Association between a Serotonin Transporter Length Polymorphism and Primary Insomnia

Deuschle, Michael; Schredl, Michael; Schilling, Cláudia; Wüst, Stefan; Frank, Josef; Witt, Stephanie H.; Rietschel, Marcella; Buckert, Magdalena; Meyer‐Lindenberg, Andreas; Schulze, Thomas G.

doi:10.1093/sleep/33.3.343

Cited by 97 publications

(70 citation statements)

References 29 publications

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“…An implication of our finding is that identification of genes for one of the three symptoms can help search genes for the other symptoms. Recent molecular genetic studies have shown that the serotonin system genes are involved in susceptibilities to all three symptoms (Deuschle et al, 2010;Falkenberg et al, 2011;Uher & McGuffin, 2008), which support our results. In our best-fitting model, symptom-specific genetic variances were relatively small.…”

Section: Discussionsupporting

confidence: 91%

The Genetic and Environmental Structure of the Covariation Among the Symptoms of Insomnia, Fatigue, and Depression in Adult Females

2012

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Although the co-occurrence among symptoms of insomnia, fatigue, and depression has been frequently reported, the etiology of this co-occurrence remains poorly understood. A total of 3,758 adult female twins in the United Kingdom completed a mail-out survey including six questions concerning frequency and severity of symptoms of insomnia, fatigue, and depression. Correlations among the scores of the three symptoms ranged from 0.35 to 0.44. Among various multivariate models we tested, the common-pathway model explained the data best. In the best-fitting model, the common factor was explained approximately equally by genetic and unique environmental factors (49% and 51%, respectively). In addition to the common variance, there was a significant specific variance in each symptom, where unique environmental factors were much larger than genetic factors. These results imply that although there are shared genetic liabilities for the development of symptoms of depression, fatigue, and insomnia, it is environmental experiences that make etiological distinctions among three symptoms.

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Section: Discussionsupporting

confidence: 91%

The Genetic and Environmental Structure of the Covariation Among the Symptoms of Insomnia, Fatigue, and Depression in Adult Females

2012

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“…Indeed, two studies to date have found that the 'short' allele conferred greater risk for sleep disturbances, including problems such as insomnia. (91,92) However, a recent candidate gene study focusing on 5HTTLPR by our group found that 'long-long' homozygotes experienced poorer sleep quality than carriers of at least one 'short' allele. (93) It is possible that these discrepant findings are due to differences in sample composition.…”

Section: Specifying Genes and Environmentsmentioning

confidence: 94%

Quantitative genetic research on sleep: A review of normal sleep, sleep disturbances and associated emotional, behavioural, and health-related difficulties

Barclay¹,

Gregory²

2013

Sleep Medicine Reviews

116

107

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Over the past 50 years, well over 100 twin studies have focussed on understanding factors contributing to variability in normal sleep-wake characteristics and sleep disturbances.Whilst we have gained a great deal from these studies, there is still much to be learnt. Twin studies can be used in multiple ways to answer questions beyond simply estimating heritability. This paper provides a comprehensive review of some of the most important findings from twin studies relating to sleep to date, with a focus on studies investigating genetic and environmental influences contributing to i) objective and subjective measures of normal sleep characteristics (e.g. sleep stage organisation, sleep quality); as well as sleep disturbances and disorders such as dyssomnias (e.g. insomnia, narcolepsy) and parasomnias (e.g. sleepwalking, bruxism); ii) the persistence of sleep problems from childhood to adulthood, and the possibility that the aetiological influences on sleep change with age; iii) the associations between sleep disturbances, emotional, behavioural and health-related problems; and iv) processes of gene-environment correlation and interaction. We highlight avenues for further research, emphasising the need to further consider the aetiology of longitudinal associations between sleep disturbances and psychopathology; the genetic and environmental overlap between sleep and numerous phenotypes; and processes of geneenvironment interplay and epigenetics.

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“…32 , 34 , 35 Candidate gene studies have identifi ed gene variants that may be involved in the pathophysiology of insomnia, including Apo ε 4, 36 PER3 4/4 , 37 HLA DQB1 * 0602, 38 homozygous Clock gene 3111C/C Clock, 39 and short (s-) allele of the 5-HTTLPR. 40 A genomewide association study found numerous single-nucleotide polymorphisms (SNPs) signifi cantly associated with insomnia symptoms. 41 Th e most signifi cant SNPs occurred within genes involved in neuroplasticity (eg, ROR1, PLCB1, EPHA4, and CACNA1A), stress reactivity (eg, STK39, USP25, and MARP10), neuronal excitability (eg, GABRB1 and DLG2), and mental health (eg, NPAS3).…”

Section: Genetics Of Sleep and Insomniamentioning

confidence: 99%

The Pathophysiology of Insomnia

Levenson

Kay

Buysse

2015

Chest

289

147

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Insomnia disorder is characterized by chronic dissatisfaction with sleep quantity or quality that is associated with diffi culty falling asleep, frequent nighttime awakenings with diffi culty returning to sleep, and/or awakening earlier in the morning than desired. Although progress has been made in our understanding of the nature, etiology, and pathophysiology of insomnia, there is still no universally accepted model. Greater understanding of the pathophysiology of insomnia may provide important information regarding how, and under what conditions, the disorder develops and is maintained as well as potential targets for prevention and treatment.The aims of this report are (1) to summarize current knowledge on the pathophysiology of insomnia and (2) to present a model of the pathophysiology of insomnia that considers evidence from various domains of research. Working within several models of insomnia, evidence for the pathophysiology of the disorder is presented across levels of analysis, from genetic to molecular and cellular mechanisms, neural circuitry, physiologic mechanisms, sleep behavior, and self-report. We discuss the role of hyperarousal as an overarching theme that guides our conceptualization of insomnia. Finally, we propose a model of the pathophysiology of insomnia that integrates the various types of evidence presented.

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Association between a Serotonin Transporter Length Polymorphism and Primary Insomnia

Abstract: This finding contributes to the understanding of the pathophysiology of primary insomnia and suggests a biological basis between the prevalent comorbidity of primary insomnia and other psychiatric disorders.

Cited by 97 publications

References 29 publications

The Genetic and Environmental Structure of the Covariation Among the Symptoms of Insomnia, Fatigue, and Depression in Adult Females

The Genetic and Environmental Structure of the Covariation Among the Symptoms of Insomnia, Fatigue, and Depression in Adult Females

Quantitative genetic research on sleep: A review of normal sleep, sleep disturbances and associated emotional, behavioural, and health-related difficulties

The Pathophysiology of Insomnia

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