Shared Family Environmental Factors Research Articles

Body mass index in parents and their adult offspring: A systematic review and meta-analysis.

Obesity may track across generations, due to genetics and shared family environmental factors, or possibly intrauterine programming. However, many studies only assess associations between maternal body mass index (BMI) and offspring BMI in childhood. To determine whether maternal and paternal associations with offspring BMI differ and whether associations persist into adulthood, a systematic review and meta-analysis was done. PubMed, Embase, Web of Science, and Google Scholar (to October 2022) were searched. Observational studies reporting associations between maternal or paternal BMI and adult offspring BMI were included. Offspring BMIs were reported as continuous or categorical measures. Forty-six studies were included in the systematic review. Meta-analyses were conducted using random-effects models. Parental BMI was positively associated with offspring BMI in adulthood. The pooled mother-offspring standardized mean difference (SMD) was 0.23 (95% confidence interval [CI]: 0.20, 0.26), and father-offspring SMD was similar: 0.22 (95% CI: 0.19, 0.25) in adjusted models. Offspring of mothers with overweight or obesity had the same risk of higher BMI as offspring of fathers with overweight or obesity. If these associations are causal, they support interventions targeting all family members, rather than focusing solely on mothers, to obtain a healthy weight development among offspring.

Acute appendicitis and ulcerative colitis: a population-based sibling comparison study

ObjectiveTo assess the inverse relationship between acute appendicitis and ulcerative colitis (UC) using a sibling comparison design to adjust for unmeasured familial genetic and environmental factors.DesignThe cohort comprised 3.1 million...

Environmental factors in offspring of parents with mood disorders and their role in parent\u2013child transmission: findings from a 14-year prospective high-risk study

BackgroundThe factors involved in the transmission of mood disorders are only partially elucidated. Aside from genes, the family environment might play a crucial role in parent–child transmission. Our goals were to (1) assess the associations of parental bipolar disorder (BPD) and Major Depressive Disorder (MDD) with individual or shared family environmental factors, including traumatic events in offspring, parental separation, family cohesion and parental attitudes; and 2) test whether these factors were mediators of the association between exposure to parental mood disorders and the onset of these disorders in offspring.MethodsThe sample stems from an ongoing family high-risk study of mood disorders conducted in the French-speaking part of Switzerland. Given the strong impact of the age of onset of parental disorders on their transmission to children, parental disorders were dichotomized according to the onset (cut-off 21 years). Probands with early-onset (n = 30) and later-onset BPD (n = 51), early-onset (n = 21) and later-onset MDD (n = 47) and controls (n = 65), along with their spouses (n = 193) and offspring (n = 388; < 18 years on study inclusion), were assessed over a mean follow-up duration of 14 years (s.d: 4.6). The environmental measures were based on reports by offspring collected before the onset of their first mood episode.ResultsOffspring of probands with later-onset BPD and offspring of probands with both early-onset and later-onset MDD reported traumatic events more frequently than comparison offspring, whereas exposure to parental separation was more frequent in all groups of high-risk offspring. Moreover, several familial environment scores including parenting attitudes differed between offspring of probands with BPD and comparison offspring. However, none of these factors were mediators of the parent–child transmission of BPD. Among the environmental factors, traumatic events were shown to be modest mediators of the transmission of early-onset MDD.ConclusionsOur data do not support the implication of the assessed environmental factors in the parent–child transmission of BPD. In contrast to BPD, traumatic events partially mediate the parent–child transmission of early-onset MDD, which has important implications for intervention and prevention. Early therapeutic efforts in offspring exposed to these events are likely to reduce their deleterious impact on the risk of subsequent MDD.

Mechanisms linking parental educational attainment with child ADHD, depression, and academic problems: a study of extended families in The Norwegian Mother, Father and Child Cohort Study.

BackgroundLow educational attainment in parents is associated with child psychopathology. It is not clear whether the associations are due to risk factors that family members share or due to effects of maternal or paternal education on the offspring. We investigate whether associations between maternal and paternal educational attainment and child symptoms of attention deficit/hyperactivity disorder (ADHD), depression, and academic problems are due to shared genetic factors, shared family environmental factors, or effects of the parental phenotype educational attainment itself.MethodsThis study is based on the Norwegian Mother, Father and Child Cohort Study (MoBa). The sample comprised 34,958 children (17,128 girls) in 28,372 extended‐family units. We used data from related nuclear families linked by siblings in the parent generation. We applied a quasi‐experimental extended children‐of‐twins design that included siblings in both generations and took account of nonrandom mating by including partners. Educational attainment was self‐reported by mothers and fathers. Mothers reported children's symptoms of ADHD, symptoms of depression, and academic problems by questionnaire when the children were 8 years old.ResultsChildren of lowly educated parents scored higher on all outcomes and had an approximate doubling of the risk of high symptom levels. The association between maternal and paternal educational attainment and child symptoms of ADHD and academic problems persisted after controlling for shared genetic and family environmental factors. Phenotypic transmission to depression was weaker and in the best fitting model fully explained by genetic factors shared by the two generations.ConclusionsAssociations between educational attainment of mothers and fathers and child symptoms of ADHD and academic problems could not be ascribed to shared familial risk factors, whereas associations with symptoms of depression could. Parental education or resources and behaviors resulting from low education might be targets of interventions aimed at reducing symptoms of ADHD and academic problems.

