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Soo Hyun Rhee

Publications and source records attributed to Soo Hyun Rhee.

At least 19 recordsLinked to original sources
PubMed2006

The inclusion of measured covariates in the Neale and Kendler model fitting approach.

Neale and Kendler (1995, Am J Hum Genet 57:935-953) described 13 comorbidity models, providing the most comprehensive set of alternative hypotheses regarding the possible causes of comorbidity to date. This research note describes an extension of the Neale and Kendler model fitting approach that permits the inclusion of measured covariates. An example of 13 models examining the comorbidity between alcohol dependence and illicit drug dependence is presented.

Alcoholism↗
PubMed2006

A genome-wide scan for loci influencing adolescent cannabis dependence symptoms: evidence for linkage on chromosomes 3 and 9.

OBJECTIVE: Cannabis is the most frequently abused illicit substance among adolescents and young adults. Genetic risk factors account for part of the variation in the development of cannabis dependence symptoms; however, no linkage studies have been performed for cannabis dependence symptoms. This study aimed to identify such loci. METHOD: Three hundred and twenty-four sibling pairs from 192 families were assessed for cannabis dependence symptoms. Probands (13-19 years of age) were recruited from consecutive admissions to substance abuse treatment facilities. The siblings of the probands ranged in age from 12 to 25 years. A community-based sample of 4843 adolescents and young adults was utilized to define an age- and sex-corrected index of cannabis dependence vulnerability. DSM-IV cannabis dependence symptoms were assessed in youth and their family members with the Composite International Diagnostic Instrument-Substance Abuse Module. Siblings and parents were genotyped for 374 microsatellite markers distributed across the 22 autosomes (average inter-marker distance=9.2cM). Cannabis dependence symptoms were analyzed using Merlin-regress, a regression-based method that is robust to sample selection. RESULTS: Evidence for suggestive linkage was found on chromosome 3q21 near marker D3S1267 (LOD=2.61), and on chromosome 9q34 near marker D9S1826 (LOD=2.57). CONCLUSIONS: This is the first reported linkage study of cannabis dependence symptoms. Other reports of linkage regions for illicit substance dependence have been reported near 3q21, suggesting that this region may contain a quantitative trait loci influencing cannabis dependence and other substance use disorders.

Adolescent↗
PubMed2006

Cannabis receptor haplotype associated with fewer cannabis dependence symptoms in adolescents.

Cannabis is a major substance of abuse, and the gene encoding for the central cannabinoid receptor (CNR1) is a logical candidate gene for vulnerability toward developing symptoms of cannabis dependence. We studied four single-nucleotide polymorphisms (SNPs) in the CNR1 gene for association with having one or more symptoms of cannabis dependence in 541 adolescent subjects who had all tried cannabis five or more times. Cases (327) were defined as those who had tried marijuana and developed one or more symptoms, and controls (214) as those who had tried marijuana but developed no dependence symptoms. Cannabis dependence symptoms were assessed in these youth when they were 17 or older with the Composite International Diagnostic Interview--Substance Abuse Module. Univariate (single-marker) association tests demonstrated that SNP rs806380, located in intron 2 of the CNR1 gene, was significantly associated with developing one or more cannabis dependence symptoms, with the G allele having a protective effect (P < 0.02). This was consistent with the results of the global haplotype test (P < 0.01). One of the common haplotypes examined (present in 21% of the subjects) was significantly associated with a lower rate of having one or more cannabis dependence symptoms. Our findings provide evidence suggesting that a common CNR1 haplotype is associated with developing fewer cannabis dependence symptoms among adolescents who have experimented with cannabis.

Adolescent↗
PubMed2006

The role of conduct disorder in explaining the comorbidity between alcohol and illicit drug dependence in adolescence.

BACKGROUND: Conduct disorder (CD), alcohol dependence (AD), and illicit drug dependence (IDD) frequently co-occur. This paper describes the result of an investigation of the extent to which comorbid alcohol and illicit drug dependence in adolescents are explained by etiological factors in common with conduct disorder. METHODS: Participants were 645 MZ twin pairs, 702 DZ twin pairs, 429 biological sibling pairs, and 96 adoptive sibling pairs, aged 12-18 years, from a community based sample. Conduct disorder was measured using the Diagnostic Interview Schedule for Children-IV. Alcohol and illicit drug dependence were assessed using the Composite International Diagnostic Interview-Substance Abuse Module (CIDI-SAM). For each outcome, subjects were categorized into those with no symptoms, those with one or more symptoms but no diagnosis, and those with a diagnosis. RESULTS: The heritability estimates for CD, AD, and IDD were 58, 66, and 36%, respectively. The genetic correlation between AD and IDD was partially explained by the genetic risk they both share with conduct disorder. CONCLUSIONS: We conclude that conduct disorder in adolescents explains, in part, the co-occurrence of alcohol and illicit drug dependence. Specifically, the genetic contribution to their covariation is explained partially by the genetic contribution in common with conduct disorder.

