Relative Contribution Of Genes Research Articles

Genetic parameters of fear-related behaviors in Nigerian indigenous turkey poults: A pilot study

Accurate estimates of genetic parameters will enable turkey breeders to determine the effect of selection on fear-related behaviors in breeding programs. Currently, no published reports exist on genetic parameters of fear-related behaviors in Nigerian indigenous turkey (NIT). The objective of this pilot study was to estimate genetic parameters of fear-related behaviors in NIT poults to know the relative contribution of genes and environment to these traits. Three behavioral tests were used as measures of fear response in randomly selected 200 NIT poults generated from mating of 10 sires and 20 dams. Emergence, inversion and open field tests were conducted at 9, 12, and 14 days of age, respectively. Fear tests were conducted in early life to measure innate fear and not learned fear. Heritability, genetic and phenotypic correlations were estimated for latency to emerge from a dark box (EMG), duration of wing flapping during inversion (INV), and behavioral activities performed during open field test such as preening frequency (PN), preening duration (PD), wall pecking duration (DPW), number of times a bird rested on its chest (NRC), duration of movement (DM), total number of floor squares explored (BE) and percentage of floor squares explored (PBC). Variance and covariance parameters of the fear-related behaviors were estimated using restricted maximum likelihood method. Heritability estimates ranged from very low to moderate. The lowest heritability (0.004) was estimated for NRC performed during the open field test while the highest heritability (0.364) was estimated for EMG. All genetic correlations between all pairs of fear-related behaviors were low except between INV and NRC (0.8132); INV and DM (0.7326), and between INV and PN (0.7115). Positive phenotypic correlations were found between INV and other fear-related behaviors while negative phenotypic correlations were found between NRC and the other fear-related behaviors. The highest phenotypic correlation was found between INV and BE (0.9985) while the lowest was between EMG and NRC (-0.0001). The very low to moderate heritability estimated for most of the fear-related behaviors indicates little genetic contribution to fear-related behaviors in NIT, suggesting that fearfulness can be best reduced in these birds by improving the rearing environment. The high genetic correlation between INV and NRC; DPW and PN; INV and DM as well as between INV and PN may indicate that the genes that contribute to these pairs of fear-related behaviors are co-inherited.

Sex-Specific Transmission of Anxiety Disorders From Parents to Offspring

Although anxiety disorders are known to run in families, the relative contribution of genes and environment is unclear. Patterns of sex-specific transmission of anxiety may point to different pathways in how parents pass anxiety disorders down to their children; however, the association of parent and offspring sex with the transmission of anxiety disorders has not been previously studied. To examine whether the transmission of anxiety from parents to children is sex specific. This cross-sectional family study recruited participants from the general population (enriched for familial risk of mood disorders) in Nova Scotia, Canada, from February 1, 2013, to January 31, 2020. Anxiety disorder in the same-sex or opposite-sex parent. Semistructured interviews were used to establish lifetime diagnoses of anxiety disorder in parents and offspring. The association between anxiety disorder in the same-sex or opposite-sex parent and anxiety disorders in the offspring was tested with logistic regression. A total of 398 offspring (203 female offspring with a mean [SD] age of 11.1 [3.7] years and 195 male offspring with a mean [SD] age of 10.6 [3.1] years) of 221 mothers and 237 fathers participated in the study. Anxiety disorders in the same-sex parent (odds ratio [OR], 2.85; 95% CI, 1.52-5.34; P = .001) were associated with increased rates of anxiety disorders in the offspring, whereas anxiety disorders in the opposite-sex parent (OR, 1.51; 95% CI, 0.81-2.81; P = .20) were not. Sharing a household with a same-sex parent without anxiety was associated with lower rates of offspring anxiety (OR, 0.38; 95% CI, 0.22-0.67; P = .001), but the presence of an opposite-sex parent without anxiety was not (OR, 0.96; 95% CI, 0.56-1.63; P = .88). In this cross-sectional study of families, an association between the same-sex parent's anxiety disorder and anxiety disorders in offspring suggests an environmental mechanism, such as modeling. Future studies should establish whether treating parents' anxiety may protect their children from developing an anxiety disorder.