Paternal antidepressant use as a negative control for maternal use: assessing familial confounding on gestational length and anxiety traits in offspring

BackgroundMaternal antidepressant use in pregnancy has been associated with both shorter gestational length and child anxiety. We employed paternal antidepressant use as a negative-control exposure to indirectly assess whether confounding by genetic or shared familial environmental factors associated with depression may explain these associations.MethodsThe study sample came from the population-based Norwegian Mother and Child Cohort Study (MoBa) that recruited participants from 1999 to 2008. We included 70 959 families where the father completed a questionnaire about medication use in the 6 months prior to pregnancy. In 42 511 infants who completed the 3-year follow-up, we computed Z-scores for the anxiety domain of the Child Behavior Checklist. We used linear and logistic regression to assess the association between paternal antidepressant use, gestational age at birth and child anxiety.ResultsAntidepressants were used by 1.1% (n = 755) of fathers. Paternal antidepressant use was not associated with gestational age at birth [β = 0.63 days, 95% confidence interval (CI) –1.56, 0.31] whereas it was positively associated with a child anxiety symptom Z-score and high anxiety symptoms (odds ratio 1.33, 95% CI 0.90, 1.97) in unadjusted analyses. This association was attenuated when controlling for maternal and paternal history of depression and other measured factors (odds ratio 1.14, 95% CI 0.76, 1.69).ConclusionsThese results support the suggested effect of maternal use of antidepressants in pregnancy on shorter gestation; however, they suggest familial confounding could explain the association between maternal use of antidepressants and anxiety traits in the offspring.

Applying the demand-control-support model on burnout in managers and non-managers

Purpose – The purpose of this paper is to study the demand-control-support (DCS) model on burnout in male and female managers and non-managers, taking into account genetic and shared family environmental factors, contributing to the understanding of mechanisms of how and when work stress is related to burnout. Design/methodology/approach – A total of 5,510 individuals in complete same-sex twin pairs from the Swedish Twin Registry were included in the analyses. Co-twin control analyses were performed using linear mixed modeling, comparing between-pairs and within-pair effects, stratified by zygosity and sex. Findings – Managers scored higher on demands and control in their work than non-managers, and female managers seem to be particularly at risk for burnout facing more demands which are not reduced by a higher control as in their male counterparts. Co-twin analyses showed that associations between control and burnout as well as between demands and burnout seem to be affected by shared family environmental factors in male non-managers but not in male managers in which instead the associations between social support and burnout seem to be influenced by shared family environment. Practical implications – Taken together, the study offers knowledge that shared environment as well as sex and managerial status are important factors to consider in how DCS is associated to exhaustion. Originality/value – Using twin data with possibilities to control for genetics, shared environment, sex and age, this study offers unique insight into the DCS research, which focusses primarily on the workplace environment rather than individual factors.

Genetic and environmental risk factors in males for self-report externalizing traits in mid-adolescence and criminal behavior through young adulthood

Externalizing traits or behaviors are typically assessed by self-report scales or criminal records. Few genetically informative studies have used both methods to determine whether they assess the same genetic or environmental risk factors. We examined 442 male Swedish twin pairs with self-reported externalizing behaviors at age 16–17 years [externalizing traits (EXT), self-reported delinquency (SRD), impulsivity (IMP), grandiosity (GRD) and callousness (CLS)] and criminal behavior (CB) from the National Suspect Registry from age 13 to 25 years. Multivariate structural equation modeling was conducted with Mx. The best-fit model contained one genetic, one shared environmental and two non-shared environmental common factors, and variable specific genetic and non-shared environmental factors. The risk for CB was influenced substantially by both genetic (a2=0.48) and familial–environmental factors (c2=0.22). About one-third of the genetic risk for CB but all of the shared environmental risk was indexed by the self-report measures. The degree to which the individual measures reflected genetic versus familial–environmental risks for CB varied widely. GRD and CLS were correlated with CB mainly through common genetic risk factors. SRD and CB covaried largely because of shared familial–environmental factors. For EXT and IMP, observed correlations with CB resulted in about equal parts from shared genetic and shared familial–environmental factors. In adolescence, measures of grandiose and callous temperament best tap the genetic liability to CB.Measures of antisocial behaviors better index familial–environmental risks for CB. A substantial proportion of the genetic risk to CB was not well reflected in any of the self-report measures.

