scholarly journals Continuity of genetic and environmental influences on clinically assessed major depression from ages 18 to 45

2018 ◽  
Vol 49 (15) ◽  
pp. 2582-2590
Author(s):  
Fartein Ask Torvik ◽  
Kristin Gustavson ◽  
Eivind Ystrom ◽  
Tom H. Rosenström ◽  
Nathan Gillespie ◽  
...  
Keyword(s):  
Risk Factors ◽  
Environmental Risk ◽  
Genetic Risk ◽  
Longitudinal Design ◽  
Environmental Influences ◽  
Environmental Risk Factors ◽  
Shared Environment ◽  
Term Stability ◽  
Long Term Stability

AbstractBackgroundStudies on the stability of genetic risk for depression have relied on self-reported symptoms rather than diagnoses and/or short follow-up time. Our aim is to determine to what degree genetic and environmental influences on clinically assessed major depressive disorder (MDD) are stable between age 18 and 45.MethodsA population-based sample of 11 727 twins (6875 women) born between 1967 and 1991 was followed from 2006 to 2015 in health registry data from primary care that included diagnoses provided by treating physicians. Individuals with schizophrenia or bipolar disorder (n = 163) were excluded. We modelled genetic and environmental risk factors for MDD in an accelerated longitudinal design.ResultsThe best-fitting model indicated that genetic influences on MDD were completely stable from ages 18 to 45 and explained 38% of the variance. At each age, the environmental risk of MDD was determined by the risk at the preceding observation, plus new environmental risk, with an environmental correlation of +0.60 over 2 years. The model indicated no effects of shared environment and no environmental effects stable throughout the observational period. All long-term stability was therefore explained by genetic factors.ConclusionsDifferent processes unfolded in the genetic and environmental risk for MDD. The genetic component is stable from later adolescence to middle adulthood and accounted for nearly all long-term stability. Therefore, molecular genetic studies can use age-heterogenous samples when investigating genetic risk variants of MDD. Environmental risk factors were stable over a short span of years with associations rapidly decreasing and no evidence of permanent environmental scarring.

Genetic and environmental influences on last-year major depression in adulthood: a highly heritable stable liability but strong environmental effects on 1-year prevalence

2017 ◽  
Vol 47 (10) ◽  
pp. 1816-1824 ◽  
Author(s):  
K. S. Kendler ◽  
C. O. Gardner
Keyword(s):  
Risk Factors ◽  
Major Depression ◽  
Environmental Effects ◽  
Environmental Risk ◽  
Structural Equation ◽  
Environmental Influences ◽  
Diagnostic Error ◽  
Environmental Risk Factors ◽  
Multiple Time ◽  
The Impact

BackgroundThis study seeks to clarify the contribution of temporally stable and occasion-specific genetic and environmental influences on risk for major depression (MD).MethodOur sample was 2153 members of female–female twin pairs from the Virginia Twin Registry. We examined four personal interview waves conducted over an 8-year period with MD in the last year defined by DSM-IV criteria. We fitted a structural equation model to the data using classic Mx. The model included genetic and environmental risk factors for a latent, stable vulnerability to MD and for episodes in each of the four waves.ResultsThe best-fit model was simple and included genetic and unique environmental influences on the latent liability to MD and unique wave-specific environmental effects. The path from latent liability to MD in the last year was constant over time, moderate in magnitude (+0.65) and weaker than the impact of occasion-specific environmental effects (+0.76). Heritability of the latent stable liability to MD was much higher (78%) than that estimated for last-year MD (32%). Of the total unique environmental influences on MD, 13% reflected enduring consequences of earlier environmental insults, 17% diagnostic error and 70% wave-specific short-lived environmental stressors.ConclusionsBoth genetic influences on MD and MD heritability are stable over middle adulthood. However, the largest influence on last-year MD is short-lived environmental effects. As predicted by genetic theory, the heritability of MD is increased substantially by measurement at multiple time points largely through the reduction of the effects of measurement error and short-term environmental risk factors.