Adolescent↗
PubMed2006

Genetic and environmental vulnerabilities underlying adolescent substance use and problem use: general or specific?

Are genetic and environmental risks for adolescent substance use specific to individual substances or general across substance classes? We examined this question in 645 monozygotic twin pairs, 702 dizygotic twin pairs, 429 biological sibling pairs, and 96 adoptive (biologically unrelated) sibling pairs ascertained from community-based samples, and ranging in age from 12 to 18 years. Substance use patterns and symptoms were assessed using structured psychiatric interviews. Biometrical model fitting was carried out using age- and sex-specific thresholds for (a) repeated use and (b) problem use, defined as one or more DSM-IV symptoms of abuse or dependence. We hypothesized that problem use would be more heritable than use in adolescence, and that both genetic and environmental risks underlying tobacco, alcohol, and marijuana use and problem use would be significantly correlated. Results of univariate analyses suggested significant heritable factors for use and problem use for all substances with the exception of alcohol use. Shared environmental factors were important in all cases and special twin environmental factors were significant for tobacco use, tobacco problem use, and alcohol use. Multivariate analyses yielded significant genetic correlations between each of the substances (for both levels studied), and significant shared environmental correlations among use variables only. Our results suggest that tobacco, alcohol, and marijuana problem use are mediated by common genetic influences, but shared environmental influences may be more substance-specific for problem use.

Adolescent↗
PubMed2006

Genetic and environmental contributions to common psychopathologies of childhood and adolescence: a study of twins and their siblings.

We report findings based on analyses of self-reports of six common adolescent psychopathologies (attention deficit/hyperactivity disorder, ADHD; conduct disorder, CD; oppositional defiant disorder, ODD; generalized anxiety disorder, GAD; separation anxiety disorder, SAD; and major depressive disorder, MDD) in a sample of 1,162 male and female adolescent (12-19 years) twin pairs and 426 siblings. Prevalence statistics for past year and lifetime reports confirm differences between genders for CD, GAD, SAD, and MDD, and a lack of differences between twins and their non-twin siblings. Biometrical modeling was conducted to ascertain the relative influences of genes, and shared and non-shared environments contributing to these disorders. A more robust estimate of these parameters was obtained by including non-twin siblings. Age-specific thresholds were integrated into the analyses to appropriately model the developmental patterns of behavior. We found evidence for both genetic and non-shared environmental influences for all disorders. Shared environmental influences also seem to be important for MDD and lifetime GAD.

Adolescent↗
PubMed2006

Comorbidity between alcohol dependence and illicit drug dependence in adolescents with antisocial behavior and matched controls.

BACKGROUND: Knowledge regarding the causes of comorbidity among substance use disorders can have significant impact on future research examining the etiology of these disorders. Unfortunately, the conclusions of past studies examining the comorbidity among substance use disorders are conflicting; some studies emphasize familial influences common to multiple substances, while others emphasize substance-specific influences. Discrepancies in results may reflect different analytical approaches or differences in the samples. Here, we examine the causes of comorbidity between alcohol dependence and illicit drug dependence in adolescents. METHODS: We ascertained a clinical sample of adolescents treated for antisocial behavior and substance use disorders and their siblings and a matched control sample. A model fitting approach was used to test 13 alternative hypotheses for the causes of comorbidity. RESULTS: The best supported hypothesis for the comorbidity between alcohol dependence and illicit drug dependence was a model hypothesizing that comorbid disorders are alternate forms of a single underlying liability. The next best fitting models were two of the correlated liabilities models (correlated risk factors and reciprocal causation). DISCUSSION: The results suggest that the best hypotheses explaining the comorbidity between alcohol and illicit drug dependence in adolescents are that alcohol dependence and illicit drug dependence are manifestations of a single general liability to develop substance dependence or that there are separate liabilities that are highly correlated.