Visual search: Heritability and association with general intelligence.

Visual search guides goal-directed action in humans and many other species, and it has been studied extensively in the past. Yet, no study has investigated the relative contributions of genes and environments to individual differences in visual search performance, or to which extent etiologies are shared with broader cognitive phenotypes. To address this gap, we studied visual search and general intelligence in 156 monozygotic (MZ) and 158 same-sex dizygotic (DZ) twin pairs. We found that different indexes of visual search performance (response latency and visual search efficiency) were moderately heritable. Phenotypic correlations between visual search and intelligence were small-to-moderate, and only a small proportion of the genetic variance in visual search was shared with genetic variance in intelligence. We discuss these findings in the context of the "generalist genes hypothesis" stating that different cognitive functions have a common genetic basis.

Reproductive phenotype predicts adult bite‐force performance in sex‐reversed dragons (Pogona vitticeps)

Sex-related differences in morphology and behavior are well documented, but the relative contributions of genes and environment to these traits are less well understood. Species that undergo sex reversal, such as the central bearded dragon (Pogona vitticeps), offer an opportunity to better understand sexually dimorphic traits because sexual phenotypes can exist on different chromosomal backgrounds. Reproductively female dragons with a discordant sex chromosome complement (sex reversed), at least as juveniles, exhibit traits in common with males (e.g., longer tails and greater boldness). However, the impact of sex reversal on sexually dimorphic traits in adult dragons is unknown. Here, we investigate the effect of sex reversal on bite-force performance, which may be important in resource acquisition (e.g., mates and/or food). We measured body size, head size, and bite force of the three sexual phenotypes in a colony of captive animals. Among adults, we found that males (ZZm) bite more forcefully than either chromosomally concordant females (ZWf) or sex-reversed females (ZZf), and this difference is associated with having relatively larger head dimensions. Therefore, adult sex-reversed females, despite apparently exhibiting male traits as juveniles, do not develop the larger head and enhanced bite force of adult male bearded dragons. This pattern is further illustrated in the full sample by a lack of positive allometry of bite force in sex-reversed females that is observed in males. The results reveal a close association between reproductive phenotype and bite force performance, regardless of sex chromosome complement.

Isolating and quantifying the role of developmental noise in generating phenotypic variation.

Genotypic variation, environmental variation, and their interaction may produce variation in the developmental process and cause phenotypic differences among individuals. Developmental noise, which arises during development from stochasticity in cellular and molecular processes when genotype and environment are fixed, also contributes to phenotypic variation. While evolutionary biology has long focused on teasing apart the relative contribution of genes and environment to phenotypic variation, our understanding of the role of developmental noise has lagged due to technical difficulties in directly measuring the contribution of developmental noise. The influence of developmental noise is likely underestimated in studies of phenotypic variation due to intrinsic mechanisms within organisms that stabilize phenotypes and decrease variation. Since we are just beginning to appreciate the extent to which phenotypic variation due to stochasticity is potentially adaptive, the contribution of developmental noise to phenotypic variation must be separated and measured to fully understand its role in evolution. Here, we show that variation in the component of the developmental process corresponding to environmental and genetic factors (here treated together as a unit called the LALI-type) versus the contribution of developmental noise, can be distinguished for leopard gecko (Eublepharis macularius) head color patterns using mathematical simulations that model the role of random variation (corresponding to developmental noise) in patterning. Specifically, we modified the parameters of simulations corresponding to variation in the LALI-type to generate the full range of phenotypic variation in color pattern seen on the heads of eight leopard geckos. We observed that over the range of these parameters, variation in color pattern due to LALI-type variation exceeds that due to developmental noise in the studied gecko cohort. However, the effect of developmental noise on patterning is also substantial. Our approach addresses one of the major goals of evolutionary biology: to quantify the role of stochasticity in shaping phenotypic variation.

