Common Genetic (common + genetic)

Distribution by Scientific Domains

Terms modified by Common Genetic

  • common genetic abnormality
  • common genetic alteration
  • common genetic background
  • common genetic factor
  • common genetic influence
  • common genetic mechanism
  • common genetic risk factor
  • common genetic variants
  • common genetic variation

  • Selected Abstracts


    Common Genetic Contributions to Alcohol and Cannabis Use and Dependence Symptomatology

    ALCOHOLISM, Issue 3 2010
    Carolyn E. Sartor
    Background:, Despite mounting evidence that use of and dependence on alcohol and cannabis are influenced by heritable factors, the extent to which heritable influences on these phenotypes overlap across the 2 substances has only rarely been explored. In the current study, we quantified cross-substance overlap in sources of variance and estimated the degree to which within-substance associations between use and dependence measures are attributable to common genetic and environmental factors for alcohol and cannabis. Methods:, The sample was comprised of 6,257 individuals (2,761 complete twin pairs and 735 singletons) from the Australian Twin Registry, aged 24 to 36 years. Alcohol and cannabis use histories were collected via telephone diagnostic interviews and used to derive an alcohol consumption factor, a frequency measure for cannabis use, and DSM-IV alcohol and cannabis dependence symptom counts. Standard genetic analyses were conducted to produce a quadrivariate model that provided estimates of overlap in genetic and environmental influences across the 4 phenotypes. Results:, Over 60% of variance in alcohol consumption, cannabis use, and cannabis dependence symptoms, and just under 50% of variance in alcohol dependence (AD) symptoms were attributable to genetic sources. Shared environmental factors did not contribute significantly to the 4 phenotypes. Nearly complete overlap in heritable influences was observed for within-substance measures of use and dependence symptoms. Genetic correlations across substances were 0.68 and 0.62 for use and dependence symptoms, respectively. Conclusions:, Common heritable influences were evident for alcohol and cannabis use and for AD and cannabis dependence symptomatology, but findings indicate that substance-specific influences account for the majority of the genetic variance in the cannabis use and dependence phenotypes. By contrast, the substantial correlations between alcohol use and AD symptoms and between cannabis use and cannabis dependence symptoms suggest that measures of heaviness of use capture much of the same genetic liability to alcohol- and cannabis-related problems as dependence symptomatology. [source]


    Evidence for an Interaction Between Age at First Drink and Genetic Influences on DSM-IV Alcohol Dependence Symptoms

    ALCOHOLISM, Issue 12 2009
    Arpana Agrawal
    Background:, Research suggests that individuals who start drinking at an early age are more likely to subsequently develop alcohol dependence. Twin studies have demonstrated that the liability to age at first drink and to alcohol dependence are influenced by common genetic and environmental factors, however, age at first drink may also environmentally mediate increased risk for alcohol dependence. In this study, we examine whether age at first drink moderates genetic and environmental influences, via gene × environment interactions, on DSM-IV alcohol dependence symptoms. Methods:, Using data on 6,257 adult monozygotic and dizygotic male and female twins from Australia, we examined the extent to which age at first drink (i) increased mean alcohol dependence symptoms and (ii) whether the magnitude of additive genetic, shared, and nonshared environmental influences on alcohol dependence symptoms varied as a function of decreasing age. Twin models were fitted in Mx. Results:, Risk for alcohol dependence symptoms increased with decreasing age at first drink. Heritable influences on alcohol dependence symptoms were considerably larger in those who reported an age at first drink prior to 13 years of age. In those with later onset of alcohol use, variance in alcohol dependence was largely attributable to nonshared environmental variance (and measurement error). This evidence for unmeasured gene × measured environment interaction persisted even when controlling for the genetic influences that overlapped between age at first drink and alcohol dependence symptoms. Conclusions:, Early age at first drink may facilitate the expression of genes associated with vulnerability to alcohol dependence symptoms. This is important to consider, not only from a public health standpoint, but also in future genomic studies of alcohol dependence. [source]


