Genetic and environmental risk factors in males for self-report externalizing traits in mid-adolescence and criminal behavior through young adulthood

2013 ◽  
Vol 43 (10) ◽  
pp. 2161-2168 ◽  
Author(s):  
K. S. Kendler ◽  
C. J. Patrick ◽  
H. Larsson ◽  
C. O. Gardner ◽  
P. Lichtenstein

BackgroundExternalizing traits or behaviors are typically assessed by self-report scales or criminal records. Few genetically informative studies have used both methods to determine whether they assess the same genetic or environmental risk factors.MethodWe examined 442 male Swedish twin pairs with self-reported externalizing behaviors at age 16–17 years [externalizing traits (EXT), self-reported delinquency (SRD), impulsivity (IMP), grandiosity (GRD) and callousness (CLS)] and criminal behavior (CB) from the National Suspect Registry from age 13 to 25 years. Multivariate structural equation modeling was conducted with Mx.ResultsThe best-fit model contained one genetic, one shared environmental and two non-shared environmental common factors, and variable specific genetic and non-shared environmental factors. The risk for CB was influenced substantially by both genetic (a2 = 0.48) and familial–environmental factors (c2 = 0.22). About one-third of the genetic risk for CB but all of the shared environmental risk was indexed by the self-report measures. The degree to which the individual measures reflected genetic versus familial–environmental risks for CB varied widely. GRD and CLS were correlated with CB mainly through common genetic risk factors. SRD and CB covaried largely because of shared familial–environmental factors. For EXT and IMP, observed correlations with CB resulted in about equal parts from shared genetic and shared familial–environmental factors.ConclusionsIn adolescence, measures of grandiose and callous temperament best tap the genetic liability to CB. Measures of antisocial behaviors better index familial–environmental risks for CB. A substantial proportion of the genetic risk to CB was not well reflected in any of the self-report measures.

2017 ◽  
Vol 20 (4) ◽  
pp. 319-329 ◽  
Author(s):  
Shin-Ho Park ◽  
Adam J. Guastella ◽  
Michael Lynskey ◽  
Arpana Agrawal ◽  
John N. Constantino ◽  
...  

Neuroticism, a ‘Big Five’ personality trait, has been associated with sub-clinical traits of both autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD). The objective of the current study was to examine whether causal overlap between ASD and ADHD traits can be accounted for by genetic and environmental risk factors that are shared with neuroticism. We performed twin-based structural equation modeling using self-report data from 12 items of the Neo Five-Factor Inventory Neuroticism domain, 11 Social Responsiveness Scale items, and 12 Adult ADHD Self-Report Scale items obtained from 3,170 young adult Australian individual twins (1,081 complete pairs). Univariate analysis for neuroticism, ASD, and ADHD traits suggested that the most parsimonious models were those with additive genetic and unique environmental components, without sex limitation effects. Heritability of neuroticism, ASD, and ADHD traits, as measured by these methods, was moderate (between 40% and 45% for each respective trait). In a trivariate model, we observed moderate phenotypic (between 0.45 and 0.62), genetic (between 0.56 and 0.71), and unique environmental correlations (between 0.37and 0.55) among neuroticism, ASD, and ADHD traits, with the highest value for the shared genetic influence between neuroticism and self-reported ASD traits (rg = 0.71). Together, our results suggest that in young adults, genetic, and unique environmental risk factors indexed by neuroticism overlap with those that are shared by ASD and ADHD.


2021 ◽  
Vol 12 ◽  
Author(s):  
Natassia Robinson ◽  
Sarah E. Bergen

Schizophrenia (SZ) and bipolar disorder (BD) are severe psychiatric disorders which result from complex interplay between genetic and environmental factors. It is well-established that they are highly heritable disorders, and considerable progress has been made identifying their shared and distinct genetic risk factors. However, the 15–40% of risk that is derived from environmental sources is less definitively known. Environmental factors that have been repeatedly investigated and often associated with SZ include: obstetric complications, infections, winter or spring birth, migration, urban living, childhood adversity, and cannabis use. There is evidence that childhood adversity and some types of infections are also associated with BD. Evidence for other risk factors in BD is weaker due to fewer studies and often smaller sample sizes. Relatively few environmental exposures have ever been examined for SZ or BD, and additional ones likely remain to be discovered. A complete picture of how genetic and environmental risk factors confer risk for these disorders requires an understanding of how they interact. Early gene-by-environment interaction studies for both SZ and BD often involved candidate genes and were underpowered. Larger samples with genome-wide data and polygenic risk scores now offer enhanced prospects to reveal genetic interactions with environmental exposures that contribute to risk for these disorders. Overall, although some environmental risk factors have been identified for SZ, few have been for BD, and the extent to which these account for the total risk from environmental sources remains unknown. For both disorders, interactions between genetic and environmental risk factors are also not well understood and merit further investigation. Questions remain regarding the mechanisms by which risk factors exert their effects, and the ways in which environmental factors differ by sex. Concurrent investigations of environmental and genetic risk factors in SZ and BD are needed as we work toward a more comprehensive understanding of the ways in which these disorders arise.