Free Will, Determinism, and Intuitive Judgments About the Heritability of Behavior.

The fact that genes and environment contribute differentially to variation in human behaviors, traits and attitudes is central to the field of behavior genetics. Perceptions about these differential contributions may affect ideas about human agency. We surveyed two independent samples (N = 301 and N = 740) to assess beliefs about free will, determinism, political orientation, and the relative contribution of genes and environment to 21 human traits. We find that lay estimates of genetic influence on these traits cluster into four distinct groups, which differentially predict beliefs about human agency, political orientation, and religiosity. Despite apparent ideological associations with these beliefs, the correspondence between mean lay estimates and published heritability estimates for the surveyed traits is large (r = .77). Belief in genetic determinism emerges as a modest predictor of accuracy in these lay estimates. Additionally, educated mothers with multiple children emerge as particularly accurate in their estimates of the genetic contribution to these traits.

Family history of prostate and colorectal cancer and risk of colorectal cancer in the Women\u2019s health initiative

BackgroundEvidence suggests that risk of colorectal and prostate cancer is increased among those with a family history of the same disease, particularly among first-degree relatives. However, the aggregation of colorectal and prostate cancer within families has not been well investigated.MethodsAnalyses were conducted among participants of the Women’s Health Initiative (WHI) observational cohort, free of cancer at the baseline examination. Subjects were followed for colorectal cancer through August 31st, 2009. A Cox-proportional hazards regression modeling approach was used to estimate risk of colorectal cancer associated with a family history of prostate cancer, colorectal cancer and both cancers among first-degree relatives of all participants and stratified by race (African American vs. White).ResultsOf 75,999 eligible participants, there were 1122 colorectal cancer cases diagnosed over the study period. A family history of prostate cancer alone was not associated with an increase in colorectal cancer risk after adjustment for confounders (aHR =0.94; 95% CI =0.76, 1.15). Separate analysis examining the joint impact, a family history of both colorectal and prostate cancer was associated with an almost 50% increase in colorectal cancer risk (aHR = 1.48; 95% CI = 1.04, 2.10), but similar to those with a family history of colorectal cancer only (95% CI = 1.31; 95% CI = 1.11, 1.54).ConclusionsOur findings suggest risk of colorectal cancer is increased similarly among women with colorectal cancer only and among those with both colorectal and prostate cancer diagnosed among first-degree family members. Future studies are needed to determine the relative contribution of genes and shared environment to the risk of both cancers.

East Meets West: The Increasing Incidence of Inflammatory Bowel Disease in Asia as a Paradigm for Environmental Effects on the Pathogenesis of Immune-Mediated Disease

East Meets West: The Increasing Incidence of Inflammatory Bowel Disease in Asia as a Paradigm for Environmental Effects on the Pathogenesis of Immune-Mediated Disease

Individual Differences in Exercise Behavior: Stability and Change in Genetic and Environmental Determinants From Age 7 to 18

Exercise behavior during leisure time is a major source of health-promoting physical activity and moderately tracks across childhood and adolescence. This study aims to investigate the absolute and relative contribution of genes and the environment to variance in exercise behavior from age 7 to 18, and to elucidate the stability and change of genetic and shared environmental factors that underlie this behavior. The Netherlands Twin Register collected data on exercise behavior in twins aged approximately 7, 10, 12, 14, 16 and 18years (N=27,332 twins; 48% males; 47% with longitudinal assessments). Three exercise categories (low, middle, high) were analyzed by means of liability threshold models. First, a univariate model was fitted using the largest available cross-sectional dataset with linear and quadratic effects of age as modifiers on the means and variance components. Second, a simplex model was fitted on the longitudinal dataset. Heritability was low in 7-year-olds (14% in males and 12% in females), but gradually increased up to age 18 (79% in males and 49% in females), whereas the initially substantial relative influence of the shared environment decreased with age (from 80 to 4% in males and from 80 to 19% in females). This decrease was due to a large increase in the genetic variance. The longitudinal model showed the genetic effects in males to be largely stable and to accumulate from childhood to late adolescence, whereas in females, they were marked by both transmission and innovation at all ages. The shared environmental effects tended to be less stable in both males and females. In sum, the clear age-moderation of exercise behavior implies that family-based interventions might be useful to increase this behavior in children, whereas individual-based interventions might be better suited for adolescents. We showed that some determinants of individual differences in exercise behavior are stable across childhood and youth, whereas others come into play at specific ages. In view of the many benefits of regular exercise, identifying these determinants at specific ages should be a public health priority.

