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(searched for: doi:10.1017/s0001566000000945)
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Monika A. Hersberger-Zurfluh, Spyridon N. Papageorgiou, Melih Motro, Alpdogan Kantarci, Leslie A. Will, Theodore Eliades
The Angle orthodontist, Volume 91, pp 384-390; https://doi.org/10.2319/060520-515.1

Abstract:
Objectives: To determine the additive genetic and environmental contributions to the vertical growth of craniofacial structures. Materials and Methods: The sample consisted of 64 untreated monozygotic (44 male, 20 female) and 61 untreated dizygotic twins (32 male, 29 female). Lateral cephalograms taken at 15 and 18 years of age were traced to analyze the sella-nasion–nasal line angle (SN-NL), nasal line–mandibular line angle (ML-NL), sella-nasion–mandibular line angle (SN-ML), sella-nasion–sella-gnathion angle (Y-axis), posterior face height/anterior face height (PFH/AFH), and lower anterior face height/anterior face height (LAFH/AFH). The genetic and environmental components of variance were analyzed with structural equation modeling for multilevel mixed effects. Results: At 15 years of age, strong dominant genetic control was seen for NL-ML (81%), LAFH/AFH (73%), and Y-axis (57%), whereas strong additive genetic components were found for PFH/AFH (78%), SN-NL (58%), and SN-ML (57%). Unique environmental factors accounted for 18–42% of observed variance, with SN-NL being affected the most (42%). At 18 years of age, only LAFH/AFH (86%) was under strong dominant genetic control, whereas the remainder were under additive genetic influence. The sole exception was SN-NL, which changed from additive to unique environmental influence. Conclusions: Either additive or dominant genetic components were found at 15 or 18 years of age for most vertical variables. Environmental factors accounted for about 10–40%, with SN-NL being mostly affected.
, Nicola L. Barclay, Wichor M. Bramer, Philip R. Gehrman, Eus J.W. Van Someren
Published: 27 January 2021
Sleep medicine reviews, Volume 59; https://doi.org/10.1016/j.smrv.2021.101448

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Monika A. Hersberger‐Zurfluh, , Melih Motro, , Leslie A. Will,
Published: 19 November 2019
Orthodontics & Craniofacial Research, Volume 23, pp 192-201; https://doi.org/10.1111/ocr.12358

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, Anna Neustaeter, Nomdo M. Jansonius, Harold Snieder
Published: 20 June 2019
Survey of ophthalmology, Volume 64, pp 835-851; https://doi.org/10.1016/j.survophthal.2019.06.002

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Monika A. Hersberger-Zurfluh, , Melih Motro, Alpdogan Kantarci, ,
American Journal of Orthodontics and Dentofacial Orthopedics, Volume 154, pp 683-692; https://doi.org/10.1016/j.ajodo.2018.01.020

Abstract:
Although monozygotic twins possess the same genetic material, differences in the soft tissues were found. This supports the complex developmental mechanism of the human face and the varying influence of genetic and environmental factors.
, Carl J. Lavie, James O. Hill
Published: 12 June 2018
Progress in cardiovascular diseases, Volume 61, pp 89-102; https://doi.org/10.1016/j.pcad.2018.06.002

Abstract:
The debate on the relative contributions of presumptive etiologic factors in the development of obesity is becoming increasingly speculative, insular, and partisan. As the global prevalence of obesity continues to rise, the sheer volume of unfounded conjecture threatens to obscure well-established evidence. We posit that the failure to distinguish between causal factors and mere statistical associations engendered the proliferation of misleading and demonstrably false research programs and failed public health initiatives. Nevertheless, scientific progress necessitates the elimination of unsupported speculation via critical examinations of contrary evidence. Thus, the purpose of this review is to present a concise survey of potentially falsifying evidence for the major presumptive etiologic factors inclusive of ‘diet’, ‘genes’, physical activity, and non-physiologic factors from the social sciences. Herein, we advance two ‘Fundamental Questions of Obesity’ that provide a conceptually clear but challenging constraint on conjecture. First, why would an individual (i.e., human or non-human animal) habitually consume more calories than s/he expends? And second, why would the excess calories be stored predominantly as ‘fat’ rather than as lean tissue? We posit that the conceptual constraint presented by these questions in concert with the parallel trends in body-mass, adiposity, and metabolic diseases in both human and non-human mammals offer a unique opportunity to refute the oversimplification, causal reductionism, and unrestrained speculation that impede progress. We conclude this review with an attempt at consilience and present two novel paradigms, the ‘Metabolic Tipping Point’ and the ‘Maternal Resources Hypothesis’, that offer interdisciplinary explanatory narratives on the etiology of obesity and metabolic diseases across mammalian species.
Published: 15 January 2018
Philosophical Transactions B, Volume 373; https://doi.org/10.1098/rstb.2016.0450