Similar birth-cohort patterns in Crohn’s disease and multiple sclerosis

2017 ◽  
Vol 24 (2) ◽  
pp. 140-149 ◽  
Author(s):  
Amnon Sonnenberg ◽  
Vladeta Ajdacic-Gross
Keyword(s):  
Risk Factors ◽  
Multiple Sclerosis ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Birth Cohort ◽  
Environmental Risk ◽  
Time Trends ◽  
The United States ◽  
Environmental Risk Factors

Background: The etiology of Crohn’s disease and multiple sclerosis is unknown. Genetic susceptibility and environmental factors are believed to play a role in both diseases. Objectives: To compare the long-term time trends of the two diseases and thus gain insight about their etiology. Methods: We analyzed mortality data of Crohn’s disease and multiple sclerosis from Canada, England, Italy, the Netherlands, Switzerland, and the United States during the past 60 years. Age–period–cohort (APC) analyses based on logit models served to disentangle the separate influences of age, period, and cohort effects on the overall time trends. Results: The long-term time trends of Crohn’s disease and multiple sclerosis have been shaped by strikingly similar birth-cohort patterns. In both diseases alike, mortality increased in all generations born prior to 1910. It peaked among generations born between 1910 and 1930 and then declined in all subsequent generations. Similar birth-cohort patterns of Crohn’s disease and multiple sclerosis were found in each country analyzed separately. Conclusion: The birth-cohort patterns indicate that the development of Crohn’s disease and multiple sclerosis is influenced by exposure to environmental risk factors during an early period of life. These environmental risk factors may be similar or even identical in Crohn’s disease and multiple sclerosis.

Multivariate genetic analysis of the causes of temperance board registrations

1998 ◽  
Vol 172 (3) ◽  
pp. 268-272 ◽  
Author(s):  
Kenneth S. Kendler ◽  
Laura M. Karkowski ◽  
Carol A. Prescott ◽  
Michael C. Neale ◽  
Nancy L. Pedersen
Keyword(s):  
Risk Factors ◽  
Environmental Risk ◽  
Genetic Risk ◽  
Genetic Risk Factors ◽  
Environmental Risk Factors ◽  
Driving Under The Influence ◽  
Multivariate Genetic Analysis ◽  
Best Fitting ◽  
Alcohol Related Problems ◽  
Fitting Model

BackgroundThe Temperance Boards in Sweden registered individuals for three reasons: public drunkenness, driving under the influence of alcohol and committing a crime in connection with alcohol. We wanted to ascertain whether these three forms of alcohol-related problems result from similar or different genetic and environmental risk factors.MethodWe conducted a trivariate twin analysis of these three causes of registration in all male-female twin pairs of known zygosity born in Sweden, 1926–1949 (n=5177 twin pairs).ResultsPrevalences of registration for public drunkenness, drink-driving and alcohol-related crime were, respectively, 9.0, 3.6 and 4.0%. The best-fitting model had one general genetic and one general familial – environmental factor with specific genetic risk factors for drink-driving and specific familial – environmental risk factors for alcohol-related crime.ConclusionsThe three causes for alcohol registration in Sweden largely reflect the same genetic and environmental risk factors. Estimated heritabilities were similar for the three forms of registration. However, specific genetic risk factors exist for drink-driving and specific familial – environmental risk factors for alcohol-related crime. Genetic factors are somewhat less important and familial –environmental factors more important for public drunkenness than for drink-driving and alcohol related crime.

scholarly journals The Relationship Between the Genetic and Environmental Influences on Common Externalizing Psychopathology and Mental Wellbeing

2011 ◽  
Vol 14 (6) ◽  
pp. 516-523 ◽  
Author(s):  
Kenneth S. Kendler ◽  
John M. Myers ◽  
Corey L. M. Keyes
Keyword(s):  
Risk Factors ◽  
Environmental Risk ◽  
Genetic Risk ◽  
Genetic Risk Factors ◽  
Environmental Risk Factors ◽  
Mental Wellbeing ◽  
Negatively Associated ◽  
Externalizing Psychopathology ◽  
Internalizing Psychopathology ◽  
The Relationship