Racial differences in heritability of cigarette smoking in adolescents and young adults

IntroductionAlthough epidemiologic studies suggest low levels of cigarette use among African American adolescents relative to White U.S. adolescents, it is not known whether this may be due to racial differences in the relative contribution of genes and environment to cigarette use initiation and progression to regular use. MethodsUsing data from White (n=2665) and African American (n=809) twins and full siblings sampled in the National Longitudinal Study of Adolescents, we fitted age-, sex- and race-specific variance decomposition models to estimate the magnitude of genetic and environmental effects on cigarette use initiation and cigarette use quantity in Whites and African Americans across adolescence and adulthood. We employ a causal-contingent-common pathway model to estimate the amount of variance explained in quantity of cigarettes smoked contingent on cigarette use initiation. ResultsAfrican Americans had lower cigarette use prevalence from adolescence through adulthood, and used cigarettes less heavily than Whites. Race-specific causal-contingent-common pathway models indicate that racial differences in genetic and environmental contributions to cigarette use initiation and cigarette use quantities are not present in adolescence but appear in young adulthood. Additive genetic factors were an important risk factor for cigarette use initiation for White but not African American young adults and adults. ConclusionsGenetic and environmental contributions for cigarette use are similar by race in adolescence. In adulthood, genes have a stronger influence for cigarette use among White adolescents while the influence of the environment is minimal. For African Americans, both genetic and environmental influences are important in young adulthood and adulthood.

Genetic and environmental factors in conjunctival UV autofluorescence.

Conjunctival UV autofluorescence (CUVAF) photography was developed to detect and characterize preclinical sunlight-induced ocular damage. Ocular sun exposure has been related to cases of pterygia and was recently negatively correlated with myopia. Hence, CUVAF has excellent potential as an objective biomarker of sun exposure. However, much variation in CUVAF has been observed, and the relative contributions of genes and environment to this variation have not yet been identified. To investigate sources of variation in CUVAF in relation to its potential clinical relevance. We performed a cross-sectional analysis of 3 population-based cohort studies in the general community, including the Twins Eye Study in Tasmania, the Brisbane Adolescent Twin Study, and the Western Australian Pregnancy Cohort (Raine) Study. The twin studies were conducted between 2001 and 2009, and the 20-year follow-up of the Raine Study was completed between March 2010 and February 2012. We included genotypic and phenotypic data from 295 Australian families in the Tasmanian and Brisbane twin studies and from 661 participants in the 20-year follow-up of the Raine Study. We compared CUVAF levels in the 3 cohorts and performed a classic twin study to partition variation in CUVAF. We also conducted a genome-wide association analysis to identify specific genetic variants associated with CUVAF. The total area of CUVAF, heritability of CUVAF, and single-nucleotide polymorphisms (SNPs) associated with CUVAF from the genome-wide association study. Within twin cohorts, individuals living closer to the equator (latitude, 27.47° S) had higher levels of CUVAF compared with individuals from southern regions (latitude, 42.88° S) (median [interquartile range], 45.4 [26.8-68.5] vs 28.7 [15.0-42.3] mm2; P < .001). The variation in CUVAF explained by the additive genetic component was 0.37 (95% CI, 0.22-0.56), whereas the variation due to the common environment was 0.50 (95% CI; 0.29-0.71). The SNP rs1060043, located approximately 800 base pairs away from the SLC1A5 gene, a member of the solute carrier family 1, had a genome-wide significant association with a P value of 3.2 × 10-8. Gene-based analysis did not improve our power to detect association with other genes. Our findings confirm that, although a large environmental component to CUVAF (equivalent of sun exposure) exists, genes also play a significant role. We identified a SNP (rs1060043) as being significantly associated with CUVAF; replication of this finding in future studies is warranted.

