Why twin studies really don't tell us much about human heritability

1999 ◽  
Vol 22 (5) ◽  
pp. 904-905 ◽  
Author(s):  
Sidney J. Segalowitz

The derivation of heritability from human twin studies involves serious methodological flaws. Heritability is consistently overestimated because of biological confounds of twinning, consistent and often gross underestimation of the environmental variance, and nonadditive genetic influences that can hugely exaggerate heritability values. Despite this bad research design, behaviour geneticists continue to publish results implying that their heritability results are valid.

2014 ◽  
Vol 17 (6) ◽  
pp. 545-552 ◽  
Author(s):  
Yoon-Mi Hur

A twin design was used to examine the developmental nature of genetic, environmental, and phenotypic variations in hyperactivity and inattention problems (HIP). Mothers of 662 complete pairs of twins (273 monozygotic [MZ] pairs and 389 dizygotic [DZ] pairs) aged from 3 to 13 years (mean [SD] age = 8.3 [2.9] years) responded to the items of the HIP scale of the Strengths and Difficulties questionnaire via a telephone interview. Maximum likelihood MZ and DZ twin correlations in the total sample were 0.47 (95% CI: 0.37–0.55) and −0.01 (95% CI: −0.11–0.09). A standard univariate model incorporating age as a modifier was applied to the raw data. Results of model-fitting analyses showed that the phenotypic variation of HIP monotonically increased from age 3 to age 12 and that this increase was completely due to an increase in genetic variance, suggesting that it is genes that expand individual difference in ADHD symptoms with age during childhood. Child-specific environmental variance was constant during this age period. In terms of relative influences, total genetic factors increased from 33% (95% CI: 27–44%) at age 3 to 51% (95% CI: 28–71%) at age 13 and this increase was accompanied by a decrease in relative influences of child-specific environmental factors from 67% (95% CI: 56–73%) at age 3 to 49% (95% CI: 29–72%) at age 13. These estimates of genetic influences were somewhat lower than those found in most twin studies of ADHD symptoms. However, the increasing trend of genetic influences with age during childhood was consistent with the results of a recent meta-analysis of ADHD symptoms.


2006 ◽  
Vol 9 (2) ◽  
pp. 185-193 ◽  
Author(s):  
Annica Dominicus ◽  
Juni Palmgren ◽  
Nancy L. Pedersen

AbstractIncomplete data on trait values may bias estimates of genetic and environmental variance components obtained from twin analyses. If the nonresponse mechanism is ‘ignorable’ then methods such as full information maximum likelihood estimation will produce consistent variance component estimates. If, however, nonresponse is ‘nonignorable’, then the situation is more complicated. We demonstrate that a within-pair correlation of nonresponse, possibly different for monozygotic (MZ) and dizygotic (DZ) twins, may well be compatible with ‘ignorability’. By means of Monte Carlo simulation, we assess the potential bias in variance component estimates for different types of nonresponse mechanisms. The simulation results guide the interpretation of analyses of data on perceptual speed from the Swedish Adoption/Twin Study of Aging. The results suggest that the dramatic decrease in genetic influences on perceptual speed observed after 13 years of follow-up is not attributable solely to dropout from the study, and thus support the hypothesis that genetic influences on some cognitive abilities decrease with age in late life.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 1026-1026
Author(s):  
Alice Kim ◽  
Alyssa Kam ◽  
Maxwell Kofman ◽  
Christopher Beam

Abstract Heritability of cognitive ability changes across late adulthood, although whether genetic variance increases or decreases in importance is not understood well. We performed a systematic review of the heritability of cognitive ability derived from longitudinal twin studies of middle-aged and older adult twins. Using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, articles were identified in APA PsycINFO and Clarivate Web of Science electronic databases. Identified articles were screened by title and abstract; remaining full-text articles were then fully evaluated. Reference sections served as an additional method for identification of relevant articles. In total, 3,106 articles were identified and screened, 28 of which were included and were based on data from 10 longitudinal twin studies published from 1994-2021. There are large genetic influences on an initial level of cognitive performance across domains whereas there are small to moderate genetic influences on change in performance with age. Evidence was less definitive about whether the same or different genetic factors contribute to both level and change. Non-shared environmental influences appeared to drive individual changes in cognitive performance. Heritability tended to either be stable or decline after 65 years, possibly because of the increasing importance of non-shared environmental influences on cognitive ability. Recent studies report increases in heritability across specific subtests and domains. Shared environmental variance accounted for little variance in cognitive ability. Emerging research questions and future directions for understanding genetic and environment influences in the context of gene-environment interplay are highlighted in this review.


