All but one subject in the present study had astigmatism of at least 0.25 D in one eye or the other. While this is more than has commonly been reported earlier, in most studies astigmatism has usually begun from a level of either 0.5 D or 0.75 D.
19,20 Although our study design does not permit general conclusions to be drawn on the prevalence of astigmatism in the population, the prevalence of astigmatism of ≥0.5 D (71.2% in the right and 70.0% in the left eye) found in the present study does not differ greatly from that reported by Schellini et al.,
20 in a Brazilian population aged 70 years or older (71.7% had astigmatism of ≥0.5 D). In the National Health and Nutrition Examination Survey, the prevalence of astigmatism of ≥1.0 D was 50.1% in persons aged 60 years or older; whereas in our study, this grade of astigmatism in one eye or the other was found in 46.3% of cases.
21 Thus the main difference between the prevalence found here and that reported in most previous studies is probably due to the fact that astigmatism in our study started at 0.25 D.
Some studies have shown a positive relationship between the amount of astigmatism and ametropia and myopia.
1,22 In the present study, no significant correlations between astigmatism and SE were found. The small proportions of myopics and cases of high ametropia in this study could be one explanation for the nonsignificant relationships observed between the amount of astigmatism and spherical ametropia.
The main aim of this study was to calculate the impact of heredity on refractive astigmatism. In the present study, only approximately one-third of the variation of astigmatism was explained by additive genetic effects, which is less than in some previous studies among somewhat younger subjects. Moreover, no significant dominant effects could be calculated. In a population-based sample of Norwegian twins, aged from birth to 31 years, additive genetic effects explained 9% (95% CI, 0–40 years), and dominant genetic effects 54% (95% CI, 20–69 years) of the variation in the liability to self-reported astigmatism.
8 In the study of Hammond et al.,
9 among 49- to 79-year-old twins, additive genetic effects accounted for 1% to 4% (95% CI, 0%–13%) and dominant effects for 47% to 49% (95% CI, 37%–55%) of the variance of total astigmatism. In the Hammond et al.
9 study and our study, the MZ correlations for astigmatism were very similar (0.4 to 0.5), while the DZ correlations in Hammond et al.
9 were 0.2 to 0.10 and in ours negative. Despite the larger sample size in Hammond et al.,
9 neither study had the power to distinguish unambiguously between additive and nonadditive genetic sources of variation. Given the differences in sample size and in characteristics resulting in some variation in the actual variance/covariance matrices underlying the pairwise correlations, it was not unexpected that the best-fitting model differed in the two studies. Both studies point to the importance of genetic factors, but whether additive or nonadditive factors are more important cannot be stated. Thus, in Hammond et al.,
9 an ADE model for astigmatism fit better than an AE model for the left but not the right eye in the univariate models. In the bivariate models, Hammond et al.
9 only present results for an ADE model and no results for an AE model.
Higher ICC values were observed between the MZ pairs of sisters for astigmatism in the WTR and ATR subgroups of astigmatism than in the whole sample. Thus, it could be supposed that the heredity of astigmatism could be higher in those subgroups; but due to the small sample size, it was not possible to calculate a meaningful model.
As far as we know, there are no previous studies on the heredity of the polar values of astigmatisms. In the present study, significant ICC values between the twin pairs emerged only for the value of J45. Further, the ICC values for J45 between the MZ sisters were lower than those for the amount of astigmatism, suggesting that the heredity of polar values is lower than the amount of astigmatism alone.
In our earlier studies on the same subjects, 83% and 81% of the variance in spherical equivalent and corneal refraction, respectively, were explained by heritable factors.
11,12 Based on the results of this study and the results of our earlier studies on the same subjects, it is reasonable to conclude that the impact of heredity among elderly females is highest on spherical equivalent refraction and corneal refraction, while environmental factors have a stronger influence on the amount of corneal and refractive astigmatism.
The amount and direction of astigmatism has been shown to vary with age.
2–5 The low impact of heredity on astigmatism found in the present study with elderly females would support the theory that the influence of environmental factors on astigmatism increases at older ages. Possible changes in astigmatism should be taken into account when controlling for refraction and prescribing new glasses, and when planning refractive surgery, especially when doing costumed corneal ablations. Emmetropic nonastigmatic refraction achieved by refractive surgery at a young age may turn to astigmatic refraction later on during the life course.