2010 ◽  
Vol 41 (4) ◽  
pp. 819-828 ◽  
Author(s):  
T. D. Wade ◽  
G. Zhu ◽  
N. G. Martin

BackgroundThree cognitive constructs are risk factors for eating disorders: undue influence of weight and shape, concern about weight and shape, and body dissatisfaction (BD). Undue influence, a diagnostic criterion for eating disorders, is postulated to be closely associated with self-esteem whereas BD is postulated to be closely associated with body mass index (BMI). We understand less about the relationships with concern about weight and shape. The aim of the current investigation was examine the degree of overlap across these five phenotypes in terms of latent genetic and environmental risk factors in order to draw some conclusions about the similarities and differences across the three cognitive variables.MethodA sample of female Australian twins (n=1056, including 348 complete pairs), mean age 35 years (s.d.=2.11, range 28–40), completed a semi-structured interview about eating pathology and self-report questionnaires. An independent pathways model was used to investigate the overlap of genetic and environmental risk factors for the five phenotypes.ResultsIn terms of variance that was not shared with other phenotypes, self-esteem emerged as being separate, with 100% of its variance unshared with the other phenotypes, followed by undue influence (51%) and then concern (34%), BD (28%) and BMI (32%).ConclusionsIn terms of shared genetic risk, undue influence and concern were more closely related than BD, whereas BMI and BD were found to share common sources of risk. With respect to environmental risk factors, concern, BMI and BD were more closely related to each other than to undue influence.


2019 ◽  
Vol 125 ◽  
pp. 04001
Author(s):  
Blego Sedionoto ◽  
Sueptrakool Wasessombat ◽  
Chuchard Punsawad ◽  
Witthaya Anamnart

The prevalence of hookworm infection and strongyloidiasis is serious public health concern globally. In rural East Kalimantan, Indonesia has high-risk environmental factors of the prevalence of hookworm infection and strongyloidiasis. In this study would show the infection rates, correlation analysis between environmental risk factors and prevalence of hookworm infection with statistical analysis. We performed a cross-sectional study among 213 participants from rural community of East Kalimantan Province, Indonesia. In this study used two diagnostic methods: Kato Katz and Koga agar plate culture/KAP culture for diagnosing of hookworm and Strongyloides infections. Chi-square analysis was used for study correlation between environmental factors and hookworm infection. Hookworm, strongyloides, and ascaris infections were found in this study; 44.1%, 16.4%, and 7.5% respectively. Environmental risk factors such as; rainy season, quality of soil and infection hookworm and strongyloides in pet have significant correlation (p-value < 0.05) with hookworm infection and strongyloidiasis. The prevalence of hookworm infection and strongyloidiasis has correlation with environmental factors, and the finding in this research could be contributed to decreasing program of hookworm infection and strongyloidiasis especially in rural community area.


2013 ◽  
Vol 44 (9) ◽  
pp. 1913-1925 ◽  
Author(s):  
K. S. Kendler ◽  
S. Larsson Lönn ◽  
N. A. Morris ◽  
J. Sundquist ◽  
N. Långström ◽  
...  