    Relationship between obesity, adipocytokines, and blood pressure: Possible common genetic and environmental factors

    AMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 1 2009
    Ia Pantsulaia
    Adipokines may link adipose tissue to the inflammatory, metabolic, and immune dysregulation. The variation of adipokine levels within individuals, intercorrelations, and relationships to well-established measures of adiposity are incompletely defined. The main goal of the present study was quantitative evaluation of the genetic interrelationships between obesity and adipokines in normal human population. The study sample comprised 272 families of various sizes, including 530 men and 531 women aged 18,80 years, randomly recruited in rural population living in Russia. Various fatness and fat distribution measures (OB), blood pressure (BP), and plasma levels of several adipokines (AC), such as adiponectin, leptin, resistin, and IGFBP-1, have been measured. The likelihood ratio tests clearly revealed that genetic effect for all studied phenotypes was highly significant (P < 0.001) and accounted for 45.9% ± 8.1%, 33.7% ± 7.9%, 35.7% ± 9.8% of variation for AC, OB, and BP, respectively. The pairwise bivariate analyses showed that strong phenotypic correlation between the obesity (OB) and adipocytokines (AC) was caused by both common genetic and environmental factors (rG = 0.597 ± 0.116, rE = 0.671 ± 0.051). The phenotypic correlation between BP and OB is explained by shared genetic factors only (rG = 0.532 ± 0.109), whereas the phenotypic correlation between BP and AC has only common environment basis (rE = ,0.212 ± 0.081) and was mostly due to the correlation observed in females. Our results suggest that genetic factors play a significant role in regulation of variation of the examined traits. The variation of OB traits is almost fully due to genes influencing variation of AC, whereas the correlation between BP and AC is only marginally significant and caused only by shared environment. Am. J. Hum. Biol., 2009. © 2008 Wiley-Liss, Inc. [source]


    Too early to dismiss Yersinia enterocolitica infection in the aetiology of Graves' disease: evidence from a twin case,control study

    CLINICAL ENDOCRINOLOGY, Issue 3 2008
    Thomas H. Brix
    Summary Background,Yersinia enterocolitica (YE) infection has long been implicated in the pathogenesis of Graves' disease (GD). The association between YE and GD could, however, also be due to common genetic or environmental factors affecting the development of both YE infection and GD. This potential confounding can be minimized by investigation of twin pairs discordant for GD. Aim, To examine whether YE infection is associated with GD. Design, We first conducted a classical case,control study of individuals with (61) and without (122) GD, and then a case,control study of twin pairs (36) discordant for GD. Methods, Immunoglobulin (Ig)A and IgG antibodies to virulence-associated Yersinia outer membrane proteins (YOPs) were measured. Main outcome measures, The prevalence of YOP IgA and IgG antibodies. Results, Subjects with GD had a higher prevalence of YOP IgA (49%vs. 34%, P = 0·054) and YPO IgG (51%vs. 35%, P = 0·043) than the external controls. The frequency of chronic YE infection, reflected by the presence of both IgA and IgG YOP antibodies, was also higher among cases than controls (49%vs. 33%, P = 0·042). Similar results were found in twin pairs discordant for GD. In the case,control analysis, individuals with GD had an increased odds ratio (OR) of YE infection: IgA 1·84 (95% CI 0·99,3·45) and IgG 1·90 (95% CI 1·02,3·55). In the co-twin analysis, the twin with GD also had an increased OR of YE infection: IgA 5·5 (95% CI 1·21,24·81) and IgG 5·0 (95% CI 1·10,22·81). Conclusion, The finding of an association between GD and YE in the case,control study and within twin pairs discordant for GD supports the notion that YE infection plays an aetiological role in the occurrence of GD, or vice versa. Future studies should examine the temporal relationship of this association in more depth. [source]