RESUMEN
BACKGROUND AND AIMS: Poor quality of life is a main complaint among individuals with irritable bowel syndrome (IBS). Self-rated health (SRH) is a powerful predictor of clinical outcomes, and also reflects psychological and social aspects of life and an overall sense of well-being. This population-based twin study evaluates how IBS affects ratings of physical and mental health, and influences perceptions of hindrance of daily activity by physical or mental health. Further, we examine how IBS is related to these SRH measures. METHODS: The sample included 5288 Norwegian twins aged 40-80, of whom 575 (10.9%) suffer from IBS. Hierarchical regressions were used to estimate the impact of IBS on perceptions of health, before and after accounting for other chronic physical and mental health conditions. Two dimensions of SRH, physical and mental, and two aspects of functional limitations, the extent to which physical or mental health interferes with daily activities, were included as outcomes in separate models. Co-twin control analyses were used to explore whether the relationships between IBS and the four measures of SRH are causal, or due to shared genetic or shared environment effects. RESULTS: IBS was an independent predictor of poor self-rated physical health (OR = 1.82 [1.41; 2.33]), the size of this effect was comparable to that predicted by chronic somatic conditions. However, in contrast to somatic diseases, IBS was associated with the perception that poorer ratings of mental health (OR = 1.45 [1.02; 2.06]), but not physical health (OR = 1.23 [0.96; 1.58]), interfered with daily activity. The co-twin control analyses suggest that causal mechanisms best explain the relationships between IBS with self-rated physical health and with hindrance of daily activities. In contrast, the relationship between IBS and self-rated mental health was consistent with shared genetic effects. CONCLUSION: IBS is predictive of poor self-rated physical health. The relationship between IBS and self-rated mental health is best explained by shared genetic effects which might partially explain why mental health interferes with daily activity to a larger degree among those with IBS.
Asunto(s)
Síndrome del Colon Irritable , Trastornos Mentales , Ansiedad , Enfermedad Crónica , Humanos , Síndrome del Colon Irritable/psicología , Salud Mental , Calidad de VidaRESUMEN
Social relationships play a critical role in health and well-being throughout life. We analyzed the genetic and environmental variance co-variance structure for social support and strain across four sets of relationships including with one's co-twin, spouse/partner, family and friends. The sample included 5288 Norwegian twins aged 40-80. Older people reported less support from their co-twin and friends and less strain from their family and friends. Genetic influences contribute importantly to variation across all the measures, with estimates ranging from 0 to 58%; variance due to shared environmental influences was most important for the twin-relationship, ranging from 0.11 to 0.42%. Social support was negatively correlated with social strain across all sets of relationships. With the exception of the co-twin relationship, these associations were primarily mediated by genetic and non-shared environmental effects.
Asunto(s)
Relaciones Familiares/psicología , Apoyo Social , Gemelos/psicología , Adulto , Anciano , Anciano de 80 o más Años , Intervalos de Confianza , Femenino , Humanos , Masculino , Persona de Mediana Edad , Modelos Biológicos , Gemelos Dicigóticos/psicología , Gemelos Monocigóticos/psicologíaRESUMEN
BACKGROUND: We aimed to disentangle genetic and environmental causes in lung cancer while considering smoking status. METHODS: Four Nordic twin cohorts (43â 512 monozygotic (MZ) and 71â 895 same sex dizygotic (DZ) twin individuals) had smoking data before cancer diagnosis. We used time-to-event analyses accounting for censoring and competing risk of death to estimate incidence, concordance risk and heritability of liability to develop lung cancer by smoking status. RESULTS: During a median of 28.5â years of follow-up, we recorded 1508 incident lung cancers. Of the 30 MZ and 28 DZ pairs concordant for lung cancer, nearly all were current smokers at baseline and only one concordant pair was seen among never smokers. Among ever smokers, the case-wise concordance of lung cancer, that is the risk before a certain age conditional on lung cancer in the co-twin before that age, was significantly increased compared with the cumulative incidence for both MZ and DZ pairs. This ratio, the relative recurrence risk, significantly decreased by age for MZ but was constant for DZ pairs. Heritability of lung cancer was 0.41 (95% CI 0.26 to 0.56) for currently smoking and 0.37 (95% CI 0.25 to 0.49) for ever smoking pairs. Among smoking discordant pairs, the pairwise HR for lung cancer of the ever smoker twin compared to the never smoker co-twin was 5.4 (95% CI 2.1 to 14.0) in MZ pairs and 5.0 (95% CI 3.2 to 7.9) in DZ pairs. CONCLUSIONS: The contribution of familial effects appears to decrease by age. The discordant pair analysis confirms that smoking causes lung cancer.
