scholarly journals Social inequalities in reception of social welfare support: A population based twin study

2016 ◽  
Vol 26 (1-2) ◽  
Author(s):  
Eivind Ystrom ◽  
Ragnhild Ørstavik ◽  
Ted Reichborn-Kjennerud ◽  
Fartein Ask Torvik
Keyword(s):  
Risk Factors ◽  
Social Welfare ◽  
Genetic Factors ◽  
Social Inequalities ◽  
Familial Risk ◽  
Population Based ◽  
Drop Out ◽  
Historical Event ◽  
Relative Contribution ◽  
Specific Risk

Social welfare support runs in families. Recent studies using Nordic registry data have found individual<br />differences in genetic factors to be of substantial importance for medical benefits. However, to date there has<br />been no genetically informative studies on receiving social welfare support. To prevent young adults to not<br />drop out of the work life and become recipients of social welfare support, it is of substantial interest to<br />clarify to what extent the familiarity of social welfare support is due to genetic or social differences between<br />families. We used data from the Historical-Event Database on 7,698 Norwegian twins born 1967-1979 to<br />estimate the relative contribution of genetic factors, the effective familial environment (i.e. the “shared<br />environment”), and individual-specific environmental factors. We found that the two forms of familial risk,<br />genetic and shared environmental, explained 39% and 45%, respectively, of the risk for receiving social<br />welfare support among young Norwegian twins. Only 17% of the variance in risk factors could be explained<br />by individual-specific risk factors. It appears that risk for receiving social welfare support can to a great<br />extent be explained by environmental differences between families. Therefore prevention strategies targeting<br />social inequalities between families would indeed be effective. Furthermore, genetic risk factors are also<br />important in explaining risk for receiving social welfare support. These effects could be mediated through<br />heritable traits related to substance abuse, psychiatric disorders, and personality. Individual-specific risk factors<br />were of very little importance. Hence, with regard to receiving social welfare support, family matters.

scholarly journals Predictors of disordered eating in adolescence and young adulthood

2013 ◽  
Vol 38 (2) ◽  
pp. 128-138 ◽  
Author(s):  
Dawit Shawel Abebe ◽  
Leila Torgersen ◽  
Lars Lien ◽  
Gertrud S. Hafstad ◽  
Tilmann von Soest
Keyword(s):  
Risk Factors ◽  
Disordered Eating ◽  
Young Adulthood ◽  
Early Adolescence ◽  
Developmental Psychopathology ◽  
Population Based ◽  
Specific Risk ◽  
Random Intercept ◽  
Developmental Phases ◽  
Gender Specific

We investigated longitudinal predictors for disordered eating from early adolescence to young adulthood (12–34 years) across gender and different developmental phases among Norwegian young people. Survey data from a population-based sample were collected at four time points (T) over a 13-year time span. A population-based sample of 5,679 females and males at T1 and T2, 2,745 at T3 and 2,718 at T4 were included in analyses, and linear regression and random intercept models were applied. In adolescence, initial disordered eating and parental overprotectiveness were more strongly related to disordered eating among females, whereas loneliness was a stronger predictor for adolescent males. Initial disordered eating during early adolescence predicted later disordered eating more strongly in late- than mid-adolescence. In young adulthood, no significant gender-specific risk factors were found. The findings provide support for both shared and specific risk factors for the developmental psychopathology of disordered eating.

Distribution and Heritability of Recurrent Ear Infections

1997 ◽  
Vol 106 (8) ◽  
pp. 624-632 ◽  
Author(s):  
Kari J. Kvaerner ◽  
Jennifer R. Harris ◽  
Kristian Tambs ◽  
Per Magnus
Keyword(s):  
Structural Equation ◽  
Genetic Factors ◽  
Age Of Onset ◽  
Population Based ◽  
Equation Modeling ◽  
Relative Contribution ◽  
Genes And Environment ◽  
Ear Infections ◽  
The Mean ◽  
Familial Environment

