The Heritability of CHD Mortality in Danish Twins After Controlling for Smoking and BMI

2005 ◽  
Vol 8 (1) ◽  
pp. 53-59 ◽  
Author(s):  
Andreas Wienke ◽  
Anne M. Herskind ◽  
Kaare Christensen ◽  
Axel Skytthe ◽  
Anatoli I. Yashin
Keyword(s):  
Environmental Factors ◽  
Structural Equation ◽  
Equation Model ◽  
Mortality Data ◽  
Best Fitting ◽  
Genetic And Environmental Factors ◽  
Individual Frailty ◽  
Fitting Model ◽  
Model Approach

AbstractCause-specific mortality data on Danish monozygotic and dizygotic twins are used to analyze heritability estimates of susceptibility to coronary heart disease (CHD) after controlling for smoking and Body Mass Index (BMI). The sample includes 1209 like-sexed twin pairs born between 1890 and 1920, where both individuals were still alive in 1966. The participants completed a questionnaire in 1966 which included questions on smoking, height and weight. The analysis was conducted with both sexes pooled due to the relatively small number of twin pairs. Follow-up was conducted from January 1, 1966 to December 31, 1993. The correlated gammafrailty model with observed covariates was used for the genetic analysis of frailty to account for censoring and truncation in the lifetime data. During the follow-up, 1437 deaths occurred, including 435 deaths due to CHD. Proportions of variance of frailty attributable to genetic and environmental factors were analyzed using the structural equation model approach. Different standard biometric models are fitted to the data to evaluate the magnitude and nature of genetic and environmental factors on mortality. Using the best-fitting model without covariates, heritability of frailty to CHD was found to be 0.45 (0.11). This result changes only slightly to 0.55 (0.13) in a DE model after controlling for smoking and BMI. This analysis underlines the existence of a substantial genetic influence on individual frailty associated with mortality caused by CHD.

The Heritability of Mortality Due to Heart Diseases: A Correlated Frailty Model Applied to Danish Twins

Twin Research ◽  
2001 ◽  
Vol 4 (4) ◽  
pp. 266-274 ◽  
Author(s):  
Andreas Wienke ◽  
Niels V. Holm ◽  
Axel Skytthe ◽  
Anatoli I. Yashin
Keyword(s):  
Environmental Factors ◽  
Parametric Analysis ◽  
Structural Equation ◽  
Heart Diseases ◽  
Frailty Model ◽  
Equation Model ◽  
Shared Environment ◽  
Males And Females ◽  
Genetic And Environmental Factors

AbstractData of the Danish Twin Registry on monozygotic and dizygotic twins are used to analyse genetic and environmental influences on susceptibility to heart diseases for males and females, respectively. The sample includes 7955 like-sexed twin pairs born between 1870 and 1930. Follow-up was from 1 January 1943 to 31 December 1993 which results in truncation (twin pairs were included in the study if both individuals were still alive at the beginning of the follow-up) and censoring (nearly 40% of the study population was still alive at the end of the follow-up). We use the correlated gamma-frailty model for the genetic analysis of frailty to account for this censoring and truncation. During the follow-up 9370 deaths occurred, 3393 deaths were due to heart diseases in general, including 2476 deaths due to coronary heart disease (CHD). Proportions of variance of frailty attributable to genetic and environmental factors were analyzed using the structural equation model approach. Different standard biometric models are fitted to the data to evaluate the magnitude and nature of genetic and environmental factors on mortality. Using the best fitting model heritability of frailty (liability to death) was found to be 0.55 (0.07) and 0.53 (0.11) with respect to heart diseases and CHD, respectively, for males and 0.52 (0.10) and 0.58 (0.14) for females in a parametric analysis. A semi-parametric analysis shows very similar results. These analyses may indicate the existence of a strong genetic influence on individual frailty associated with mortality caused by heart diseases and CHD in both, males and females. The nature of genetic influences on frailty with respect to heart diseases and CHD is probably additive. No evidence for dominance and shared environment was found.

A quantitative genetic analysis of schizotypal personality traits

2003 ◽  
Vol 33 (5) ◽  
pp. 803-816 ◽  
Author(s):  
Y. M. LINNEY ◽  
R. M. MURRAY ◽  
E. R. PETERS ◽  
A. M. MacDONALD ◽  
F. RIJSDIJK ◽  
...  
Keyword(s):  
Structural Equation ◽  
Model Fitting ◽  
Twin Studies ◽  
Equation Model ◽  
Common Pathway ◽  
Schizotypal Personality ◽  
Quantitative Genetic ◽  
Best Fitting ◽  
Limited Power ◽  
Fitting Model

Background. Previous twin studies investigating the heritability of schizotypy have often had limited power and have failed to measure the disorganization/social anxiety component.Method. Seven hundred and thirty-three female twin pairs, drawn from the Institute of Psychiatry Volunteer Twin Register, completed the Oxford–Liverpool Inventory of Feelings and Experiences and the Peters et al. Delusions Inventory. Structural equation modelling was carried out on scores for MZ and DZ twin pairs.Results. The best fitting models for all scales comprised additive genetic and unique environmental effects. Heritability was estimated at approximately 50% for most scales, although it was lower at 37% for the PDI scale. Multivariate structural equation model fitting revealed a best-fitting model in which additive genetic and unique environmental influences act through a single common pathway for Cognitive Disorganization, Unusual Experiences and the PDI, and through a separate common pathway for Cognitive Disorganization and Introvertive Anhedonia.Conclusions. The various components of schizotypy are moderately heritable. Multivariate model fitting indicates that at least two latent factor structures are required to account for the covariation between the various components of schizotypy. The positive and negative components of schizotypy are relatively genetically independent, although each in turn may be related to Cognitive Disorganization.

