scholarly journals Genetic and Environmental Influences on Disgust Proneness, Contamination Sensitivity, and Their Covariance

2020 ◽  
Vol 8 (6) ◽  
pp. 1054-1061 ◽  
Author(s):  
Joshua M. Tybur ◽  
Laura W. Wesseldijk ◽  
Patrick Jern

Dozens of studies have indicated that individuals more prone to experiencing disgust have stronger symptoms of anxiety disorders—especially contamination sensitivity. However, no work has informed the degree to which this relationship arises from genetic factors versus environmental factors. In the present study, we fill this gap by measuring disgust proneness and contamination sensitivity in a sample of 7,199 twins and siblings of twins, including 1,411 complete twin pairs. Disgust proneness was related to contamination sensitivity, r = .32. Multivariate twin modeling revealed that genetic factors accounted for 34% and 40% of the variance in disgust proneness and contamination sensitivity, respectively, and that the correlation between the two traits reflected overlapping genetic (54%) and unshared environmental (46%)—but not shared environmental—influences. Although consistent with work indicating that disgust proneness relates to contamination sensitivity, results suggest that prevailing parental-modeling hypotheses for explaining this relationship be reevaluated.

2020 ◽  
Author(s):  
Joshua M. Tybur ◽  
Laura Wesseldijk ◽  
Patrick Jern

Dozens of studies indicate that individuals more prone to experiencing disgust have stronger symptoms of anxiety disorders – especially contamination sensitivity. However, no work has informed the degree to which this relationship arises from genetic versus environmental factors. The present study fills this gap by measuring disgust proneness and contamination sensitivity in a sample of 7,199 twins and siblings of twins, including 1,411 complete twin pairs. Disgust proneness was related to contamination sensitivity, r = .32. Multivariate twin modeling revealed that genetic factors accounted for 34% and 40% of the variance in disgust proneness and contamination sensitivity, respectively, and that the correlation between the two traits reflected overlapping genetic (54%) and unshared environmental (46%) – but not shared environmental – influences. While consistent with work indicating that disgust proneness relates to contamination sensitivity, results suggest that parental-modeling hypotheses for explaining this relationship be re-evaluated.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yisong Huang ◽  
Shaoyong Su ◽  
Harold Snieder ◽  
Frank Treiber ◽  
Gaston Kapuku ◽  
...  

AbstractIncreased arterial stiffness measured by pulse wave velocity (PWV) is an important parameter in the assessment of cardiovascular risk. Our previous longitudinal study has demonstrated that carotid-distal PWV showed reasonable stability throughout youth and young adulthood. This stability might be driven by genetic factors that are expressed consistently over time. We aimed to illustrate the relative contributions of genetic and environmental factors to the stability of carotid-distal PWV from youth to young adulthood. We also examined potential ethnic differences. For this purpose, carotid-distal PWV was measured twice in 497 European American (EA) and African American (AA) twins, with an average interval time of 3 years. Twin modelling on PWV showed that heritability decreased over time (62–35%), with the nonshared environmental influences becoming larger. There was no correlation between the nonshared environmental factors on PWV measured at visit 1 and visit 2, with the phenotypic tracking correlation (r = 0.32) completely explained by shared genetic factors over time. Novel genetic influences were identified accounting for a significant part of the variance (19%) at the second measurement occasion. There was no evidence for ethnic differences. In summary, novel genetic effects appear during development into young adulthood and account for a considerable part of the variation in PWV. Environmental influences become larger with age for PWV.


2019 ◽  
Vol 25 (10) ◽  
pp. 2556-2566 ◽  
Author(s):  
John P. Hegarty ◽  
Luiz F. L. Pegoraro ◽  
Laura C. Lazzeroni ◽  
Mira M. Raman ◽  
Joachim F. Hallmayer ◽  
...  

Abstract Atypical growth patterns of the brain have been previously reported in autism spectrum disorder (ASD) but these alterations are heterogeneous across individuals, which may be associated with the variable effects of genetic and environmental influences on brain development. Monozygotic (MZ) and dizygotic (DZ) twin pairs with and without ASD (aged 6–15 years) were recruited to participate in this study. T1-weighted MRIs (n = 164) were processed with FreeSurfer to evaluate structural brain measures. Intra-class correlations were examined within twin pairs and compared across diagnostic groups. ACE modeling was also completed. Structural brain measures, including cerebral and cerebellar gray matter (GM) and white matter (WM) volume, surface area, and cortical thickness, were primarily influenced by genetic factors in TD twins; however, mean curvature appeared to be primarily influenced by environmental factors. Similarly, genetic factors accounted for the majority of variation in brain size in twins with ASD, potentially to a larger extent regarding curvature and subcortical GM; however, there were also more environmental contributions in twins with ASD on some structural brain measures, such that cortical thickness and cerebellar WM volume were primarily influenced by environmental factors. These findings indicate potential neurobiological outcomes of the genetic and environmental risk factors that have been previously associated with ASD and, although preliminary, may help account for some of the previously outlined neurobiological heterogeneity across affected individuals. This is especially relevant regarding the role of genetic and environmental factors in the development of ASD, in which certain brain structures may be more sensitive to specific influences.


