Exploring factors underlying ethnic differences in age-related macular degeneration (AMD) prevalence

Abstract

Purpose : To explore factors underlying ethnic differences in AMD prevalence in White and Asian population-based samples.

Methods : Demographic, AMD-related genetic and lifestyle data collected from the Blue Mountains Eye Study (BMES, whites) and Singapore Prospective Study 2 (SP2, Asians) were used (BMES n=2085, SP2 n=546). We compared age-adjusted AMD prevalence between the two cohorts. We used dietary patterns, computed from exploratory factor analysis loadings, and Alternative Healthy Eating Index (AHEI) to test associations between diet and AMD, adjusted for age, polygenic risk score, and smoking. We used mediation analyses to examine the extent to which the ethnicity effect on AMD was explained by genes and diet.

Results : BMES cohort showed higher age-adjusted prevalence of early and late AMD (18.5% and 1.4%) than SP2 (7.8% and 0.4%). The percentage of subjects carrying two risk alleles of rs1061170 was 13.7% in BMES and 0.2% in SP2, and for rs10490924 were 4.4% in BMES and 18.8% in SP2. The likelihood of having AMD increased with increasing scores of a traditional Western dietary pattern and decreased with increasing scores of an Asian dietary pattern. However, such associations were no longer present within each cohort, nor after adjusting for ethnicity in models including both cohorts. AHEI scores overlapped substantially between the two cohorts but SP2 had significantly higher mean AHEI (52.0, 95% CI 51.6, 52.5) than BMES (44.3, CI 43.9, 44.7, p<0.001). AHEI was not associated with AMD in each cohort after adjusting for polygenic score, nor in models including both cohorts adjusting for ethnicity. After adjusting for ethnicity, age, polygenic score and smoking, polyunsaturated fatty acid (PUFA) consumption was significantly associated with AMD (OR 0.98, CI 0.96, 1.0). SP2 had significantly lower likelihood of having AMD (OR 0.57, CI 0.46, 0.72) than BMES. Mediation analyses revealed that compared to whites, Asians had 5-6% AMD risk reduction, of which 19% (CI 7%, 63%) was mediated via genetics and 7% (CI 0.3%, 16%) via PUFA consumption differences. The mediation effects of AHEI (6%, CI -6%, 17.7%) and smoking (1.6%, CI -0.1%, 3.9%) were not significant.

Conclusions : In understanding the ethnic differences in AMD, we found that genetics explain more of the risk difference than diet but the majority of the ethnic difference remains unexplained.

This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.