Table 2.
Time period | Exposure | Model | PD* (587 cases total; 213 in WHIMS; 374 in WHIMS-ECHO) | MCI (671 cases total; 325 in WHIMS; 346 in WHIMS-ECHO) | PD or MCI (1047 cases total; 455 in WHIMS; 592 in WHIMS-ECHO) | |||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| ||||||||||||||
HR | 95°% CI | P value | HR | 95°% CI | P value | HR | 95°% CI | P value | ||||||
WHIMS (1995–2007) and WHIMS-ECHO (2008–2016) | DHA+EPA† (per 1 SD) | 1 | 0.92 | 0.84 | 1.00 | 0.0434 | 0.96 | 0.89 | 1.05 | 0.3751 | 0.95 | 0.89 | 1.02 | 0.1399 |
2 | 0.92 | 0.84 | 1.00 | 0.0454 | 0.97 | 0.89 | 1.05 | 0.3880 | 0.95 | 0.90 | 1.02 | 0.1463 | ||
3 | 0.92 | 0.84 | 1.00 | 0.0498 | 0.97 | 0.89 | 1.05 | 0.4466 | 0.96 | 0.90 | 1.02 | 0.1741 | ||
S1 | 0.91 | 0.83 | 0.99 | 0.0293 | 0.95 | 0.88 | 1.03 | 0.2284 | 0.94 | 0.88 | 1.00 | 0.0647 | ||
S2 | 0.92 | 0.83 | 1.01 | 0.0929 | 1.00 | 0.90 | 1.10 | 0.9501 | 0.96 | 0.89 | 1.04 | 0.3430 | ||
DHA (per 1 SD) | 3 | 0.92 | 0.85 | 1.01 | 0.0799 | 0.97 | 0.90 | 1.06 | 0.5226 | 0.96 | 0.90 | 1.02 | 0.2032 | |
EPA (per 1 SD) | 3 | 0.93 | 0.85 | 1.02 | 0.1244 | 0.97 | 0.89 | 1.05 | 0.4376 | 0.97 | 0.91 | 1.03 | 0.3357 | |
WHIMS | DHA+EPA (per 1 SD) | 3 | 0.85 | 0.73 | 0.99 | 0.0429 | 0.95 | 0.86 | 1.07 | 0.4098 | 0.96 | 0.87 | 1.05 | 0.3575 |
WHIMS-ECHO | DHA+EPA (per 1 SD) | 3 | 0.95 | 0.86 | 1.05 | 0.3162 | 0.98 | 0.87 | 1.09 | 0.6704 | 0.95 | 0.88 | 1.03 | 0.2344 |
Model 1 = RBC omega-3 FA content, HT trial arm (4 levels: estrogen-only trial: active treatment or placebo; estrogen and progestin trial: active treatment or placebo), age at baseline, education, race/ethnicity (black, white or other). Educational attainment was analyzed as an 11-level ordinal variable, ranging from 1 (no formal education) to 11 (doctoral degree). For simplicity, these 11 levels were collapsed to three broader categories in Table 1. Cubic spline transformations of age and education with knots at the 10th, 50th and 90th percentiles were used to allow for non-linear relationships with the study outcomes.
Model 2 = Model 1 + cardiovascular disease, hypertension, diabetes.
Model 3 = Model 2 + BMI (cubic spline transformation), current smoking status, status as prior alcohol user, current average servings of alcohol per week (cubic spline transformation).
Model S1 (sensitivity analysis 1) = Model 3 + baseline 3MS score (cubic spline transformation).
Model S2 (sensitivity analysis 2) = Model 3 + APOE genotype (none vs. 1+ ε4 alleles). Note: the S2 sensitivity analysis included only participants for whom data on APOE genotype were available.
Probable dementia was the primary endpoint.
RBC DHA+EPA was the primary exposure.