scholarly journals Genetic and Environmental Influences on Smoking Behavior across Adolescence and Young Adulthood in the Virginia Twin Study of Adolescent Behavioral Development and the Transitions to Substance Abuse Follow-Up

2015 ◽  
Vol 18 (1) ◽  
pp. 43-51 ◽  
Author(s):  
Elizabeth K. Do ◽  
Elizabeth C. Prom-Wormley ◽  
Lindon J. Eaves ◽  
Judy L. Silberg ◽  
Donna R. Miles ◽  
...  
Keyword(s):  
Environmental Factors ◽  
Young Adulthood ◽  
Twin Study ◽  
Smoking Behavior ◽  
Smoking Initiation ◽  
Study Results ◽  
Adolescence And Young Adulthood ◽  
Genetic And Environmental Factors ◽  
The Relationship

Little is known regarding the underlying relationship between smoking initiation and current quantity smoked during adolescence into young adulthood. It is possible that the influences of genetic and environmental factors on this relationship vary across sex and age. To investigate this further, the current study applied a common causal contingency model to data from a Virginia-based twin study to determine: (1) if the same genetic and environmental factors are contributing to smoking initiation and current quantity smoked; (2) whether the magnitude of genetic and environmental factor contributions are the same across adolescence and young adulthood; and (3) if qualitative and quantitative differences in the sources of variance between males and females exist. Study results found no qualitative or quantitative sex differences in the relationship between smoking initiation and current quantity smoked, though relative contributions of genetic and environmental factors changed across adolescence and young adulthood. More specifically, smoking initiation and current quantity smoked remain separate constructs until young adulthood, when liabilities are correlated. Smoking initiation is explained by genetic, shared, and unique environmental factors in early adolescence and by genetic and unique environmental factors in young adulthood; while current quantity smoked is explained by shared environmental and unique environmental factors until young adulthood, when genetic and unique environmental factors play a larger role.

scholarly journals The role of perceived stress and cognitive function on the relationship between neuroticism and depression among the elderly: a structural equation model approach

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Mukda Banjongrewadee ◽  
Nahathai Wongpakaran ◽  
Tinakon Wongpakaran ◽  
Tanyong Pipanmekaporn ◽  
Yodying Punjasawadwong ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Structural Equation Model ◽  
Perceived Stress ◽  
Structural Equation ◽  
The Elderly ◽  
Equation Model ◽  
The Relationship ◽  
Model Approach

scholarly journals Exploring the Drivers behind Self-Reported and Measured Food Wastage

2019 ◽  
Vol 11 (20) ◽  
pp. 5677 ◽  
Author(s):  
Elimelech ◽  
Ert ◽  
Ayalon
Keyword(s):  
Food Waste ◽  
Structural Equation ◽  
Equation Model ◽  
The Sustainable Development ◽  
Self Reports ◽  
Negative Effect ◽  
Development Goals ◽  
Meal Planning ◽  
Food Wastage

Understanding households’ food waste drivers is crucial for forming a coherent policy to meet the sustainable development goals. However, current studies have documented mixed evidence regarding food waste determinants. Most studies have relied on self-reports, assuming they reflect actual behaviors. This study applies a structural equation model that evaluates both self-reported and measured food wastage, and how they are affected by different households’ attributes, attitudes, and behaviors. As such, it also provides a test for the underlying logic that self-reports are a proxy for actual food waste. Results show that measured food wastage is, at best, weakly correlated with self-reports. Moreover, drivers affecting self-reported and measured food wastage are not necessarily the same. Household size affects only measured food wastage. Source separation behavior negatively affects self-reported and measured food wastage, while environmental attitudes have a negative effect only on self-reports. Meal planning, unplanned shopping, and food purchased have no impact on self-reported and measured food wastage. The relation between self-reported and actual food waste and their drivers are even less understood than we thought. The distinction between self-reports and actual waste is crucial for follow-up research on this subject as well as assessing policy measures.

A longitudinal study of personality and major depression in a population-based sample of male twins

2007 ◽  
Vol 37 (8) ◽  
pp. 1163-1172 ◽  
Author(s):  
AYMAN H. FANOUS ◽  
MICHAEL C. NEALE ◽  
STEVEN H. AGGEN ◽  
KENNETH S. KENDLER
Keyword(s):  
Major Depression ◽  
Environmental Factors ◽  
Structural Equation ◽  
Causal Effect ◽  
Population Based ◽  
Twin Model ◽  
Genetic Overlap ◽  
Genetic And Environmental Factors ◽  
One Year ◽  
Time To Onset

ABSTRACTBackgroundThe relationship between personality and psychiatric illness is complex. It is not clear whether one directly causes the other.MethodIn a population-based sample of male twins (n=3030), we attempted to predict major depression (MD) from neuroticism (N) and extraversion (E) and vice versa, to evaluate the causal, scar, state, and prodromal hypotheses. In a longitudinal, structural equation twin model, we decomposed the covariation between N and MD into (a) genetic and environmental factors that are common to both traits, as well as specific to each one and (b) direct causal effects of N at time 1 on subsequent MD, as well as between MD and subsequent N.ResultsE was negatively correlated with lifetime and one-year prevalence of MD. N predicted the new onset of MD, and was predicted by both current and past MD. It did not predict the time to onset of MD. All of the covariation between N and MD was due to additive genetic and individual-specific environmental factors shared by both traits and a direct causal path between MD and N assessed later. No genetic factors were unique to either trait.ConclusionsIn men, N may be a vulnerability factor for MD but does not cause it directly. However, MD may have a direct causal effect on N. The genetic overlap between N and MD in men may be greater than in women.

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