Adolescent↗
PubMed2006

The moderating effects of religiosity on the genetic and environmental determinants of smoking initiation.

Although a number of studies have shown that various measures of religiosity are inversely correlated with smoking behavior, none of these studies have used genetically informative samples to test for a gene-environment interaction between the determinants of smoking initiation and religiosity. We tested the moderating effects of three measures of religiosity (religious affiliation, organizational religious activity, and self-rated religiousness) on the genetic and environmental determinants of smoking initiation in 237 monozygotic twin pairs, 315 dizygotic twin pairs, 779 full-sibling pairs, and 233 half-sibling pairs in young adults surveyed from the third wave of the National Longitudinal Study of Adolescent Health. Primary analyses incorporated all sibling pairs, irrespective of whether they were concordant or discordant for the environmental moderator, in models designed to account for the confounding effects of a gene-environment correlation. High levels of self-rated religiousness attenuated the additive genetic component for smoking initiation and were associated with a lower prevalence of smoking initiation. Although all three measures of religiosity were associated with lower rates of smoking initiation, only self-rated religiousness moderated genetic influences on the liability for smoking.

Adolescent↗
PubMed2006

Common and specific genetic influences on aggressive and nonaggressive conduct disorder domains.

OBJECTIVE: To explore the genetic and environmental influences on DSM-IV conduct disorder (CD) aggressive and nonaggressive subscales, taking into account age and sex differences. METHOD: A community sample of 1,100 twin pairs (ages 11-18) was interviewed using the Diagnostic Interview Schedule for Children. Bivariate analyses, using variable threshold models accounting for age and sex differences, were used to determine the extent to which the genetic and environmental influences on aggressive and nonaggressive CD domains are shared or unique. RESULTS: The phenotypic correlation between aggressive and nonaggressive CD domains was 0.32. The most parsimonious bivariate model included additive genetic effects and nonshared environmental effects only (AE model). CONCLUSIONS: The results of behavior genetic model fitting suggest that the DSM-IV CD domains are influenced by unique genetic and environmental factors, but also share some common genetic and environmental influences. A large percentage of the covariation (61%) is caused by genetic factors. These results are consistent with a previous report on the bivariate heritability of aggressive and nonaggressive antisocial behavior, but extend the findings to DSM-IV domains.

Adolescent↗
PubMed2006

Examination of the causes of covariation between conduct disorder symptoms and vulnerability to drug dependence.

Conduct disorder (CD) symptoms and substance dependence commonly co-occur. Both phenotypes are highly heritable and a common genetic influence on the covariation has been suggested. The aim of this study was to determine the extent to which genes and environment contribute to the covariance between CD and drug dependence using twins from the Colorado Longitudinal Twin Sample and the Colorado Twin Registry. A total of 880 twin pairs (237 monozygotic [MZ] female, 195 MZ male, 116 dizygotic [DZ] female, 118 DZ male and 214 DZ opposite-sex) aged 13 to 18 (mean = 15.65) were included in the analysis. CD was assessed by lifetime Diagnostic and Statistical Manual of Mental Disorders (4th ed.; DSM-IV; American Psychiatric Association, 1994) symptom count and a polysubstance dependence vulnerability index was developed from responses to the Composite International Diagnostic Interview--Substance Abuse Module. A bivariate Cholesky Decomposition model was used to partition the cause of variation and covariation of the two phenotypes. No sex-limitation was observed in our data, and male and female parameter estimates were constrained to be equal. Both CD symptoms and dependence vulnerability were significantly heritable, and genes, shared environment and nonshared environment all contributed to the covariation between them. Genes contributed 35% of the phenotypic covariance, shared environment contributed 46%, and nonshared environmental influences contributed the remaining 19% to the phenotypic covariance. Therefore, there appears to be pleiotropic genetic influence on CD symptoms and dependence vulnerability.

Adolescent↗
PubMed2005

A genome-wide search for quantitative trait Loci that influence antisocial drug dependence in adolescence.