Genetic Analysis of Age-at-Onset for Cardiovascular Risk Factors in a Brazilian Family Study

Background/Aims: Statistical analysis of age-at-onset involving family data is particularly complicated because there is a correlation pattern that needs to be modeled and also because there are measurements that are censored. In this paper, our main purpose was to evaluate the effect of genetic and shared family environmental factors on age-at-onset of three cardiovascular risk factors: hypertension, diabetes and high cholesterol. Methods: The mixed-effects Cox model proposed by Pankratz et al. [2005] was used to analyze the data from 81 families, involving 1,675 individuals from the village of Baependi, in the state of Minas Gerais, Brazil. Results: The analyses performed showed that the polygenic effect plays a greater role than the shared family environmental effect in explaining the variability of the age-at-onset of hypertension, diabetes and high cholesterol. The model which simultaneously evaluated both effects indicated that there are individuals which may have risk of hypertension due to polygenic effects 130% higher than the overall average risk for the entire sample. For diabetes and high cholesterol the risks of some individuals were 115 and 45%, respectively, higher than the overall average risk for the entire population. Conclusions: Results showed evidence of significant polygenic effects indicating that age-at-onset is a useful trait for gene mapping of the common complex diseases analyzed. In addition, we found that the polygenic random component might absorb the effects of some covariates usually considered in the risk evaluation, such as gender, age and BMI.

Adolescent alcohol use is a risk factor for adult alcohol and drug dependence: evidence from a twin design

Early alcohol use is associated with abuse and dependence of licit and illicit substances later in life. The role of genetic and environmental factors in this association is not conclusive. In 1992, data on substance use, abuse/dependence and psychiatric disorders were collected from 8169 male twin members of the Vietnam Era Twin Registry. The interview obtained age of onset of regular drinking (one drink/month for 6 or more months). Regression analyses of twin pairs discordant for early alcohol use tested whether the association between early drinking (before age 17) and adult substance use and abuse/dependence remained after controlling for genetic factors, family environment and covariates. Twin models tested for common genetic and/or environmental influences on early drinking and adult alcohol dependence and ever use and abuse/dependence on marijuana and other drugs. Co-twin analyses suggested the association between early regular alcohol use and adult alcohol dependence, marijuana and other drug use, and marijuana and other drug abuse/dependence could not be entirely explained by common genetic and shared family environmental factors. Genetic contributions to early regular drinking were significantly correlated with those on use of marijuana (rA=0.59), use of other drugs (rA=0.64), alcohol dependence (rA=0.54) and abuse/dependence of marijuana and other drugs (rA=0.63 and 0.66). Small but significant unique environmental correlations (rE range 0.11-0.22) indicated that familial factors could not entirely explain the association between early alcohol use and later substance use, abuse and dependence. Early regular drinking is associated with later alcohol dependence and use, abuse/dependence on drugs. The association is not entirely explained by genetic or shared family environmental factors. This suggests unique environmental factors contribute to transitions from early regular alcohol drinking to use, abuse and dependence on alcohol and other substances.

Genes and family environment explain correlations between blood pressure and body mass index.

The correlations between systolic blood pressure (SBP) and diastolic blood pressure (DBP), and between SBP and body mass index (BMI), might result from genetic or environmental factors that determine variation in 2 or more phenotypes and are shared by family members. In 767 adult nuclear families (n=2912 individuals, including 66 pairs of monozygotic twins and 84 pairs of dizygotic twins), we used a multivariate normal model and the software FISHER to estimate genetic and environmental components of variation and covariation. Mean phenotypes were adjusted for age, gender, and generation, and for antihypertensive treatment. Genetic and shared family environmental factors accounted for 46% and 31% of total variance in SBP, respectively. Adjustment of SBP for DBP reduced considerably both the additive genetic (86.7 to 21.0) and shared environmental (59.7 to 21.0) components of variance. Smaller reductions in genetic (86.7 to 84.9) and shared environmental (59.7 to 51.1) components were observed after adjustment of SBP for BMI. For SBP and DBP, the correlation between the effects of genes was 1.00 and between shared environmental effects was 0.52. For SBP and BMI the correlations were 0.30 for genetic and 0.22 for shared environmental effects. Our findings suggest that the same genes and many of the same family environmental factors determine variation in both SBP and DBP. In contrast, SBP and BMI share genetic and family environmental determinants to a lesser degree. These observations are relevant to multifactorial cardiovascular risk reduction based on genetic and family environmental approaches.

