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  • With the AR gene previous research has found associations of

    2020-08-03

    With the AR gene, previous research has found associations of the short Etomoxir sale of both the CAG and GGC repeat polymorphisms with behavioural characteristics typical of high P. In the present study, the short CAG genotype was significantly associated with high P in males only. In females, the trend was for higher P in the group homozygous for short alleles, but this did not even approach statistical significance. For the GGC polymorphism, there were no significant associations with P, although the trend was for the short alleles to be associated with higher P. If there is a real association of AR polymorphisms with P, then the effects must be quite small given the sample size of the current study. For males, the power to detect a small difference (0.2 standard deviation units) between long and short alleles is approximately 81% for the CAG repeat polymorphism and around 74% for the GGC repeat polymorphism (P<0.05, 2-tailed) (Cohen, 1977). For females, the power to detect a small difference between the short/short and other genotypes is approximately 81% for CAG repeats and 80% for GGC repeats. In addition to these findings with P, there were some significant associations of AR polymorphisms with BAS Drive. For females, the homozygous short CAG group had higher Drive scores, while for males the GGC short allele was associated with higher scores. Neither of these associations was predicted. Given that 28 statistical tests were carried out, it is possible that these are Type I errors, particularly as associations were not observed with other BAS scales which are correlated with the Drive scale. Although the present results are negative, we believe it is important to report all findings to avoid biases in the literature. The present sample has also been genotyped for several other polymorphisms which might plausibly be associated with personality traits, but again there have been largely negative results. While some of these results have been previously published, others have not. In order to provide a complete record of the results, we have presented them as Appendix A to this paper. Only 2 of the 33 statistical comparisons in this appendix are statistically significant. One of these did not replicate across sub-samples (Henderson et al., 2000) and the other involved heterozygotes having a higher score, which is not biologically plausible. A potential weakness of the present study is that it involved population controls rather than family controls, which are a better way of controlling the effects of population stratification (e.g. ethnic group differences in allele frequencies). On the other hand, general population samples do have their own advantages (Jorm & Easteal, 2000). They are not affected by the referral biases of clinic samples and not subject to transmission ratio distortion (Paterson & Petronis, 1999), which can produce spurious associations with family controls. In conclusion, the present study failed to find support for the predicted association of DBH and AR polymorphisms with P, despite the large sample size. However, we cannot rule out that there are very small associations or that other polymorphisms of these genes have associations with P.