To determine the relationship between the genetic and environmental risk factors for externalizing psychopathology and mental wellbeing, we examined detailed measures of emotional, social and psychological wellbeing, and a history of alcohol-related problems and smoking behavior in the last year in 1,386 individual twins from same-sex pairs from the MIDUS national US sample assessed in 1995. Cholesky decomposition analyses were performed withthe Mx program. The best fit model contained one highly heritable common externalizing psychopathology factor for both substance use/abuse measures, and one strongly heritable common factor for the three wellbeing measures. Genetic and environmental risk factors for externalizing psychopathology were both negatively associated with levels of mental wellbeing and accounted for, respectively, 7% and 21% of its genetic and environmental influences. Adding internalizing psychopathology assessed in the last year to the model, genetic risk factors unique for externalizing psychopathology were now positively related to levels of mental wellbeing, although accounting for only 5% of the genetic variance. Environmental risk factors unique to externalizing psychopathology continued to be negatively associated with mental wellbeing, accounting for 26% of the environmental variance. When both internalizing psychopathology and externalizing psychopathology are associated with mental wellbeing, the strongest risk factors for low mental wellbeing are genetic factors that impact on both internalizing psychopathology and externalizing psychopathology, and environmental factors unique to externalizing psychopathology. In this model, genetic risk factors for externalizing psychopathology predict, albeit weakly, higher levels of mental wellbeing.

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

2013 ◽  
Vol 43 (10) ◽  
pp. 2161-2168 ◽  
Author(s):  
K. S. Kendler ◽  
C. J. Patrick ◽  
H. Larsson ◽  
C. O. Gardner ◽  
P. Lichtenstein
Keyword(s):  
Risk Factors ◽  
Environmental Factors ◽  
Environmental Risk ◽  
Genetic Risk ◽  
Criminal Behavior ◽  
Environmental Risk Factors ◽  
Environmental Risks ◽  
The Self ◽  
Self Report ◽  
Equation Modeling

BackgroundExternalizing 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.MethodWe 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.ResultsThe 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.ConclusionsIn 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.

The structure of genetic and environmental risk factors for three measures of disordered eating

1999 ◽  
Vol 29 (4) ◽  
pp. 925-934 ◽  
Author(s):  
T. WADE ◽  
N. G. MARTIN ◽  
M. C. NEALE ◽  
M. TIGGEMANN ◽  
S. A. TRELOAR ◽  
...  
Keyword(s):  
Risk Factors ◽  
Disordered Eating ◽  
Environmental Risk ◽  
Genetic Factors ◽  
Structured Interview ◽  
Environmental Risk Factors ◽  
Self Report ◽  
Shared Environment ◽  
Similar Degree ◽  
Psychiatric Interview

Background. The study explored the genetic and environmental risk factors for both the behaviours and attitudes characteristic of disordered eating.Methods. In three waves of data collection, information was collected from female twins regarding their eating and attitudes towards eating, weight and shape. The first assessment consisted of a self-report questionnaire (1988–9) with 1682 women. The second assessment consisted of a semi-structured psychiatric interview schedule (1992–3), completed by 1852 women, many of whom had completed Wave 1 assessment. The third assessment, with 325 women chosen from Waves 1 and 2 (1995–6), consisted of a semi-structured interview (the Eating Disorder Examination).Results. As only one twin pair was concordant for lifetime bulimia nervosa at Wave 3 assessment, ordinal measures of all assessments were used in a multivariate genetic analysis. Results indicated that additive genetic and non-shared environmental influences best explained variance in liability to disordered eating, with about 60% (95% CI 50–68) of the variance explained by genetic factors. Comparison with a model allowing for the effects of shared environment indicated genetic factors accounted for a similar degree of variance (59%, 95% CI 36–68).Conclusion. Liability to the development of the behaviours and attitudes characteristic of eating disorders is best explained by both environmental and genetic factors, with covariation between the three measures best explained by a single latent phenotype of disordered eating which has a heritability of 60%.