Author(s):  
Tracey D. Wade

The current chapter reviews our progress in understanding how genes influence eating and eating disorders (EDs) by addressing the following areas: (1) how recognition of genetic influences on eating and EDs emerged; (2) the complex nature of genetic action; (3) what twin studies can tell us about genetic influences; and (4) the current state of linkage and association studies. It is concluded that genes are an important part of the explanatory framework for the etiology of EDs, with an important contribution of the shared environment to the development of cognition and attitudes that may initiate disordered eating practices, and a critical contribution of the environment in providing a context within which genetic risk is more likely to be expressed. We currently have a limited understanding of the specific genes that are implicated, and the ways in which genes and the environment work together to increase risk for disordered eating.


2019 ◽  
Vol 11 (4) ◽  
pp. 433-450 ◽  
Author(s):  
Lea Klassen ◽  
Eike F. Eifler ◽  
Anke Hufer ◽  
Rainer Riemann

Although many previous studies have emphasized the role of environmental factors, such as parental home and school environment, on achievement motivation, classical twin studies suggest that both additive genetic influences and non-shared environmental influences explain interindividual differences in achievement motivation. By applying a Nuclear Twin Family Design on the data of the German nationally representative of TwinLife study, we analyzed genetic and environmental influences on achievement motivation in adolescents and young adults. As expected, the results provided evidence for the impact of additive genetic variation, non-additive genetic influences, as well as twin specific shared environmental influences. The largest amount of variance was attributed to non-shared environmental influences, showing the importance of individual experiences in forming differences in achievement motivation. Overall, we suggest a revision of models and theories that explain variation in achievement motivation by differences in familial socialization only.


2010 ◽  
Vol 25 (5) ◽  
pp. 264-267 ◽  
Author(s):  
N.L. Pedersen ◽  
A. Fiske

AbstractIt has been well established that suicidal behavior is familial. Twin studies provide a unique opportunity to distinguish genetic effects from other familial influences. Consistent with findings from previous twin studies, including case series and selected samples, data from the population-based Swedish Twin Registry clearly demonstrate the importance of genetic influences on suicide. Twin studies of suicidal ideation and suicide attempts also implicate genetic influences, even when accounting for the effects of psychopathology. Future work is needed to evaluate the possibility of age and gender differences in heritability of suicide and nonfatal suicidal behavior.


Author(s):  
Ted Reichborn-Kjennerud ◽  
Kenneth S. Kendler

This chapter reviews the evidence for genetic contributions to the etiology of personality disorders (PDs) as defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM; 5th ed.). This approach and some of the controversial issues associated with its development are briefly described in the first section. The second section evaluates the evidence for genetic influence on DSM PDs from family and twin studies using quantitative genetic methods. Studies that move beyond individual PDs are also reviewed, together with studies on the extent to which common genetic factors influence PDs and normal personality traits and PDs and pathological personality trait domains. Stability of genetic influences on PDs over time are also examined. Molecular genetic studies are reviewed in the third section. The fourth section deals with gene environment interplay, and the final section discusses future directions in the exploration of genetic influences on PDs.


Twin Research ◽  
2002 ◽  
Vol 5 (4) ◽  
pp. 277-286 ◽  
Author(s):  
Dan A. Svensson ◽  
Bo Larsson ◽  
Elisabet Waldenlind ◽  
Nancy L. Pedersen

AbstractTo explore age-related mechanisms in the expression of recurrent headache, we evaluated whether genetic and environmental influences are a function of the reporting age using questionnaire information that was gathered in 1973 for 15- to 47-year-old Swedish twins (n =12,606 twin pairs). Liability to mixed headache (mild migraine and tension-type headache) was explained by non-additive genetic influences (49%) in men aged from 15 to 30 years and additive genetic plus shared environmental influences (28%) in men aged from 31 to 47 years. In women, the explained proportion of variance, which was mainly due to additive genetic effects, ranged from 61% in adolescent twins to 12% in twins aged from 41 to 47 years, whereas individual specific environmental variance was significantly lower in twins aged from 15 to 20 years than in twins aged from 21 to 30 years. Liability to migrainous headache (more severe migraine) was explained by non-addi-tive genetic influences in men, 32% in young men and 45% in old men, while total phenotypic variance was significantly lower in young men than in old men. In women, the explained proportion of variance ranged from 91% in the youngest age group to 37% in the oldest age group, with major contributions from non-additive effects in young and old women (15–20 years and 41–47 years, respectively) and additive genetic effects in intermediate age groups (21–40 years). While total variance showed a positive age trend, genetic variance tended to be stable across age groups, whereas individual specific environmental variance was significantly lower in adolescent women as compared to older women.


2010 ◽  
Vol 64 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Teresa Lee ◽  
Julie D. Henry ◽  
Julian N. Trollor ◽  
Perminder S. Sachdev

Addiction ◽  
2008 ◽  
Vol 103 (7) ◽  
pp. 1069-1081 ◽  
Author(s):  
Arpana Agrawal ◽  
Michael T. Lynskey

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