Abstract 1297: The heritability of melanoma differs between light- and dark-skinned individuals of European descent

Abstract Melanoma is strongly associated with exposure to ultraviolet radiation (UV). The prevalence of melanoma is much higher in lighter-skinned Caucasians as compared to darker-skinned Caucasians who have a higher concentration of melanin in their skin which absorbs UV radiation and prevents it from reaching deeper layers of the skin to cause DNA damage. This suggests that the relative contributions of genes and environment in the etiology of melanoma and the genetic architecture of melanoma susceptibility may differ between these two groups. To test this hypothesis, we assessed the heritability of melanoma separately in self-reported light- and dark-skinned Caucasians using data from a previously published melanoma GWAS of 2000 cases and 1000 controls (Amos et al, 2011). Employing the GCTA method developed by Visscher et al (Yang et al, 2011), which estimates the additive genetic contributions of all genotyped single nucleotide polymorphisms (SNPs) to phenotypic variance, we observed that melanoma was highly heritable in dark-skinned Caucasians (h2 = 66%, SE = 25%, p = 0.0058), but not significantly heritable in light-skinned Caucasians (h2 = 15%, SE = 22%, p = 0.25). This suggests that whereas inherited common genetic variation contributes significantly to melanoma susceptibility in dark-skinned Caucasians, this is not the case in lighter-skinned Caucasians. To determine the consequences of this difference in heritability on melanoma risk, we investigated the enrichment of expression quantitative trait loci (eQTLs) separately in light-skinned Caucasians and dark-skinned Caucasians using a permutation-based strategy. We generated 1000 permutations of the melanoma GWAS, shuffling case-control status each time. In each of the permuted datasets, we calculated the percentage of significant disease-associated variants that are also eQTLs. Then we compared the actual percentage of GWAS hits that are eQTLs to the expected percentage under the null based on the permutations to assess whether there is a significant enrichment of functional variants in the GWAS. We found a significant enrichment of skin and lymphoblastoid cell line (LCL) eQTLs in among the melanoma-associated SNPs (p &amp;lt; 10-4) in the GWAS of light-skinned but not dark-skinned Caucasians. Furthermore the target genes of these eQTLs showed a functional enrichment of response pathways to ultraviolet radiation (UV), the major cause of melanoma. Taken together, these findings indicate that melanoma susceptibility not only has varying contributions of genes and environment but also different genetic architectures in light- vs dark- Caucasians. More broadly, heritability can provide important insights into variable contributions of genetics and environment to cancer and other complex diseases, and can be used to divide patients into genetically homogenous subsets to maximize power to detect significant genotype-disease associations. Citation Format: Imge Hulur, Andrew Skol, Kenan Onel. The heritability of melanoma differs between light- and dark-skinned individuals of European descent. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1297. doi:10.1158/1538-7445.AM2014-1297

Familial aggregation of gout and relative genetic and environmental contributions: a nationwide population study in Taiwan

ObjectiveTo examine familial aggregation of gout and to estimate the heritability and environmental contributions to gout susceptibility in the general population.MethodsUsing data from the National Health Insurance (NHI) Research Database...