Genetic and environmental risk factors for the weight and shape concerns characteristic of bulimia nervosa

1998 ◽  
Vol 28 (4) ◽  
pp. 761-771 ◽  
Author(s):  
T. WADE ◽  
N. G. MARTIN ◽  
M. TIGGEMANN
Keyword(s):  
Risk Factors ◽  
Bulimia Nervosa ◽  
Environmental Risk ◽  
Environmental Influences ◽  
Model Fitting ◽  
Environmental Risk Factors ◽  
Weight Concern ◽  
Contrast Model ◽  
Shape Concern

Background. This study seeks to identify the genetic and environmental risk factors for the overvalued ideas that are characteristic of bulimia nervosa, using a biometrical model fitting approach with twin data.Methods. The Eating Disorder Examination (EDE), which can be used to gain continuous measures of dietary restraint, eating concern, weight concern and shape concern, was administered to 325 female twins, both monozygotic (MZ) and dizygotic (DZ). For each subscale, questions were asked concerning the month prior to interview and lifetime prevalence (‘ever’).Results. Model fitting indicated that there is a powerful role of the environment in shaping women's attitude towards weight, shape, eating and food, ranging from 38% to 100% of the variance. For all subscales, with the exception of weight concern, the best explanation for individual variation was one that incorporated additive genetic and non-shared environmental influences. In contrast, model fitting indicated that non-shared and shared environmental influences best explained the variance of weight concern.Conclusions. With the exception of the Shape Concern subscale, environmental factors make a greater contribution than genetic factors to the development of the overvalued ideas that are seen to be one of the triggers for the development of bulimia nervosa. Given this substantial role of the environment influences, it seems likely that environmental manipulation can be effective in the prevention of bulimia nervosa.

scholarly journals Maternal and environmental risk factors for neonatal AKI and its long-term consequences

2018 ◽  
Vol 14 (11) ◽  
pp. 688-703 ◽  
Author(s):  
Norberto Perico ◽  
David Askenazi ◽  
Monica Cortinovis ◽  
Giuseppe Remuzzi
Keyword(s):  
Risk Factors ◽  
Environmental Risk ◽  
Environmental Risk Factors ◽  
Long Term Consequences

scholarly journals Interactions of established risk factors and a GWAS-based genetic risk score on the risk of venous thromboembolism

2016 ◽  
Vol 116 (10) ◽  
pp. 705-713 ◽  
Author(s):  
Marta Crous-Bou ◽  
Immaculata De Vivo ◽  
Carlos A. Camargo ◽  
Raphaëlle Varraso ◽  
Francine Grodstein ◽  
...  
Keyword(s):  
Risk Factors ◽  
Venous Thromboembolism ◽  
Risk Score ◽  
Environmental Risk ◽  
Genetic Risk ◽  
Genetic Risk Score ◽  
Environmental Risk Factors ◽  
Health Study ◽  
Targeted Prevention ◽  
Genome Wide

SummaryMultiple genetic and environmental risk factors contribute to venous thromboembolism (VTE) risk. Understanding how genes and environmental risk factors interact may provide key insight into the pathophysiology of VTE and may identify opportunities for targeted prevention and treatment. It was our aim to examine the main effects and the potential effect-modification between single nucleotide polymorphisms (SNPs) at established loci and lifestyle risk factors for VTE. We performed a nested case-control study using data on 1,040 incident VTE cases and 16,936 controls from the Nurses’ Health Study, Nurses’ Health Study II, and Health Professionals Follow-up Study cohorts, who gave blood, were selected as participants in a previous genome-wide association study (GWAS), and completed a biennial questionnaire at time of blood draw. We selected SNPs that were associated with VTE risk in previous GWAS studies. A genetic risk score (GRS) was constructed to evaluate the combined effect of the 16 SNPs that have reached genome-wide significance in previous GWAS of VTE. Interactions between SNPs and VTE risk factors (BMI and smoking) were also assessed. We found a significant association between our GRS and VTE risk. The risk of VTE among individuals in the highest GRS tertile was 2.02 times that of individuals in the lowest GRS tertile (p-trend = 9.69x10-19). The OR was 1.52 (p=1.03x10-8) for participants in the highest GRS tertile compared to those in the medium GRS tertile. However, while BMI and smoking were associated with VTE, and their effects were additive to each other we did not observe any significant multiplicative gene-environment interactions.Supplementary Material to this article is available online at www.thrombosis-online.com.

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