Levitan R D, Kaplan A S, Masellis M, Basile V S, Richter M A, Kennedy J L
Mood and Anxiety Division, Centre for Addiction and Mental Health, University of Toronto, Department of Psychiatry, Canada.
Eur Neuropsychopharmacol. 2006 Jan;16(1):1-6. doi: 10.1016/j.euroneuro.2005.04.016. Epub 2005 Jun 6.
There is significant evidence that eating disorders have an important biological overlap with obsessive-compulsive disorder (OCD), though the specific mediators of this relationship remain unclear. Recent evidence suggests that the G861C polymorphism of the 5HT-1Dbeta receptor gene and the G allele in particular may play a role in OCD. We thus hypothesized that, among a heterogenous group of probands with bulimia nervosa (BN), this same G allele might predict the presence and/or severity of OCD pathology.
165 consecutive female probands with BN were genotyped for the G861C polymorphism of the 5HT-1Dbeta receptor gene. Rates of full syndrome OCD, partial syndrome OCD and no OCD were compared across the three genotypic groups defined by this polymorphism.
45 out of 165 BN probands (27.3%) had either full or partial syndrome OCD. In the full sample, there was a significant difference in the distribution of the three diagnostic groups by genotype (chi2=10.07, df=4, p=.039). The G861C polymorphism did not strongly predict which probands had any vs. no OCD pathology. However, among the 45 probands with OCD symptoms, the G861C polymorphism did strongly differentiate full syndrome vs. partial syndrome OCD (chi2=9.26, df=2, p=.01; odds ratio for full syndrome OCD with GG genotype=7.69, 95% CI=1.45-40.9).
In women with BN, the G861C polymorphism of the 5HT-1Dbeta gene does not appear to be associated with the generation of OCD symptoms; however, it might directly or indirectly be associated with a modulatory effect on syndrome severity in probands otherwise predisposed to OCD. While preliminary and in need of replication in other samples, this is the first association study to suggest how a particular gene might influence OCD pathology in an eating disorder population.
有大量证据表明，饮食失调与强迫症（OCD）在生物学上有重要重叠，尽管这种关系的具体介导因素仍不清楚。最近的证据表明，5HT - 1Dβ受体基因的G861C多态性，特别是G等位基因，可能在强迫症中起作用。因此，我们假设，在一组异质性的神经性贪食症（BN）先证者中，同样的G等位基因可能预示着强迫症病理的存在和/或严重程度。
对165名连续的患有BN的女性先证者进行5HT - 1Dβ受体基因G861C多态性的基因分型。比较由这种多态性定义的三个基因分型组中完全综合征强迫症、部分综合征强迫症和无强迫症的发生率。
165名BN先证者中有45名（27.3%）患有完全或部分综合征强迫症。在整个样本中，三个诊断组的基因型分布存在显著差异（χ2 = 10.07，自由度 = 4，p = 0.039）。G861C多态性并不能强烈预测哪些先证者有或没有强迫症病理。然而，在45名有强迫症症状的先证者中，G861C多态性确实能强烈区分完全综合征与部分综合征强迫症（χ2 = 9.26，自由度 = 2，p = 0.01；GG基因型的完全综合征强迫症的优势比 = 7.69，95%置信区间 = 1.45 - 40.9）。
在患有BN的女性中，5HT - 1Dβ基因的G861C多态性似乎与强迫症症状的产生无关；然而，它可能直接或间接地与对原本易患强迫症的先证者的综合征严重程度的调节作用有关。虽然这是初步研究且需要在其他样本中重复验证，但这是第一项表明特定基因可能如何影响饮食失调人群中强迫症病理的关联研究。
