Table 6.
Authors | Study subjects | Concordance rates | Genetic heritability |
---|---|---|---|
Jahanfar et al. (94) | 193 subjects [inclusive of same gender twins (n = 176) and females from opposite sex twin sets (n = 17)] | 43.0% in monozygotic and 46.8% in dizygotic twins. Proband-wise concordance for PMS was higher in monozygotic (0.81) than in dizygotic twins (0.67), indicating a strong genetic effect | Quantitative genetic modelling found that a model comprising of additive genetic (A) and unique environment (E) factors provided the best fit of A: 95%, E: 5% suggesting 95% genetic heritability |
Treloar et al. (95) | 720 female twin pairs (454 monozygotic and 266 dizygotic) Australian National Health and Medical Research Council Twin Register |
Genetic correlations of 0.62 between reported PMS and neuroticism, and 0.70 with lifetime major depression, 39% of the genetic variance of PMS was not explained by these factors | Indicating weaker genetic effect |
Kendler et al. (72) | Virginia Twin Registry two assessments, 72 h apart 314 monozygotic and 181 dizygotic twin pairs |
Stability of psychological symptoms of PMS. | A best-fitting twin-measurement model estimated the heritability of the stable component of premenstrual symptoms at 56% and showed no impact of family environment factors |
Dalton et al. (97) | 31 pairs of twins Prospectively examined premenstrual symptoms |
Significantly higher concordance rate in monozygotic pairs (93%, 14 of 15) than in dizygotic pairs (44%, 7 of 16) | Indicating a strong genetic effect |
Condon et al. (98) | 157 monozygotic and 143 dizygotic female twin pairs Self-report questionnaire on premenstrual syndrome (PMS) |
Correlation in global PMS scores nearly twice as great for monozygotic twins (r = 0.55) as for dizygotic (r = 0.28) pairs | Indicating a strong genetic effect |