BackgroundTo clarify the role of genetic and environmental factors in criminal behavior (CB), we examined all CB and violent and non-violent subtypes (VCB and NVCB, respectively) in a Swedish national sample of adoptees and their relatives.MethodCB was defined by a conviction in the Swedish Crime Register with standard definitions for VCB and NVCB subtypes. We examined adoptees born 1950–1991 (n = 18 070) and their biological (n = 79 206) and adoptive (n = 47 311) relatives.ResultsThe risk for all CB was significantly elevated in the adopted-away offspring of biological parents of which at least one had CB [odds ratio (OR) 1.5, 95% confidence interval (CI) 1.4–1.6] and in the biological full and half-siblings of CB adoptees (OR 1.4, 95% CI 1.2–1.6 and OR 1.3, 95% CI 1.2–1.3, respectively). A genetic risk index (including biological parental/sibling history of CB and alcohol abuse) and an environmental risk index (including adoptive parental and sibling CB and a history of adoptive parental divorce, death, and medical illness) both strongly predicted probability of CB. These genetic and environmental risk indices acted additively on adoptee risk for CB. Moderate specificity was seen in the transmission of genetic risk for VCB and NVCB between biological parents and siblings and adoptees.ConclusionsCB is etiologically complex and influenced by a range of genetic risk factors including a specific liability to CB and a vulnerability to broader externalizing behaviors, and by features of the adoptive environment including parental CB, divorce and death. Genetic risk factors for VCB and NVCB may be at least partially distinct.


2015 ◽  
Vol 28 (1) ◽  
pp. 111-125 ◽  
Author(s):  
Leslie E. Roos ◽  
Philip A. Fisher ◽  
Daniel S. Shaw ◽  
Hyoun K. Kim ◽  
Jenae M. Neiderhiser ◽  
...  

AbstractRisk factors for the childhood development of co-occurring internalizing and externalizing symptoms are not well understood, despite a high prevalence and poor clinical outcomes associated with this co-occurring phenotype. We examined inherited and environmental risk factors for co-occurring symptoms in a sample of children adopted at birth and their birth mothers and adoptive mothers (N = 293). Inherited risk factors (i.e., birth mothers' processing speed and internalizing symptoms) and environmental risk factors (i.e., adoptive mothers' processing speed, internalizing symptoms, and uninvolved parenting) were examined as predictors for the development of internalizing-only, externalizing-only, or co-occurring symptoms using structural equation modeling. Results suggested a unique pattern of predictive factors for the co-occurring phenotype, with risk conferred by adoptive mothers' uninvolved parenting, birth mothers' slower processing speed, and the birth mothers' slower processing speed in tandem with adoptive mothers' higher internalizing symptoms. Additional analyses indicated that when co-occurring-symptom children were incorporated into internalizing and externalizing symptom groups, differential risk factors for externalizing and internalizing symptoms emerged. The findings suggest that spurious results may be found when children with co-occurring symptoms are not examined as a unique phenotypic group.


2018 ◽  
Vol 98 (1) ◽  
pp. 77-83 ◽  
Author(s):  
M.J. Silva ◽  
N.M. Kilpatrick ◽  
J.M. Craig ◽  
D.J. Manton ◽  
P. Leong ◽  
...  

The etiology of hypomineralized second primary molars (HSPM) is unclear, but genetic and environmental factors have been proposed. The aim of this study was to investigate the relative contribution of genes and environment to the etiology of HSPM and to identify potential environmental risk factors in a longitudinal twin cohort. Children from twin pregnancies ( N = 250) were recruited antenatally, and detailed demographic, health, and phenotypic data were collected at recruitment, 24- and 36-wk gestation, birth, and 18 mo of age. 25-Hydroxyvitamin D was quantified for mothers at 28-wk gestation and infants at birth. Dental examinations were conducted on the twins at 6 y of age to determine the presence, severity, and extent of HSPM per standardized criteria. To investigate associations of environmental risk factors with HSPM, multiple logistic regression models were fitted with generalized estimating equations to adjust for twin correlation. Within- and between-pair analyses were performed for unshared continuous variables: birthweight and birth 25-hydroxyvitamin D. Twin-twin concordance for monozygotic (MZ) and dizygotic (DZ) pairs was calculated and compared after adjusting for identified risk factors. A total of 344 twins underwent the 6-y-old dental assessment; HSPM occurred in 68 (19.8%). After adjusting for potential confounders, vitamin D levels at birth, infantile eczema, dizygosity, in vitro fertilization, socioeconomic position, and maternal smoking beyond the first trimester of pregnancy demonstrated the strongest associations with HSPM. Overall concordance for HSPM was 0.47 (95% CI, 0.32 to 0.62) with weak evidence ( P = 0.078) of higher concordance in MZ twins (0.63; 95% CI, 0.38 to 0.89) as compared with DZ twins (0.41; 95% CI, 0.24 to 0.58). After adjusting for known risk factors, there was no evidence ( P = 0.172) for an additive genetic influence. These findings suggest that shared and unshared environmental factors, such as maternal smoking later in pregnancy and infantile eczema, are important in the etiology of HSPM.