The distribution of recurrent ear infections was obtained from a population-based sample of 2,750 pairs of Norwegian twins born between 1967 and 1974. The lifetime prevalence of self-reported recurrent ear infections was 8.9%, with a significant predominance of female cases. The mean age of onset was 4.2 years, with a gradual decrease in occurrence from 2 to 7 years of age. Among monozygotic pairs, the rate of tetrachoric correlation between co-twins was almost identical in males (0.73, SE 0.08) and females (0.74, SE 0.06), but among the dizygotic pairs the correlation was clearly higher in males (0.53, SE 0.12) than in females (0.20, SE 0.12). The value in the unlike-sexed dizygotic twins (0.25, SE 0.05) was intermediate to that of the like-sexed male and female dizygotic pairs. The relative contribution of genes and environment to variability in the predisposition to develop otitis media was estimated by means of structural equation modeling. Variation in liability to ear infections was mainly explained by additive genetic and dominance factors in females, for whom heritability was estimated at 74%. The remaining 26% of the variation in liability was explained by individual environmental factors. In males, 45% of the variation could be accounted for by genetic factors, 29% by common familial environment, and the remaining 26% by individual environmental effects.

Familial risk factors and the familial aggregation of psychiatric disorders

1990 ◽  
Vol 20 (2) ◽  
pp. 311-319 ◽  
Author(s):  
Kenneth S. Kendler
Keyword(s):  
Risk Factors ◽  
Risk Factor ◽  
Psychiatric Disorders ◽  
Genetic Factors ◽  
Familial Aggregation ◽  
Familial Risk ◽  
Significant Proportion ◽  
Potential Importance ◽  
Obstetric Injury ◽  
Familial Risk Factors

SynopsisAll major psychiatric disorders aggregate in families. For most disorders, both genes and environmental factors play an important role in this aggregation. While recent work has tended to concentrate on the importance of genetic factors, this report focuses on the potential importance of environmental risk factors which themselves aggregate in families. In particular, this article examines how much of the familial aggregation of a psychiatric disorder may result from the familial aggregation of a risk factor. The model is illustrated and then applied to putative familial risk factors for schizophrenia and depression. The results of the model suggest that if parental loss and exposure to pathogenic rearing practices are true risk factors for depression, then they could account for a significant proportion of the familial aggregation of depression. By contrast, the model predicts that even if obstetric injury and low social class are true risk factors for schizophrenia, they together would account for only a very small proportion of the tendency for schizophrenia to aggregate in families.

scholarly journals Impact of familial risk factors on management and survival of early-onset breast cancer: a population-based study

2005 ◽  
Vol 94 (2) ◽  
pp. 231-238 ◽  
Author(s):  
H M Verkooijen ◽  
P O Chappuis ◽  
E Rapiti ◽  
G Vlastos ◽  
G Fioretta ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Risk Factors ◽  
Early Onset ◽  
Familial Risk ◽  
Population Based ◽  
Early Onset Breast Cancer ◽  
Population Based Study ◽  
Familial Risk Factors

scholarly journals Community Level Disadvantage and the Likelihood of First Ischemic Stroke

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Bernadette Boden-Albala ◽  
Eric T. Roberts ◽  
Harmon Moats ◽  
Hiba Arif ◽  
Ralph L. Sacco ◽  
...  
Keyword(s):  
Risk Factors ◽  
New York ◽  
Ischemic Stroke ◽  
Census Tract ◽  
Social Inequalities ◽  
Population Level ◽  
Population Based ◽  
Community Level ◽  
Community Controls ◽  
The Impact

Background and Purpose. Residing in “disadvantaged” communities may increase morbidity and mortality independent of individual social resources and biological factors. This study evaluates the impact of population-level disadvantage on incident ischemic stroke likelihood in a multiethnic urban population. Methods. A population based case-control study was conducted in an ethnically diverse community of New York. First ischemic stroke cases and community controls were enrolled and a stroke risk assessment performed. Data regarding population level economic indicators for each census tract was assembled using geocoding. Census variables were also grouped together to define a broader measure of collective disadvantage. We evaluated the likelihood of stroke for population-level variables controlling for individual social (education, social isolation, and insurance) and vascular risk factors. Results. We age-, sex-, and race-ethnicity-matched 687 incident ischemic stroke cases to 1153 community controls. The mean age was 69 years: 60% women; 22% white, 28% black, and 50% Hispanic. After adjustment, the index of community level disadvantage (OR 2.0, 95% CI 1.7–2.1) was associated with increased stroke likelihood overall and among all three race-ethnic groups. Conclusion. Social inequalities measured by census tract data including indices of community disadvantage confer a significant likelihood of ischemic stroke independent of conventional risk factors.