Rebellious teens? Genetic and environmental influences on the social attitudes of adolescents.

Genetic and environmental influences in social attitudes were investigated in adopted and nonadopted children (N = 654) and their biological and adoptive relatives in the Colorado Adoption Project. Conservatism and religious attitudes were measured in the children annually from ages 12 to 15 and in the parents during the 12-year-old visit. Multivariate genetic model fitting indicated that both conservatism and religious attitudes are strongly influenced by shared-family environmental factors throughout adolescence. In contrast to previous findings from twin studies, which suggest that genetic influence on social attitudes does not emerge until adulthood, the present study detected significant genetic influence in conservatism as early as age 12. There was no evidence of genetic influence, however, on religious attitudes during adolescence.

Rebellious teens? Genetic and environmental influences on the social attitudes of adolescents.

Genetic and environmental influences in social attitudes were investigated in adopted and nonadopted children (N = 654) and their biological and adoptive relatives in the Colorado Adoption Project. Conservatism and religious attitudes were measured in the children annually from ages 12 to 15 and in the parents during the 12-year-old visit. Multivariate genetic model fitting indicated that both conservatism and religious attitudes are strongly influenced by shared-family environmental factors throughout adolescence. In contrast to previous findings from twin studies, which suggest that genetic influence on social attitudes does not emerge until adulthood, the present study detected significant genetic influence in conservatism as early as age 12. There was no evidence of genetic influence, however, on religious attitudes during adolescence.

Genetic and environemental factors in conduct problems and adult antisocial behavior among adult female twins.

Most twin and adoption studies of conduct problems have demonstrated modest genetic effects but substantial contributions of shared family environment. Conversely, most investigations have shown marked genetic influences but modest contributions of shared family environment in adult antisocial behavior. However, most previous work has focused on male subjects. We obtained retrospective reports of DSM-III-R-defined conduct disorder (CD) and adult antisocial behaviors from a population-based sample of female-female twin pairs. Genetic and environmental contributions to conduct problems and adult antisocial behaviors were examined using polychoric correlation coefficients and univariate structural equation modeling. Statistically significant but modest heritability was observed for conduct problems. A small, statistically nonsignificant contribution of shared family environment to CD behavior was also noted. Adult antisocial symptoms showed modest contributions of both additive genetic and shared family environmental factors. In both childhood and adulthood, the largest influence on antisocial behavior was individual-specific environment. Our findings support the importance of both genetic and environmental factors in antisocial behavior among women as well as the possibility that the relative importance of each set of influences differs by sex in both childhood and adulthood.

Personality resemblance in adoptive families: A 10-year follow-up.

Children from 181 of the 300 families of the Texas Adoption Project were recontacted after a 10year interval, at an average age of 17. They completed two standard personality tests, the Minnesota Multiphasic Personality Inventory (MMPI) and the Sixteen Personality Factor Questionnaire (16PF), plus a life events questionnaire and were rated by a parent on 24 bipolar trait scales. MMPI and 16PF scores were available from the earlier study for the adoptive parents, and MMPIs were available from the agency files for many of the adopted children's birth mothers. Parent-child correlations and regressions, sibling correlations, and comparison of the means of adopted and biological children were interpreted as indicating a modest genetic influence on personality traits (narrowsense heritability, uncorrected, of about .25), a near-zero influence of shared family environmental factors, and a substantial contribution of idiosyncratic environment. The relative emotional and social adjustment of the biological and the adopted children had shifted since the time of the first study, to the detriment of the adopted children, but most still fell in the normal range. Studying adoptive families is one way of assessing the extent to which personality differences reflect genetic differences among individuals rather than differences in their family environments. Moreover, if parents who adopt children have one or more biological children of their own, one can compare the resemblance of genetically related and genetically unrelated pairs. If information about the personality of one or both of the birth parents of an adopted child is also available, one can see what the resemblance of parent and child might be in the absence of any explicity shared experiences or interactions between them. If this resemblance is appreciable for some traits, it provides direct evidence for the influence of the genes in accounting for variation on these traits. If some of this information is available on two or more occasions, developmental questions can also be addressed. For example, do the genes play an increasing or a decreasing role in accounting for individual variation in a trait as children grow older? The Texas Adoption Project (Horn, Loehlin, & Willerman, 1979) studied 300 Texas families who had adopted one or more children through a church-related home for unwed mothers. Parents and children in these adoptive families were given various IQ and personality tests. IQ and personality test scores were also available from the agency files for many of the adopted children's birth mothers, from tests taken during their residence at the home some 3 to 14 years earlier. In this article we will report the results of a 10-year follow-up of many of the children in the