1998 ◽  
Vol 172 (3) ◽  
pp. 268-272 ◽  
Author(s):  
Kenneth S. Kendler ◽  
Laura M. Karkowski ◽  
Carol A. Prescott ◽  
Michael C. Neale ◽  
Nancy L. Pedersen

BackgroundThe Temperance Boards in Sweden registered individuals for three reasons: public drunkenness, driving under the influence of alcohol and committing a crime in connection with alcohol. We wanted to ascertain whether these three forms of alcohol-related problems result from similar or different genetic and environmental risk factors.MethodWe conducted a trivariate twin analysis of these three causes of registration in all male-female twin pairs of known zygosity born in Sweden, 1926–1949 (n=5177 twin pairs).ResultsPrevalences of registration for public drunkenness, drink-driving and alcohol-related crime were, respectively, 9.0, 3.6 and 4.0%. The best-fitting model had one general genetic and one general familial – environmental factor with specific genetic risk factors for drink-driving and specific familial – environmental risk factors for alcohol-related crime.ConclusionsThe three causes for alcohol registration in Sweden largely reflect the same genetic and environmental risk factors. Estimated heritabilities were similar for the three forms of registration. However, specific genetic risk factors exist for drink-driving and specific familial – environmental risk factors for alcohol-related crime. Genetic factors are somewhat less important and familial –environmental factors more important for public drunkenness than for drink-driving and alcohol related crime.


2011 ◽  
Vol 14 (6) ◽  
pp. 516-523 ◽  
Author(s):  
Kenneth S. Kendler ◽  
John M. Myers ◽  
Corey L. M. Keyes

To determine the relationship between the genetic and environmental risk factors for externalizing psychopathology and mental wellbeing, we examined detailed measures of emotional, social and psychological wellbeing, and a history of alcohol-related problems and smoking behavior in the last year in 1,386 individual twins from same-sex pairs from the MIDUS national US sample assessed in 1995. Cholesky decomposition analyses were performed withthe Mx program. The best fit model contained one highly heritable common externalizing psychopathology factor for both substance use/abuse measures, and one strongly heritable common factor for the three wellbeing measures. Genetic and environmental risk factors for externalizing psychopathology were both negatively associated with levels of mental wellbeing and accounted for, respectively, 7% and 21% of its genetic and environmental influences. Adding internalizing psychopathology assessed in the last year to the model, genetic risk factors unique for externalizing psychopathology were now positively related to levels of mental wellbeing, although accounting for only 5% of the genetic variance. Environmental risk factors unique to externalizing psychopathology continued to be negatively associated with mental wellbeing, accounting for 26% of the environmental variance. When both internalizing psychopathology and externalizing psychopathology are associated with mental wellbeing, the strongest risk factors for low mental wellbeing are genetic factors that impact on both internalizing psychopathology and externalizing psychopathology, and environmental factors unique to externalizing psychopathology. In this model, genetic risk factors for externalizing psychopathology predict, albeit weakly, higher levels of mental wellbeing.


1992 ◽  
Vol 22 (3) ◽  
pp. 617-622 ◽  
Author(s):  
Ellen E. Walters ◽  
Michael C. Neale ◽  
Lindon J. Eaves ◽  
Andrew C. Heath ◽  
Ronald C. Kessler ◽  
...  

SynopsisA genetic analysis of the co-occurrence of bulimia and major depression (MD) was performed on 1033 female twin pairs obtained from a population based register. Personal interviews were conducted and clinical diagnoses made according to DSM-III-R criteria.Additive genes, but not family environment, are found to play an important aetiological role in both bulimia and MD. The genetic liabilities of the two disorders are correlated 0·456. While unique environmental factors account for around half of the variation in liability to both bulimia and MD, these risk factors appear to be unrelated, i.e., each disorder has its own set of unique environmental risk factors. Thus, the genetic liability of bulimia and MD is neither highly specific nor entirely nonspecific. There is some genetic correlation between the two disorders as well as some genetic and environmental risk factors unique to each disorder. Limitations and directions for future research are discussed.


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