Abstract
The ratio of the lengths of the second and fourth finger (2D∶4D) has been described as reflecting the degree of prenatal androgen exposure in humans. 2D∶4D is smaller for males than females and is associated with traits such as left-handedness, physical aggression, attention-deficit-hyperactivity disorder and a genetic polymorphism of the androgen receptor. All of these traits are known to be correlated to the vulnerability for alcohol dependency. We therefore hypothesized low 2D∶4D in patients with alcohol dependency. In the present study on 131 patients suffering from alcohol dependency and 185 healthy volunteers, we found that alcohol dependent patients had smaller 2D∶4D ratios compared to controls with preserved sexual dimorphism but with reduced right-left differences. The detection of alcohol dependency based on 2D∶4D ratios was most accurate using the right hand of males (ROC-analysis: AUC 0.725, sensitivity 0.667, specificity 0.723). These findings provide novel insights into the role of prenatal androgen exposure in the development of alcohol dependency and for the use of 2D∶4D as a possible trait marker in identifying patients with alcohol dependency.
Highlights
The lengths of the second digit (2D) and fourth digit (4D) and their ratio have received attention because of sex differences [1]
Reliability of the three raters was high for both the right hand (2D: intra-class correlation coefficient (ICC) = 1.000; 4D: ICC = 0.998; 2D:4D: ICC = 0.988) and the left hand (2D: ICC = 0.991; 4D: ICC = 0.998; 2D:4D: ICC = 0.951)
These results indicate that alcohol dependent patients have smaller 2D:4D ratios with preserved sexual dimorphism but with reduced right-left differences
Summary
The lengths of the second digit (2D) and fourth digit (4D) and their ratio have received attention because of sex differences [1]. The ratio of 2D to 4D is smaller for males than females. Those differences are generally larger for the right hand than for the left in humans [2,3,4]. Low 2D:4D values probably result from high prenatal testosterone exposure [1,4,5]. Evidence supporting this hypothesis has recently been reviewed [6], but for an alternative critical view see Forstmeier et al, 2010 [7]
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