2008 ◽  
Vol 22 (2) ◽  
pp. 143-153 ◽  
Author(s):  
Steven Taylor ◽  
Kerry L. Jang ◽  
Murray B. Stein ◽  
Gordon J. G. Asmundson

The leading contemporary cognitive-behavioral model of excessive health anxiety (HA) emphasizes the importance of environmental factors, such as learning experiences. The model has little to say about the role of genetic factors and, by ignoring these factors, seems to imply that they are unimportant. In contrast, results from the University of British Columbia Twin Study, using a sample of 88 monozygotic and 65 dizygotic twin pairs, indicated that various facets of HA, such as excessive disease fear, unrealistic beliefs that one has a serious disease, and HA-related interference in functioning, are moderately heritable. The present study extended the analyses of this data set by investigating the extent to which the various facets of HA are due to genetic or environmental factors that are common to all facets versus specific to each facet. Results indicated that all facets of HA are influenced by a common set of genes—there was very little evidence of facet-specific genetic influences. There was considerably stronger evidence for facet-specific environmental influences, where each facet is strongly influenced by environmental experiences that are specific to that facet. However, there was also evidence that particular environmental influences—especially those that shape disease conviction—also influence some of the other HA facets (fear and interference). The importance of environmental factors is consistent with the cognitive-behavioral model of HA, although the model needs to be refined to account for the role of genetic factors. Possibilities for refining the model are discussed, along with promising research directions to better understand the role of genes and the environment in HA.


2007 ◽  
Vol 10 (4) ◽  
pp. 564-572 ◽  
Author(s):  
Kerry L. Jang ◽  
Steven Taylor ◽  
Murray B. Stein ◽  
Shinji Yamagata

AbstractPeople differ markedly in their risk for developing posttraumatic stress symptoms (PTSS) after exposure to traumatic events. Twin studies suggest that the trauma-PTSS relationship is moderated by genetic and environmental influences. The present study tested for specific types of genetic and environmental interaction effects on PTSS. A sample of 222 monozygotic and 184 dizygotic twin pairs reported on lifetime frequency of assaultive and nonassaultive trauma and associated PTSS. Biometric analyses indicated that in the case of nonassaultive trauma, PTSS were directly affected by environmental factors that also influence exposure to nonassaultive trauma. For assaultive trauma both genetic and non-shared environmental influences jointly affected PTSS, and the number of traumatic events moderated the severity of PTSS. Genetic factors were found to become less important beyond some threshold (e.g., 3 or 4 types of serious trauma) suggesting that genetic factors — which may confer either risk or resilience to PTSS — modify these symptoms within a range of human experience, beyond which environmental effects supervene.


2019 ◽  
Vol 105 (2) ◽  
pp. 443-452 ◽  
Author(s):  
Britt J van Keulen ◽  
Conor V Dolan ◽  
Ruth Andrew ◽  
Brian R Walker ◽  
Hilleke E Hulshoff Pol ◽  
...  

Abstract Context Inter-individual differences in cortisol production and metabolism emerge with age and may be explained by genetic factors. Objective To estimate the relative contributions of genetic and environmental factors to inter-individual differences in cortisol production and metabolism throughout adolescence. Design Prospective follow-up study of twins. Setting Nationwide register. Participants 218 mono- and dizygotic twins (N = 109 pairs) born between 1995 amd 1996, recruited from the Netherlands Twin Register. Cortisol metabolites were determined in 213, 169, and 160 urine samples at the ages of 9, 12, and 17, respectively. Main outcome measures The total contribution of genetic factors (broad-sense heritability) and shared and unshared environmental influences to inter-individual differences in cortisol production and activities of 5α-reductase, 5β-reductase, and 11β-hydroxysteroid dehydrogenases and cytochrome P450 3A4. Results For cortisol production rate at the ages of 9, 12, and 17, broad-sense heritability was estimated as 42%, 30%, and 0%, respectively, and the remainder of the variance was explained by unshared environmental factors. For cortisol metabolism indices, the following heritability was observed: for the A-ring reductases (5α-and 5β-reductases), broad-sense heritability increased with age (to >50%), while for the other indices (renal 11β-HSD2, global 11β-HSD, and CYP3A4), the contribution of genetic factors was highest (68%, 18%, and 67%, respectively) at age 12. Conclusions The contribution of genetic factors to inter-individual differences in cortisol production decreased between 12 and 17y, indicative of a predominant role of individual circumstances. For cortisol metabolism, distinct patterns of genetic and environmental influences were observed, with heritability that either increased with age or peaked at age 12y.