Abstract:
Individual differences in telomere length have been linked to survival and senescence. Understanding the heritability of telomere length can provide important insight into individual differences and facilitate our understanding of the evolution of telomeres. However, to gain accurate and meaningful estimates of telomere heritability it is vital that the impact of the environment, and how this may vary, is understood and accounted for. The aim of this review is to raise awareness of this important, but much under-appreciated point. We outline the factors known to impact telomere length and discuss the fact that telomere length is a trait that changes with age. We highlight statistical methods that can separate genetic from environmental effects and control for confounding variables. We then review how well previous studies in vertebrate populations including humans have taken these factors into account. We argue that studies to date either use methodological techniques that confound environmental and genetic effects, or use appropriate methods but lack sufficient power to fully separate these components. We discuss potential solutions. We conclude that we need larger studies, which also span longer time periods, to account for changing environmental effects, if we are to determine meaningful estimates of the genetic component of telomere length. This article is part of the theme issue ‘Understanding diversity in telomere dynamics'.
, Christophe Moreno, , Marsha Y. Morgan
Published: 27 August 2016
Journal of Hepatology, Volume 66, pp 195-211; https://doi.org/10.1016/j.jhep.2016.08.011

Abstract:
The susceptibility to develop alcohol dependence and significant alcohol-related liver injury is determined by a number of constitutional, environmental and genetic factors, although the nature and level of interplay between them remains unclear. The familiarity and heritability of alcohol dependence is well-documented but, to date, no strong candidate genes have emerged with the exception of variants in alcohol dehydrogenase and acetaldehyde dehydrogenase, which confer protection predominantly in individuals of East Asian ancestry. Population contamination with confounder such as drug co-dependence and psychiatric and physical co-morbidity may explain the essentially negative genome wide association studies in this disorder. The familiarity and hereditability of alcohol-related cirrhosis is not as well-documented but three strong candidate genes PNPLA3, TM6SF2 and MBOAT7, have been identified. The mechanisms by which variants in these genes confer risk and the nature of the functional interplay between them remains to be determined but, when elucidated, will undoubtedly increase our understanding of the pathophysiology of this disease. The way in which this genetic information could potentially inform patient management has yet to be determined and tested.
, H. Ohlsson, A. C. Edwards, P. Lichtenstein, K. Sundquist
Published: 21 March 2016
Psychological Medicine, Volume 46, pp 1639-1650; https://doi.org/10.1017/S003329171500224X

Abstract:
Background Twin studies have been criticized for upwardly biased estimates that might contribute to the missing heritability problem. Method We identified, from the general Swedish population born 1960–1990, informative sibships containing a proband, one reared-together full- or half-sibling and a full-, step- or half-sibling with varying degrees of childhood cohabitation with the proband. Estimates of genetic, shared and individual specific environment for drug abuse (DA), alcohol use disorder (AUD) and criminal behavior (CB), assessed from medical, legal or pharmacy registries, were obtained using Mplus. Results Aggregate estimates of additive genetic effects for DA, AUD and CB obtained separately in males and females varied from 0.46 to 0.73 and agreed with those obtained from monozygotic and dizygotic twins from the same population. Of 54 heritability estimates from individual classes of informative sibling trios (3 syndromes × 9 classes of trios × 2 sexes), heritability estimates from the siblings were lower, tied and higher than those from obtained from twins in 26, one and 27 comparisons, respectively. By contrast, of 54 shared environmental estimates, 33 were lower than those found in twins, one tied and 20 were higher. Conclusions With adequate information, human populations can provide many methods for estimating genetic and shared environmental effects. For the three externalizing syndromes examined, concerns that heritability estimates from twin studies are upwardly biased or were not generalizable to more typical kinds of siblings were not supported. Overestimation of heritability from twin studies is not a likely explanation for the missing heritability problem.
, , H. H. Maes, Kristina Sundquist
Published: 23 December 2014
Psychological Medicine, Volume 45, pp 1873-1880; https://doi.org/10.1017/s0033291714002979

