Discussion
In this cross-sectional study, we found a positive association between intraocular pressure and metabolic syndrome in nonglaucomatous postmenopausal women after adjusting for confounding variables, whereas there was no such association in premenopausal women.
Our results are in agreement with previous studies on some aspects. Chang et al, in a study examining 1,044 Taiwanese adults, reported that the number of metabolic components was independently associated with intraocular pressure. Intraocular pressure increased significantly with a larger number of metabolic syndrome components after adjusting for age and sex. However, that study did not present separate data for men and women; thus, sex difference was not fully considered. In two studies of Korean men and women, Oh et al and Lin et al revealed significant associations between intraocular pressure and metabolic syndrome. However, those studies did not fully adjust for lifestyle factors such as smoking, alcohol intake, and physical activity, which are known modifiers of intraocular pressure. Moreover, little is known about the association between intraocular pressure and metabolic syndrome according to women's menopause status. We believe that the present study is the first to focus on the role of menopause status in the relationship between intraocular pressure and metabolic syndrome.
Although the reason for the discrepancy by menopause status in the association of intraocular pressure with metabolic syndrome is unclear, some explanatory biological mechanisms may be offered. First, insulin resistance, which is the core feature of metabolic syndrome, could stimulate sympathetic activity. Hyperactivation of the ocular sympathetic nerve increases intraocular pressure. Premenopausal women have dominant parasympathetic activity and subordinate sympathetic activity compared with age-matched men, whereas there were no sex-related differences in older women. Second, estrogen could directly influence target tissues in the eye, such as the ciliary epithelia, subepithelial vascular plexus, trabecular meshwork, and episcleral venous plexus, and act on the inflow of aqueous humor. Some studies also reported that intraocular pressure was significantly lower in women taking estrogen therapy than in those who had never taken estrogen therapy. In addition, higher testosterone in postmenopausal women may influence the degree of intraocular pressure. Some researchers have demonstrated that the shift in the testosterone-to-estrogen ratio after menopause may explain the transition in cardiovascular diseases better than the fall in estrogen. In this regard, premenopausal women with metabolic syndrome seem to have lower intraocular pressure due to attenuated sympathetic activity and direct action on the eye by estrogen. In postmenopausal women with metabolic syndrome, the protective effects of estrogen may be lacking, and higher testosterone due to increased adiposity could influence intraocular pressure, which causes intraocular pressure to increase even more.
Our study has some limitations. First, our study used a cross-sectional design, and additional studies are needed to establish cause and effect between intraocular pressure and metabolic syndrome according to menopause status. Second, we could not fully exclude the effects of information bias because this study was based on a questionnaire survey. Thus, menopause status and history of glaucoma were determined using a self-administered questionnaire with a possibility for misclassification (such as underestimation), which may have introduced a bias. Lastly, we did not inquire into serum sex hormone levels and current use of oral contraceptives, estrogen, and/or progesterone because this study used secondary data from KNHANES.