Common genetic variants, acting additively, are a major source of risk for autism

BackgroundAutism spectrum disorders (ASD) are early onset neurodevelopmental syndromes typified by impairments in reciprocal social interaction and communication, accompanied by restricted and repetitive behaviors. While rare and especially de novo genetic variation are known to affect liability, whether common genetic polymorphism plays a substantial role is an open question and the relative contribution of genes and environment is contentious. It is probable that the relative contributions of rare and common variation, as well as environment, differs between ASD families having only a single affected individual (simplex) versus multiplex families who have two or more affected individuals.MethodsBy using quantitative genetics techniques and the contrast of ASD subjects to controls, we estimate what portion of liability can be explained by additive genetic effects, known as narrow-sense heritability. We evaluate relatives of ASD subjects using the same methods to evaluate the assumptions of the additive model and partition families by simplex/multiplex status to determine how heritability changes with status.ResultsBy analyzing common variation throughout the genome, we show that common genetic polymorphism exerts substantial additive genetic effects on ASD liability and that simplex/multiplex family status has an impact on the identified composition of that risk. As a fraction of the total variation in liability, the estimated narrow-sense heritability exceeds 60% for ASD individuals from multiplex families and is approximately 40% for simplex families. By analyzing parents, unaffected siblings and alleles not transmitted from parents to their affected children, we conclude that the data for simplex ASD families follow the expectation for additive models closely. The data from multiplex families deviate somewhat from an additive model, possibly due to parental assortative mating.ConclusionsOur results, when viewed in the context of results from genome-wide association studies, demonstrate that a myriad of common variants of very small effect impacts ASD liability.

Genetic, environmental and stochastic factors in monozygotic twin discordance with a focus on epigenetic differences.

Genetic-epidemiological studies on monozygotic (MZ) twins have been used for decades to tease out the relative contributions of genes and the environment to a trait. Phenotypic discordance in MZ twins has traditionally been ascribed to non-shared environmental factors acting after birth, however recent data indicate that this explanation is far too simple. In this paper, we review other reasons for discordance, including differences in the in utero environment, genetic mosaicism, and stochastic factors, focusing particularly on epigenetic discordance. Epigenetic differences are gaining increasing recognition. Although it is clear that in specific cases epigenetic alterations provide a causal factor in disease etiology, the overall significance of epigenetics in twin discordance remains unclear. It is also challenging to determine the causality and relative contributions of environmental, genetic, and stochastic factors to epigenetic variability. Epigenomic profiling studies have recently shed more light on the dynamics of temporal methylation change and methylome heritability, yet have not given a definite answer regarding their relevance to disease, because of limitations in establishing causality. Here, we explore the subject of epigenetics as another component in human phenotypic variability and its links to disease focusing particularly on evidence from MZ twin studies.

Heritability of central blood pressure and arterial stiffness

Central blood pressure and aortic stiffness have been consistently reported as strong cardiovascular risk factors. Twin studies by comparing identical with nonidentical twins produce information on the relative contribution of genes and environment. One hundred and fifty-four monozygotic (MZ) and 42 dizygotic (DZ) twin pairs (age 43 ± 17 years) from Hungary and the United States underwent brachial and central augmentation index (AIx), brachial and central pressure, and aortic pulse wave velocity (PWV) measurements with the invasively validated Arteriograph device. Bivariate Cholesky decomposition models were applied. Age-adjusted, sex-adjusted and country-adjusted heritability was 60.0% for central SBP [95% confidence interval (CI), 44.8-69.6%], 50.1% for aortic PWV (95%CI, 26.0-66.8%), 48.7% for aortic AIx (95%CI, 1.7-74.0%), 46.8% for brachial AIx (95%CI, 1.1-73.8%), 46.7% for central pulse pressure (PP) (95%CI, 12.4-61.4%), and 30.0% for brachial PP (95%CI, 0.0-53.4%). Central SBP and PP had strong bivariate correlations with brachial (r = 0.461 and 0.425) and central AIx (r = 0.457 and 0.419), as well as with aortic PWV (r = 0.341 and 0.292, all P < 0.001). Brachial PP had a weak correlation with brachial AIx (r = -0.118, P < 0.05), central AIx (r = -0.122, P < 0.05), and none with aortic PWV (r = 0.08, P = n.s.). Genetic factors explained a moderate phenotypic correlation between central PP, SBP, brachial SBP and aortic PWV. Central systolic and PPs, brachial PP, AIx, aortic PWV are moderately heritable. A moderate genetic covariance among aortic PWV and central PP, central SBP and brachial SBP was found.