Abstract:
BackgroundTwin studies have shown that criminal behavior (CB) is influenced by both genetic and shared environmental factors. Could these results be replicated using full-siblings and half-siblings?MethodIn 911 009 full-siblings reared together (FSRT), 41 872 half-siblings reared together (HSRT) and 52 590 half-siblings reared apart (HSRA), CB was assessed from the Swedish Crime Register. Modeling, including testing for age differences and rearing status, was performed using the OpenMx package.ResultsFive sibling models were fitted examining FSRT and HSRT 0–2 years different in age, and both FSRT and HSRT, and FSRT, HSRT and HSRA 0–10 years different in age with and without a specified shared environment indexing age differences. Heritability estimates for CB ranged from 33 to 55% in females and 39 to 56% in males, similar to those found in our prior twin study on the same population. Estimates for the shared environment varied from 1 to 14% in females and 10 to 23% in males, lower than those estimated in the twin study. The specified shared environment indexed by sibling age differences was significant in all models tested.ConclusionsHeritability estimates for CB from full- and half-siblings closely approximated those found from twins in the same population, validating the twin method. Shared environmental estimates were lower, suggesting the presence of shared environmental factors for CB specific to twins. When rearing status can be assessed, full- and half-siblings offer an additional method for assessing the role of genetic and environmental factors in complex disorders. However, age differences in siblings may need to be included in the models.
Psychological bulletin, Volume 140, pp 434-465; https://doi.org/10.1037/a0033564

Abstract:
There are dramatic individual differences among adolescents in how and when they become sexually active adults, and “early” sexual activity is frequently cited as a cause of concern for scientists, policymakers, and the general public. Understanding the causes and developmental impact of adolescent sexual activity can be furthered by considering genes as a source of individual differences. Quantitative behavioral genetics (i.e., twin and family studies) and candidate gene association studies now provide clear evidence for the genetic underpinnings of individual differences in adolescent sexual behavior and related phenotypes. Genetic influences on sexual behavior may operate through a variety of direct and indirect mechanisms, including pubertal development, testosterone levels, and dopaminergic systems. Genetic differences may be systematically associated with exposure to environments that are commonly treated as causes of sexual behavior (gene-environment correlation). Possible gene-environment correlations pose a serious challenge for interpreting the results of much behavioral research. Multivariate, genetically-informed research on adolescent sexual behavior compares twins and family members as a form of “quasi-experiment”: How do twins who differ in their sexual experiences differ in their later development? The small but growing body of genetically-informed research has already challenged dominant assumptions regarding the etiology and sequelae of adolescent sexual behavior, with some studies indicating possible positive effects of teenage sexuality. Studies of gene × environment interaction may further elucidate the mechanisms by which genes and environments combine to shape the development of sexual behavior and its psychosocial consequences. Overall, the existence of heritable variation in adolescent sexual behavior has profound implications for environmentally-oriented theory and research.
Published: 1 January 2014
Social science research, Volume 43, pp 184-199; https://doi.org/10.1016/j.ssresearch.2013.10.004

Abstract:
Twin studies are a major source of information about genetic effects on behavior, but they depend on a controversial assumption known as the equal environments assumption (EEA): that similarity in co-twins' environments is not predictive of similarity in co-twin outcomes. Although evidence has largely supported the EEA, critics have claimed that environmental similarity has not been measured well, and most studies of the EEA have focused on outcomes related to health and psychology. This article addresses these limitations through (1) a reanalysis of data from the most cited study of the EEA, Loehlin and Nichols (1976), using better measures, and through (2) an analysis of nationally representative twin data from MIDUS using more comprehensive controls on a wider variety of outcomes than previous studies. Results support a middle ground position; it is likely that the EEA is not strictly valid for most outcomes, but the resulting bias is likely modest.
Colin A. Ross
Published: 1 March 2013
Journal: Psychosis
Psychosis, Volume 6, pp 189-191; https://doi.org/10.1080/17522439.2013.773365

Abstract:
It is widely stated that schizophrenia is “genetic”. The main basis for this claim is the literature on twin concordance for schizophrenia in monozygotic (MZ) and dizygotic (DZ) twins. The validity of twin studies depends on the equal environments assumption. However, the low concordance rates in MZ and DZ twins prove two things: (1) schizophrenia can be at most only a little bit genetic, and (2) the equal environments assumption cannot hold. Proponents of the genetic contribution to schizophrenia must deal with a logical bind: the greater they make the gap between MZ and DZ twin concordance rates, the more they undermine the equal environments assumption; the smaller they make it, the more they undermine the genetic contribution to schizophrenia.
Jon Rasbash, , Rebecca Pillinger, Jennifer Jenkins
Journal of the Royal Statistical Society: Series A (Statistics in Society), Volume 173, pp 657-682; https://doi.org/10.1111/j.1467-985x.2010.00642.x

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, Christopher T. Dawes, , , , Björn Wallace
Proceedings of the National Academy of Sciences of the United States of America, Volume 105, pp 3721-3726; https://doi.org/10.1073/pnas.0710069105