Asunto(s)
Neoplasias Pulmonares/inducido químicamente , Neoplasias Pulmonares/genética , Fumar/efectos adversos , Gemelos Dicigóticos/genética , Gemelos Monocigóticos/genética , Estudios de Cohortes , Estudios de Seguimiento , Humanos , Incidencia , Estudios Retrospectivos , Factores de Riesgo , Factores de TiempoRESUMEN
The association between birth weight and later life outcomes is of considerable interest in life-course epidemiology. Research often relies on self-reported measures of birth weight, and its validity is consequently of importance. We assessed agreement between self-reported birth weight and official birth records for Norwegian twins born 1967-1974. The intraclass correlation between self-reported birth weight and register-based birth weight was 0.91 in our final sample of 363 twins. It could be expected that 95% of self-reported birth-weight values will deviate from official records within a maximum of +446 grams and a minimum of -478 grams - around a mean deviation of 16 grams. Self-reported birth weight had a sensitivity of 0.78-0.89 and a positive predictive value of 0.59-0.85, and an overall weighted kappa of 0.71. We further assessed agreement by conducting two linear regression models where we respectively regressed self-reported birth weight and register-based birth weight on adult body mass index, a known association. The two models were not significantly different; however, there were different levels of significance in parameter estimates that warrant some caution in using self-reported birth weight. Reliability of self-reported birth weight was also assessed, based on self-reports in another sample of twins born 1935-1960 who had reported their birth weight in two questionnaires 34 years apart. The intraclass correlation was 0.86, which indicates a high degree of reliability. In conclusion, self-reported birth weight, depending on context and age when birth weight was reported, can be cautiously used.
Asunto(s)
Peso al Nacer , Índice de Masa Corporal , Autoinforme , Gemelos , Adulto , Anciano , Anciano de 80 o más Años , Femenino , Humanos , Masculino , Persona de Mediana Edad , NoruegaRESUMEN
BACKGROUND: Social stress is related to symptom burden of irritable bowel syndrome (IBS). This study explores the associations between IBS and social strain or low support in close relationships, including spouse, friends, and family, in a Norwegian twin cohort. METHODS: The sample included 5442 Norwegian twins aged 40-80, of whom 589 suffer from IBS. We used multivariate structural equation models to estimate genetic and environmental sources of variation and covariation underlying IBS liability, measures of social stress and the relationships between these. The co-twin control design was used to explore the nature of the associations between IBS and social strain or low support using models that test for causality. KEY RESULTS: Genetic effects explained between 30% and 40% of the variation in IBS liability, social strain, and low support. The phenotypic correlations between IBS and social strain (0.20) and between IBS and low support (0.17) were primarily explained by shared genetic pathways. Surprisingly, all the genetic variation underlying the liability to develop IBS was shared with genetic influences underlying social strain and low support. In contrast, most of the nonshared environmental influences accounting for the variation of IBS risk were unique for IBS. The co-twin control analyses suggest that the relationships between IBS and the social measures reflect shared familial rather than causal effects. CONCLUSION & INFERENCES: The genetic variation of IBS risk was fully shared with genetic effects for variation in the social measures, emphasizing the contribution of genes involved in central brain-gut mechanisms to genetic variation in IBS risk.