Twin Studies of Human Obesity
Claude Bouchard in The Genetics of Obesity, 2020
Several methods have been proposed to estimate the heritability of traits. The so-called “classical” estimate of heritability4 is calculated as twice the difference between the MZ and DZ intraclass correlations. It is a simple calculation, has been popular for many years, and has been employed extensively in studies of obesity. In deriving this estimate, the assumption is made that only additive genetic effects and family (or common) environmental effects influence intrapair similarity. Additive genetic effects arise when alleles at a number of genetic loci contribute additively to the trait and there are no intraloci (dominance) or interloci (epistatic) interactions. Under such an assumption, the MZ twin correlation will be simply a function of the genetic variation within the population (denoted H) plus the common environmental variation (denoted C); thus,
Genetics of Psoriasis and Psoriatic Arthritis
Siba P. Raychaudhuri, Smriti K. Raychaudhuri, Debasis Bagchi in Psoriasis and Psoriatic Arthritis, 2017
Twin studies compare disease concordance rates between genetically identical monozygotic (MZ) and dizygotic (DZ) twins. Studies in psoriasis have shown a concordance rate ranging from 20% to 70% among MZ twins and 9% to 20% among DZ twins, indicating a higher risk of disease among the more genetically similar MZ twins [20–23]. Although these numbers still reflect both shared genes and a shared environment, twin studies do enable the dissection of phenotypic variation into additive genetic effects, dominant genetic effects, common (shared) environmental effects, and random (nonshared) environmental effects. Broad-sense heritability (H2) is defined as the proportion of phenotypic variance that can be explained by all genetic effects (additive and dominant), and it has been estimated to be quite high relative to other complex diseases, ranging from 60% to 90% [18], which suggests that shared genetics plays a much larger role than shared environment in the above estimates for psoriasis.
Elevated Psychiatric Risk in Same-Sex Married Individuals: Large-scale Evidence is Consistent with a Substantial Role of Familial Common Causes
Published in The Journal of Sex Research, 2023
Brendan P. Zietsch
The second problem with the authors’ interpretation of their results is that the term “shared familial influences” contains an important caveat (which they acknowledge in the Discussion): much of the putative familial common causes, which Xu et al. set out to investigate, are not shared among siblings. For example, genetic effects shared by siblings only comprise 50% of the total genetic effects for a trait – or less, for non-additive genetic effects or for half-siblings. Therefore, the sibling control method leaves at least half of any genetic common causes uncontrolled. As a consequence, the true extent to which familial common causes account for elevation of psychiatric risk in LGB individuals could be much greater than the already-substantial effects reported. Indeed, the authors’ analysis using adoptive siblings estimated that 98% of the association between same-sex marriage and depression could be accounted for by overlapping genetic influences, which is consistent with genetic common causes accounting for all of the elevated risk of depression among same-sex married individuals. (Probably 98% is an overestimate of the true value, though; the estimates from this analysis have low precision because of the relatively few adopted siblings and the low statistical power to differentiate genetic and shared environmental variance components.)
Familial abnormalities of endocannabinoid signaling in schizophrenia
Published in The World Journal of Biological Psychiatry, 2019
Dagmar Koethe, Franziska Pahlisch, Martin Hellmich, Cathrin Rohleder, Juliane K. Mueller, Andreas Meyer-Lindenberg, E. Fuller Torrey, Daniele Piomelli, F. Markus Leweke
The twin model is a powerful approach for determining the relative contributions of heredity apart from common and unique environmental influences on variation of disorder-associated abnormalities. Despite evidence of heterogeneity across studies, meta-analytic results from twin studies of schizophrenia are consistent with the view of schizophrenia as a complex trait that results from genetic and environmental influences. Sullivan et al. (2003) found evidence for substantial additive genetic effects by using a multi-group twin model. The point estimate of heredity in liability to schizophrenia was 81% (95% confidence interval, 73–90%). Notably, there was consistent evidence across these studies for common or shared environmental influences on liability to schizophrenia (point estimate 11% (95% confidence interval, 3–19%).
Child Maltreatment and Adult Sexual Assault Victimization: Genetic and Environmental Associations
Published in The Journal of Sex Research, 2020
Patrizia Pezzoli, Jan Antfolk, Emilia Kronlund, Pekka Santtila
To test our hypothesis H4b, we further estimated the two univariate models in women and men separately. A substantial difference between same-sex and opposite-sex DZ twins emerged in the cross-twin within-trait correlations. Correlations were positive in same-sex DZ twins (r = .16 in women, and r = .07 in men), and negative in opposite-sex DZ twins (r = − .02), suggesting that genetic factors influencing ASA in women could be, at least in part, qualitatively different from the those influencing ASA in men. The ACE model indicated that, for women, 28% of individual differences in the likelihood of experiencing ASA could be explained by additive genetic factors, 1% by shared environmental factors, and the remaining 71% by unique environmental factors. For men, we estimated no additive genetic effects, and, instead, only shared and unique environmental effects (C2 = 5.5%, E2 = 94.5%). As predicted, women showed significantly larger additive genetic influences on ASA compared to men (p < .01; ES = .28), who, in contrast, showed significantly larger unique environmental influences (p < .01; ES = .23). No dominant genetic effect emerged when we estimated the ADE model separately in the two sex groups.
Related Knowledge Centers
- Allele
- Epistasis
- Phenotype
- Quantitative Genetics
- Zygosity
- Dominance
- Locus