Abstract:
Although laboratory experiments document cooperative behavior in humans, little is known about the extent to which individual differences in cooperativeness result from genetic and environmental variation. In this article, we report the results of two independently conceived and executed studies of monozygotic and dizygotic twins, one in Sweden and one in the United States. The results from these studies suggest that humans are endowed with genetic variation that influences the decision to invest, and to reciprocate investment, in the classic trust game. Based on these findings, we urge social scientists to take seriously the idea that differences in peer and parental socialization are not the only forces that influence variation in cooperative behavior.
Published: 1 March 2008
Perspectives on Politics, Volume 6, pp 785-791; https://doi.org/10.1017/s1537592708081917

Abstract:
Using the “classical twin method,” political scientists John Alford, Carolyn Funk, and John Hibbing conclude that political ideologies are significantly influenced by genetics, an assertion that has garnered considerable media attention. Researchers have long used human twins in attempts to assess the degree of genetic influence on various behavioral traits. Today, this methodology has been largely replaced in favor of contemporary molecular genetic techniques, and thus heritability studies have seen a diminishing role in behavioral genetic research of the twenty-first century. One important reason the twin method has been superseded is that it depends upon several questionable assumptions, the most significant of which is known as the equal environments assumption. Alford, Funk, and Hibbing argue that this crucial assumption, and thus their conclusion, holds up under empirical scrutiny. They point to several studies in support of this assumption. Here, we review the evidence presented and conclude that these attempts to test the equal environments assumption are weak, suffering significant methodological and inherent design flaws. Furthermore, much of the empirical evidence provided by these studies actually argues that, contrary to the interpretation, trait-relevant equal environments assumptions have been violated. We conclude that the equal environments assumption remains untenable, and as such, twin studies are an insufficient method for drawing meaningful conclusions regarding complex human behavior.
, Zengchang Pang, Gary E Swan, Qian Guo, Shaojie Wang, Weihua Cao, , C Anderson Johnson, Liming Lee
International Journal of Epidemiology, Volume 35, pp 1278-1285; https://doi.org/10.1093/ije/dyl148

Abstract:
Background China has the world's largest concentration of smokers (350 million) and rising alcohol consumption, yet little is known about tobacco and alcohol use aetiology. In 2000, the Chinese National Twin Registry was established to provide a genetically informative resource for investigation of health behaviour including tobacco and alcohol use. Methods Using standard twin methodology, this study aimed to examine the relative contribution of genetic and environmental influences on cigarette smoking and alcohol drinking in a sample of adult Chinese twins (n = 1010 individual twins). More than half of the male twins were smokers (58%), and 32.5% reported alcohol consumption. Among male smokers, 46.4% smoked 20 or more cigarettes per day (heavy smokers) and among drinkers, 32.8% consumed one or more drinks per day. Nearly all female twins were non-smokers (99.2%) and non-drinkers (98.7%); therefore, genetic analysis was limited to male data. Results In men, current smoking was significantly heritable [75.1%, 95% confidence interval (CI) 56.7–87.5] with no evidence for a significant contribution of shared environmental effects. Heavy smoking was more strongly influenced by genes (66.2%, 95% CI 0–88.4) than shared environment (8.7%, 95% CI 0–71.0). Similarly, current drinking was more strongly influenced by genetic effects (59.5%, 95% CI 0–87.8) than by shared environmental effects (15.3%, 95% CI 0–72.1). Amount of alcohol consumed was influenced to a similar degree by genetic (42.4%, 95% CI 0–91.8) and shared environmental factors (39.2%, 95% CI 0–82.7). Conclusions These results support findings from twins of Western origin on the aetiology of tobacco and alcohol use and encourage further work in Chinese twins.
Colin A. Ross
Ethical human psychology and psychiatry, Volume 8, pp 123-131; https://doi.org/10.1891/ehpp.8.2.123

Abstract:
The purpose of this article is to analyze and critique repeated claims in the literature that there is a substantial genetic contribution to eating disorders. Data from the existing twin and family studies of eating disorders were tabulated and compared to heritability estimates resulting from complex statistical analyses of the same data. Overall, concordance in monozygotic twins is 26% for bulimia and 35% for anorexia nervosa. Among the relatives of probands with bulimia, 95.1% do not have bulimia, whereas among the relatives of probands with anorexia nervosa, 97.1% do not have the disorder. The raw data refute claims that the genetic heritability of eating disorders is as high as 80%. The erroneous conclusion that there is a substantial genetic contribution to eating disorders needs to be corrected by focusing on the raw data for twin concordance and prevalence in first-degree relatives.
Comment
Developmental Psychology, Volume 41, pp 985-988; https://doi.org/10.1037/0012-1649.41.6.985