BACKGROUND: Among adolescents, externalizing problem behavior and substance use disorders are often comorbid. Familial influences, including shared genetic risk factors, may account for part of this comorbidity. Previously we reported 2 chromosomal regions (3q24-3q25 and 9q34) likely to contain genes that influence substance dependence vulnerability (DV) in adolescence. OBJECTIVES: To identify quantitative trait loci (QTLs) that influence externalizing problem behavior in adolescence and to determine whether any identified QTL overlap chromosomal regions that influence DV. DESIGN: Regression-based QTL mapping procedures designed for selected sibling pair samples. SETTING: Patient probands were drawn from consecutive admissions to residential and outpatient (milieu-type) treatment facilities for substance abuse and delinquency operated by the University of Colorado; most of these patients were referred for treatment by juvenile justice or social service agencies. PATIENTS: A total of 249 proband-sibling pairs from 191 families were selected for the study. Patient probands were 13 to 19 years of age; siblings of the probands ranged in age from 12 to 25 years. MAIN OUTCOME MEASURES: A community-based sample of 4493 adolescents and young adults was used to define clinically significant, heritable, age- and sex-normed indexes of DV, conduct disorder symptoms (CDS), and a composite index of antisocial substance dependence (DV + CDS). Siblings and parents were genotyped for 374 microsatellite markers distributed across the 22 autosomes (mean intermarker distance, 9.2 centimorgans). RESULTS: For both DV and CDS, there was evidence of linkage to the same region on chromosome 9q34, as well as to 3q24-3q25 for DV, and a novel region on chromosome 17q12 for CDS. Our composite index (DV + CDS) yielded the strongest evidence for linkage (logarithm of odds = 2.65) to the chromosome 9q34 region. CONCLUSION: These results provide the first evidence of a potential molecular genetic basis for the comorbidity between DV and antisocial behavior.

Adolescent↗
PubMed2005

Testing hypotheses regarding the causes of comorbidity: examining the underlying deficits of comorbid disorders.

The authors examined the validity of a method commonly used to test alternative hypotheses regarding the causes of comorbidity: the examination of underlying deficits of comorbid disorders. The authors simulated data in which the true causes of comorbidity were known, then compared the patterns of underlying deficits of the comorbid disorders found in the simulated data with the predicted results. The method of examining the underlying deficits of comorbid disorders could distinguish between several comorbidity models, including those that could not be distinguished well using other methods. The ability to distinguish the correct model decreased as the sample size and the correlation between the underlying deficits and the symptom scores decreased, suggesting that the issue of power should be considered carefully.

Adult↗
PubMed2005

Genetic and environmental influences on conduct disorder: symptom, domain and full-scale analyses.

BACKGROUND: We used variable threshold models which accounted for age and gender differences to investigate the genetic and environmental influences on DSM-IV conduct disorder (CD) at the level of symptoms, aggressive versus non-aggressive domains, and full-scale. METHOD: A community sample of 1100 twin pairs (age 11-18) was interviewed using the Diagnostic Interview Schedule for Children. RESULTS: Behavior genetic model fitting suggested that genetic and environmental influences on individual symptoms varied by symptom. The best-fitting models for aggressive and non-aggressive domains, and full-scale CD included additive genetic effects and unique environmental effects only (AE models). These effects could be constrained across age cohorts and sex. The results suggest that using models that incorporate age- and gender-appropriate thresholds specific to each subject we can account for prevalence differences between cohorts. Heritability estimates were .49, .55 and .53 for the aggressive domain, non-aggressive domain, and full-scales, respectively. These results are in contrast to previous research on antisocial behavior measured with the CBCL reporting higher heritability for aggressive versus non-aggressive domains. CONCLUSIONS: Results suggest that individual symptoms of CD may be differentially heritable. Additionally, CD assessed using DSM-IV criteria may show differing patterns of heritability compared with estimates obtained for other measures of antisocial behavior such as the CBCL.

Adolescent↗
PubMed2004

Etiology of sex differences in the prevalence of ADHD: an examination of inattention and hyperactivity-impulsivity.

Several studies have examined the predictions of two models (i.e., the polygenic multiple threshold (PMT) model and the constitutional variability (CV) model) developed to explain sex differences in the prevalence of attention-deficit/hyperactivity disorder (ADHD), and the results of these studies are conflicting. Although there is substantial evidence that two distinct, moderately correlated symptom dimensions (inattention and hyperactivity-impulsivity) underlie ADHD symptoms, all of these studies have examined ADHD as a unidimensional construct. Therefore, we tested the PMT and CV models for the two ADHD symptom dimensions separately. Dizygotic twins or siblings of girls with ADHD had a higher number of ADHD symptoms than twins or siblings of boys with ADHD. This evidence for the PMT model and against the CV model was found for both inattention and hyperactivity-impulsivity, but became weaker for hyperactivity-impulsivity as symptom severity increased.