Heritability of arterial stiffness and central blood pressure

Heritability of arterial stiffness and central blood pressure

The Heritability of Premenstrual Syndrome

We aimed to determine (1) the prevalence of premenstrual syndrome in a sample of twins and (2) the relative contribution of genes and environment in premenstrual syndrome. A group of 193 subjects inclusive of same gender twins (n = 176) and females from opposite sex twin sets (n = 17) entered the study. Heritability analysis used same gender twin data only. The probandwise concordance rate for the presence or absence of premenstrual syndrome was calculated and the heritability of premenstrual syndrome was assessed by a quantitative genetic model fitting approach using MX software. The prevalence of premenstrual syndrome was 43.0% and 46.8% in monozygotic and dizygotic twins, respectively. The probandwise concordance for premenstrual syndrome was higher in monozygotic (0.81) than in dizygotic twins (0.67), indicating a strong genetic effect. Quantitative genetic modeling found that a model comprising of additive genetic (A) and unique environment (E) factors provided the best fit (A: 95%, E: 5%). No association was found between premenstrual symptom and the following variables: belonging to the opposite gender twin set, birth weight, being breast fed and vaccination. These results established a clear genetic influence in premenstrual syndrome.

Low Heritability of Tinnitus

To estimate the heritability of tinnitus. Self-report questionnaire data collected from August 1, 1995, through June 30, 1997, from individuals in the Nord-Trøndelag Hearing Loss Study (an integrated part of the Nord-Trøndelag Health Study) were used. The study also included information on first-degree family relationships, and age-corrected polychoric correlations of relatives' tinnitus status were calculated. A structural equation model was fit to the data, and the relative contributions of genes and unique environmental effects were estimated. Models that included sex-specific effects were also tested. Nord-Trøndelag County, Norway. A population-based sample of 12 940 spouses, 27 607 parent-offspring, and 11 498 siblings was used. A total of 28 066 respondents were tested twice, yielding a test-retest correlation of 0.65 for the report of tinnitus. Heritability of tinnitus. Correlations for parent-offspring ranged from 0.01 to 0.07 for the various sex combinations, sibling correlation ranged from 0.06 to 0.14, and the spouse correlation was 0.04. This family correlation pattern implies an upper limit for heritability of 0.11 with no sex differences in the heritability estimates. This is the first large population-based family study, to our knowledge, to report on the heritability of tinnitus. In contrast to previous speculations in the literature, this low heritability indicates that additive genetic effects explain only a small proportion of the variance of tinnitus in the population.

Depressive and anxiety symptomatology in ecstasy users: the relative contribution of genes, trauma, life stress and drug use

Previous research has identified elevated rates of depressive and anxiety symptoms amongst ecstasy users; however, few studies have examined which factors increase the likelihood of experiencing such symptoms. The current study aimed to determine the relationship between ecstasy use and depressive/anxiety symptomatology after controlling for known environmental and genetic (polymorphism of the serotonin transporter gene) risk factors for depression and anxiety disorders. Participants consisted of a community sample of 184 18-35-year olds who had taken ecstasy at least once in the past 12 months. Participants completed an interview and questionnaires and provided a saliva sample. Mood symptoms were assessed using the Mood and Anxiety Symptom Questionnaire. Timeline methods were used to collect information on lifetime and recent ecstasy use, as well as recent other drug use and life stress. Trauma exposure was measured using the Composite International Diagnostic Interview--Trauma List. Genomic DNA was extracted from participant saliva samples. Neither lifetime nor recent ecstasy use was associated with the severity of current mood symptoms, either alone or in combination with genetic risk factors. Rather, lifetime trauma, recent stressful life events, the frequency of tobacco use and recent polydrug use significantly predicted the severity of depressive and anxiety symptoms. These results highlight the need to consider the role of environmental factors when examining the relationship between ecstasy use and mood symptoms. Whether ecstasy exacerbates such symptoms in vulnerable individuals requires further investigation using prospective designs.