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Twin Studies of Human Obesity
Published in Claude Bouchard, The Genetics of Obesity, 2020
Joanne M. Meyer, Albert J. Stunkard
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,
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
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.)
Cohort profile and heritability assessment of familial pancreatic cancer: a nation-wide study
Published in Scandinavian Journal of Gastroenterology, 2021
Ming Tan, Klaus Brusgaard, Anne-Marie Gerdes, Michael Bau Mortensen, Sönke Detlefsen, Ove B. Schaffalitzky de Muckadell, Maiken Thyregod Joergensen
The calculated heritability using ICC represents a narrow sense additive genetic model. The estimated heritability is a narrow sense because it captures only the proportion of genetic variations that are due to additive genetic effects (i.e. dominant or recessive inheritance was not taken into account). Multiple environmental exposures within families such as heavy smoking, alcohol, obesity, etc. have been reported as risk factors for early onset of precursor lesions of pancreatic cancer [23,24]. Environmental factors may be especially relevant to FPC as these patients develop more precursor lesions with differential gene expression patterns compared to pancreatic cancer patients without familial predisposition [25–27]. Accumulative environmental exposures such as drinking and smoking confer a strong risk of pancreatic inflammation (i.e. pancreatitis) [28], while inflammatory signals have been shown to implicate both development of precursor lesions and progression to PDAC [29]. This means that sharing of the risky environmental factors within families may also contribute to family aggregation of FPC. Hence, the ICC-based approach provides an upper bound estimate of heritability. Findings of the present study emphasize the genetic component in pancreatic cancer (PC) as reflected by reports of previous population-based studies – indicating an increased risk of PDAC among FDRs to patients with PC in general [5,30,31].
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.