Attention Deficit Disorder with Hyperactivity↗
PubMed2004

The validity of the Neale and Kendler model-fitting approach in examining the etiology of comorbidity.

Given that knowledge regarding the etiology of comorbidity between disorders can have a significant impact on research regarding the classification, treatment, and etiology of the disorders, the ability to reject incorrect hypotheses regarding the causes of comorbidity is very important. A simulation study was conducted to assess the validity of the Neale and Kendler (1995) model-fitting approach in examining the etiology of comorbidity between two disorders. First, data were simulated under the assumptions of the 13 alternative comorbidity models described by Neale and Kendler. Second, model-fitting analyses testing the comorbidity models were conducted on the simulated datasets. Thirteen sets of data with varying model parameters were simulated to test Neale and Kendler's assertion that their model-fitting approach is appropriate across a range of potential prevalences and degrees of familiality. The validity of the model-fitting approach in examining unselected twin data and a combination of selected family data and unselected family data was explored. The model-fitting approach successfully discriminated several classes of comorbidity models, although discrimination between models within classes of related models was less accurate. Results suggest that the model-fitting approach can be a useful tool in examining the etiology of the comorbidity between disorders if the caveats of the present study's results are considered carefully. As predicted by Neale and Kendler, variations in the disorder prevalences and familial correlations did not affect the validity of their model-fitting approach, but affected the power to discriminate the correct model. As suggested by Neale and Kendler, the model-fitting approach can be applied to both unselected and selected data and to both twin and family data.

Comorbidity↗
PubMed2004

The relation between sluggish cognitive tempo and DSM-IV ADHD.

To test the relation between sluggish cognitive tempo (SCT) and DSM-IV ADHD symptoms, parent and teacher ratings of the 18 DSM-IV ADHD items and five potential SCT items were obtained in a community sample of 8-18 year-old twins that was overselected for ADHD and learning disabilities (n = 296). Confirmatory factor analyses revealed that a three-factor model provided the best fit to the data for both parent and teacher ratings. DSM-IV inattention and hyperactivity-impulsivity symptoms loaded on two factors consistent with the DSM-IV model, and five SCT symptoms loaded primarily on a third factor. The SCT and inattention factors were highly correlated, whereas SCT and hyperactivity-impulsivity were weakly related. Both raters indicated that children meeting symptom criteria for the combined and inattentive subtypes exhibited significantly more SCT symptoms than those meeting symptom criteria for hyperactive-impulsive type and the comparison group without ADHD. Children meeting symptom criteria for the inattentive type exhibited significantly more SCT symptoms than those meeting criteria for the combined type, based on teacher ratings. These results suggest that SCT is an internally consistent construct that is significantly associated with DSM-IV inattention.

Attention↗
PubMed2004

Comorbidity of depression with levels of smoking: an exploration of the shared familial risk hypothesis.

Comorbidity of depression and smoking is well recognized, but results from studies that have assessed alternative explanations have varied by the level of smoking and the study method. We examined all 13 etiology models of comorbidity described by Neale and Kendler (American Journal of Genetics, 57, 935-953, 1995) for depression and each of four levels of smoking to shed light on the role that differing definitions might have played in generating the conflicting findings. Data came from 979 young adults aged 26-35 years who participated in an epidemiological cohort study in southeastern Michigan. Respondent and family history data on parental smoking and depression were analyzed using the biometric modeling method for family data, which Rhee and colleagues (Journal of Child Psychology and Psychiatry and Allied Disciplines, 44, 612-636, 2003; Behavior Genetics, 34, 251-265, 2004) have shown to be valid more frequently than traditional prevalence analyses. Results of the biometric model fitting suggested that for ever smoking, the comorbidity with depression may be related to chance or a high liability threshold for smoking only. In contrast, a correlated liabilities model fit the data best for the comorbidity of depression with daily, heavy, and nicotine-dependent smoking. The familial correlations accounted for 73%-95% of the total variance shared between depression and these levels of smoking. These results differ from analyses of these data using a traditional prevalence approach, which found no evidence of shared familial liability. The conflicting findings of the studies that have examined the relationship between smoking and depression may be attributable to differences in definition of the disorders and the methods used to analyze them.

Adult↗