Abstract:
M. McGue, I. Elkins, B. Walden, and W. G. Iacono presented the findings from a twin study examining the relative contributions of genetic and environmental factors to the developmental trajectories of parent-adolescent relationships. From a behavioral genetics perspective, this study is well conceptualized, is well implemented, and raises some interesting developmental questions. Yet, the classic twin methodology and heritability estimates obfuscate the dynamic gene-ecology transactions that underlie these social developmental trajectories. There is a growing divide between the findings of quantitative behavioral genetics, with its foundational estimate of a statistical genetic influence, and developmental molecular genetics. This comment provides a brief overview of this divide and its implications for the findings of McGue et al. as well as quantitative behavioral genetics more broadly.
, Neal L. Benowitz, Peyton Jacob, Christina N. Lessov, Rachel F. Tyndale, Kirk Wilhelmsen, Ruth E. Krasnow, Mary R. McElroy, Sharyn E. Moore, Michelle Wambach
Published: 1 October 2004
Journal: Twin Research
Twin Research, Volume 7, pp 435-448; https://doi.org/10.1375/twin.7.5.435

Abstract:
This article describes a pharmacogenetic investigation of nicotine metabolism in twins. One hundred and thirty-nine twin pairs (110 monozygotic and 29 dizygotic) were recruited and assessed for smoking status, zygosity, and health conditions known or suspected to affect drug metabolism. Participants underwent a 30-minute infusion of stable isotope-labeled nicotine and its major metabolite, cotinine, followed by an 8-hour in-hospital stay. Blood and urine samples were taken at regular intervals for analysis of nicotine, cotinine, and metabolites by gas chromatography–mass spectrometry or liquid chromatography–mass spectrometry and subsequent characterization of pharmacokinetic phenotypes. DNA was genotyped to confirm zygosity and for variation in the primary gene involved in nicotine metabolism, CYP2A6. Univariate and multivariate biometric analyses planned for the future will determine genetic and environmental influences on each pharmacokinetic measure individually and in combination with each other, and in the presence and absence of covariates, including measured genotype. When the analyses are completed, this study will result in a more complete characterization of the impact of genetic and environmental influences on nicotine and cotinine metabolic pathways than has heretofore been reported. The approach taken, with its use of a quantitative model of nicotine metabolism, highly refined metabolic phenotypes, measured genotype, and advanced tools for biometric genetic analysis, provides a model for the use of twins in next-generation studies of complex drug-metabolism phenotypes.
S Van Gestel,
Published: 29 September 2003
Molecular Psychiatry, Volume 8, pp 840-852; https://doi.org/10.1038/sj.mp.4001367

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, Colin A. Ross
The journal of the American Academy of Psychoanalysis and Dynamic Psychiatry, Volume 31, pp 247-268; https://doi.org/10.1521/jaap.31.1.247.21938

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Published: 20 September 2002
Epilepsy research, Volume 51, pp 167-177; https://doi.org/10.1016/s0920-1211(02)00121-3

Abstract:
The relative importance of genetic and environmental factors in the etiology of febrile seizures was estimated using a large, unselected population-based twin sample. A total of 34 076 twins (aged 12–41 years), recruited from the Danish Twin Registry, were screened for febrile seizures by questionnaire. Information was obtained from 11 872 complete pairs. Concordance rates, odds ratios and correlations were used to assess the degree of similarity in monozygotic (MZ) and dizygotic (DZ) twins. Model fitting and estimation of heritability (proportion of the population variance attributable to genetic variation) were performed using standard biometrical methods. Significantly higher probandwise concordance rates were found for MZ compared with DZ twins (0.36 and 0.12, P<0.01). Odds ratios and correlations showed a similar pattern. An etiological model including additive genetic effects and individual-specific environmental factors provided the best fit to the data with a heritability for febrile seizures of 70% (95% CI: 61–77%). The remaining 30% of the variation could be attributed to individual-specific environmental factors. In conclusion, this study has confirmed a major impact of genetic factors in the etiology of febrile seizures. Future studies aimed at identifying the specific genetic factors and environmental exposures involved in determining febrile seizure risk are clearly warranted.
, , Harold Snieder, , Tim Spector, Philip Sambrook
Published: 1 April 2002
Journal of Bone and Mineral Research, Volume 17, pp 725-733; https://doi.org/10.1359/jbmr.2002.17.4.725

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Published: 1 January 2002
Psychiatric Quarterly, Volume 73, pp 71-82; https://doi.org/10.1023/a:1012896802713

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