who rely upon emotion-oriented coping. These data give support to the notion that arousability and maladaptive coping are key factors in the aetiology of insomnia.Journal of Sleep Research 05/2014; DOI:10.1111/jsr.12168 · 2.95 Impact Factor
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ABSTRACT: Our population-based study examined the prevalence of insomnia symptoms and its sociodemographic, subjective, and polysomnographic (PSG) sleep risk factors in young and preadolescent children. We performed a cross-sectional study of 700 children, ages 5-12 years who underwent a 9-h PSG and parent-completed sleep and development questionnaires (Penn State Child Cohort). Insomnia symptoms were defined as parent report of difficulty falling or staying asleep and sleep-disordered breathing (SDB) as an apnea hypopnea index of ⩾1. The prevalence of insomnia symptoms was 19.3% and did not significantly change (20.2%) when children with SDB were excluded. A significant interaction between gender and age revealed that the prevalence of insomnia symptoms was highest in girls ages 11 to 12 years (30.6%). This gender difference was not associated with significant differences between girls and boys ages 11-12years in anxiety and depressive symptoms. In contrast girls ages 11-12years with insomnia symptoms, but not boys of the same group, demonstrated clinically significant PSG sleep disturbances compared to those without insomnia symptoms. These data suggest that one out of five young children and preadolescents of the general population have insomnia symptoms. Importantly, the prevalence of insomnia symptoms peaks in girls ages 11 to 12 years and is associated with objective sleep disturbances which may be related to hormonal changes associated with the onset of puberty rather than anxiety and depression.Sleep Medicine 01/2014; 15(1):91-95. DOI:10.1016/j.sleep.2013.08.787 · 3.10 Impact Factor
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ABSTRACT: Sleep is a complex physiological process and still remains one of the great mysteries of science. Over the past 10 y, genetic research has provided a new avenue to address the regulation and function of sleep. Gene loci that contribute quantitatively to sleep characteristics and variability have already been identified. However, up to now, a genetic basis has been established only for a few sleep disorders. Little is yet known about the genetic background of insomnia, one of the most common sleep disorders. According to the conceptualisation of the 3P model of insomnia, predisposing, precipitating and perpetuating factors contribute to the development and maintenance of insomnia. Growing evidence from studies of predisposing factors suggests a certain degree of heritability for insomnia and for a reactivity of sleep patterns to stressful events, explaining the emergence of insomnia in response to stressful life events. While a genetic susceptibility may modulate the impact of stress on the brain, this finding does not provide us with a complete understanding of the capacity of stress to produce long-lasting perturbations of brain and behaviour. Epigenetic gene-environment interactions have been identified just recently and may provide a more complex understanding of the genetic control of sleep and its disorders. It was recently hypothesised that stress-response-related brain plasticity might be epigenetically controlled and, moreover, several epigenetic mechanisms have been assumed to be involved in the regulation of sleep. Hence, it might be postulated that insomnia may be influenced by an epigenetic control process of both sleep mechanisms and stress-response-related gene-environment interactions having an impact on brain plasticity. This paper reviews the evidence for the genetic basis of insomnia and recent theories about epigenetic mechanisms involved in both sleep regulation and brain-stress response, leading to the hypothesis of an involvement of epigenetic mechanisms in the development and maintenance of insomnia.Sleep Medicine Reviews 08/2013; DOI:10.1016/j.smrv.2013.05.002 · 9.14 Impact Factor