scholarly journals Genetic and Environmental Contributions to Long-Term Sick Leave and Disability Pension: A Population-Based Study of Young Adult Norwegian Twins

2013 ◽  
Vol 16 (4) ◽  
pp. 759-766 ◽  
Author(s):  
Line C. Gjerde ◽  
Gun Peggy Knudsen ◽  
Nikolai Czajkowski ◽  
Nathan Gillespie ◽  
Steven H. Aggen ◽  
...  
Keyword(s):  
Risk Factors ◽  
Young Adult ◽  
Environmental Factors ◽  
Sick Leave ◽  
Disability Pension ◽  
Strong Association ◽  
Population Based ◽  
Historical Event ◽  
Environmental Correlations

Although exclusion from the workforce due to long-term sick leave (LTSL) and disability pension (DP) is a major problem in many Western countries, the etiology of LTSL and DP is not well understood. These phenomena have a strong association as most patients receiving DP have first been on LTSL. However, only a few of those on LTSL end up with DP. The present study aimed to investigate the common and specific genetic and environmental risk factors for LTSL and DP. The present study utilizes a population-based sample of 7,710 young adult twins from the Norwegian Institute of Public Health Twin Panel, which has been linked to the Historical-Event Database (FD-Trygd; 1998–2008). Univariate and bivariate twin models were fitted to determine to what degree genetic and environmental factors contribute to variation in LTSL and DP. The estimated heritabilities of LTSL and DP were 0.49 and 0.66, respectively. There was no evidence for shared environmental or sex-specific factors. The phenotypic-, genetic-, and non-familial environmental correlations between the variables were 0.86, 0.82, and 0.94, respectively. Our results indicate that familial transmission of LTSL and DP is due to genetic and not environmental factors. The risk factors contributing to LTSL and DP were mainly shared, suggesting that what increases risk for LTSL also increases risk for DP. However, a non-negligible part of the genetic variance was not shared between the variables, which may contribute to explaining why some progress from LTSL to DP, whereas others return to work.

Genetic Susceptibility to Sickness Absence is Similar Among Women and Men: Findings From a Swedish Twin Cohort

2012 ◽  
Vol 15 (5) ◽  
pp. 642-648 ◽  
Author(s):  
Pia Svedberg ◽  
Annina Ropponen ◽  
Kristina Alexanderson ◽  
Paul Lichtenstein ◽  
Jurgita Narusyte
Keyword(s):  
Risk Factors ◽  
Sickness Absence ◽  
Genetic Model ◽  
Model Fitting ◽  
Heritability Estimate ◽  
Population Based ◽  
Population Based Study ◽  
Relative Contribution ◽  
Best Fitting

Previous studies of risk factors for sickness absence (SA) focus primarily on psychosocial and work environmental exposures. The aim of this study was to investigate the relative contribution of genetic influences on SA among women and men. The population-based study sample of Swedish twins (34,547) included 13,743 twin pairs of known zygosity, 3,495 monozygotic, 5,073 same-sexed dizygotic, and 5,175 opposite sexed. The point prevalence of long-term SA (≥15 days) in each zygosity and sex group was calculated. The risk of SA was estimated as an odds ratio (OR) with 95% confidence intervals (CI) where the odds for twins on SA to have a co-twin on SA was compared to the OR for SA in twins whose co-twin were not sickness absent. Intrapair correlations and probandwise concordance rates were calculated and standard biometrical genetic model-fitting methods were used to estimate the heritability of SA. The prevalence of SA was 8.8% (women 10.7%; men 6.5%). Intrapair similarity was higher among monozygotic than dizygotic twin pairs. The best-fitting model showed no sex differences in genetic effects or variance components contributing to SA. The heritability estimate was 36% (95% CI: 35–40%). Results suggest genetic contribution to the variation of SA and that environmental factors have an important role, for women and men. As SA seem to be influenced by genetic factors, future studies of associations between risk factors and SA should consider this potentially confounding effect.

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