2008 ◽  
Vol 39 (1) ◽  
pp. 115-127 ◽  
Author(s):  
K. Witting ◽  
P. Santtila ◽  
F. Rijsdijk ◽  
M. Varjonen ◽  
P. Jern ◽  
...  

BackgroundPrevious studies have shown moderate heritability for female orgasm. So far, however, no study has addressed the pattern of genetic and environmental influences on diverse sexual dysfunctions in women, nor how genetic and environmental factors contribute to the associations between them.MethodThe sample was drawn from the Genetics of Sex and Aggression (GSA) sample and consisted of 6446 female twins (aged 18–43 years) and 1994 female siblings (aged 18–49 years). The participants responded to the Female Sexual Function Index (FSFI), either by post or online.ResultsModel fitting analyses indicated that individual differences on all six subdomains of the FSFI (desire, arousal, lubrication, orgasm, satisfaction, and pain) were primarily due to non-shared (individual-specific) environmental influences. Genetic influences were modest but significant, whereas shared environmental influences were not significant. A correlated factors model including additive and non-additive genetic and non-shared environmental effects proved to have the best fit and suggested that both correlated additive and non-additive genetic factors and unique environmental factors underlie the co-occurrence of the sexual function problems.ConclusionsThe findings suggest that female sexual dysfunctions are separate entities with some shared aetiology. They also indicate that there is a genetic susceptibility for sexual dysfunctions. The unique experiences of each individual are, however, the main factors determining if, and which, dysfunction develops.


2007 ◽  
Vol 10 (2) ◽  
pp. 327-333 ◽  
Author(s):  
Gonneke Willemsen ◽  
Dorret I. Boomsma

AbstractEvidence for a relation between neuroticism and religion is scarce and inconsistent. The aims of the present study were to determine the association of religious upbringing with adult neuroticism scores and to examine the effect of religious upbringing on the heritability of neuroticism. As part of a longitudinal survey of twin families from the Netherlands Twin Register, data were collected on neuroticism and religious upbringing. Restricting the sample to persons aged 25 and over resulted in a sample of 4369 twins and 1304 siblings from 2698 families. Religious upbringing was significantly associated with neuroticism; in both men and women neuroticism levels were lower in those who had received a religious upbringing. There were no sex or twinsibling differences in neuroticism variances and covariances. Structural equation modeling showed differences in heritability between those with and without religious upbringing. In the group with religious upbringing, variation in neuroticism was determined for 41% by additive genetic factors and for the remaining 59% by unique environmental factors. In the group who had not received a religious upbringing, variation in neuroticism was determined for 55% by genetic factors, with evidence for both additive and nonadditive factors, and for the remaining 45% by unique environmental influences. In conclusion, having received a religious upbringing is associated with lower neuroticism scores and a lower heritability in adulthood.


2018 ◽  
Vol 49 (09) ◽  
pp. 1500-1509 ◽  
Author(s):  
Catherine Tuvblad ◽  
Pan Wang ◽  
Christopher J. Patrick ◽  
Leslie Berntsen ◽  
Adrian Raine ◽  
...  

AbstractBackgroundThe Triarchic Psychopathy Measure (TriPM) provides Disinhibition, Boldness, and Meanness scales for assessing the three trait domains of the triarchic model. Here we examined the genetic and environmental etiology of these three domains, including evaluation of potential sex differences.MethodsA total of 1016 men and women ages 19–20 years were drawn from the University of Southern California Risk Factors for Antisocial Behavior twin study.ResultsScores for the three TriPM scales were correlated to differing degrees, with the strongest phenotypic correlation between Disinhibition and Meanness. No sex differences were found in the genetic and environmental influences underlying these three domains, suggesting that the same genes and life experiences contribute to these traits in young men and women. For TriPM Disinhibition and Boldness, genetic factors explained about half or less of the variance, with the rest of the variance being explained by non-shared environmental factors. For TriPM Meanness, on the other hand, genetic, shared environmental, and non-shared environmental factors accounted for the variance. The phenotypic correlation between Disinhibition and Meanness was explained in part by common genes (26%), with the remainder attributable about equally to common shared (39%), and non-shared environmental influences (35%).ConclusionsThese findings contribute to our understanding of psychopathic personality traits by demonstrating the importance of heritable factors for disinhibition and boldness facets of psychopathy, and the importance of shared environmental influences for the meanness facet.


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