TABLE 2.
Combined hazard ratios (HRs) for coronary events and coronary deaths per 5% increments in energy intake from polyunsaturated fatty acids (PUFAs) or carbohydrates (CHs) in the Pooling Project of Cohort Studies on Diet and Coronary Disease1
All |
Women |
Men |
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HR (95% CI) | P value, test for between-studies heterogeneity | HR (95% CI) | P value, test for between-studies heterogeneity | HR (95% CI) | P value, test for between-studies heterogeneity | P value, test for effect modification by sex | |
Coronary events2 | |||||||
MUFAs for SFAs | |||||||
Model 13 | 1.39 (1.20, 1.61) | 1.33 (1.01, 1.74) | 1.47 (1.25, 1.73) | ||||
Model 24 | 1.19 (1.00, 1.42) | 0.32 | 1.15 (0.84, 1.58) | 0.30 | 1.23 (0.98, 1.55) | 0.32 | 0.49 |
PUFAs for SFAs | |||||||
Model 13 | 0.69 (0.59, 0.81) | 0.66 (0.54, 0.81) | 0.68 (0.52, 0.87) | ||||
Model 24 | 0.87 (0.77, 0.97) | 0.70 | 0.85 (0.68, 1.06) | 0.51 | 0.87 (0.76, 1.01) | 0.61 | 0.84 |
CHs for SFAs | |||||||
Model 13 | 1.06 (1.01, 1.12) | 0.98 (0.90, 1.06) | 1.10 (1.05, 1.16) | ||||
Model 24 | 1.07 (1.01, 1.14) | 0.51 | 1.00 (0.89, 1.12) | 0.72 | 1.11 (1.02, 1.20) | 0.37 | 0.13 |
Coronary deaths5 | |||||||
MUFAs for SFAs | |||||||
Model 13 | 1.16 (0.83, 1.60) | 0.97 (0.62, 1.52) | 1.31 (0.82, 2.09) | ||||
Model 24 | 1.01 (0.73, 1.41) | 0.18 | 0.88 (0.51, 1.54) | 0.27 | 1.10 (0.71, 1.69) | 0.18 | 0.40 |
PUFAs for SFAs | |||||||
Model 13 | 0.57 (0.42, 0.77) | 0.51 (0.29, 0.89) | 0.64 (0.46, 0.90) | ||||
Model 24 | 0.74 (0.61, 0.89) | 0.40 | 0.61 (0.37, 1.01) | 0.14 | 0.80 (0.64, 0.99) | 0.81 | 0.24 |
CHs for SFAs | |||||||
Model 13 | 0.93 (0.82, 1.06) | 0.85 (0.68, 1.07) | 1.00 (0.86, 1.15) | ||||
Model 24 | 0.96 (0.82, 1.13) | 0.05 | 0.86 (0.65, 1.13) | 0.16 | 1.03 (0.86, 1.24) | 0.14 | 0.08 |
MUFAs, monounsaturated fatty acids; SFAs, saturated fatty acids.
n = 306,244 for all; n = 215,006 for women; and n = 91,238 for men.
Model 1 included intake of MUFAs, PUFAs, trans fatty acids, protein, and CHs expressed as percentages of total energy intake (as continuous variables) and total energy intake (kcal/d) (as a continuous variable). Age at baseline (y) and the calendar year in which the baseline questionnaire was returned were entered into the model through the strata statement. Within each study, HRs with 95% CIs for the incidence of a coronary event and of mortality from coronary heart disease were calculated by using Cox proportional hazards regression with time in study (y) as the time metric. The study-specific logs of HRs were weighted by the inverse of their variances, and a combined estimate of the HRs was computed by using a random-effects model. The estimated HRs for unsaturated fatty acids and CHs can be interpreted as the estimated differences in risk of a 5% lower energy intake from SFAs and a concomitant higher energy intake from unsaturated fatty acids and CHs, respectively.
Model 2 included variables in model 1 and smoking (never smokers, former smokers, or current smoker of 1–4, 5–14, 15–24, or ≥25 cigarettes/d), BMI (in kg/m2; <23, 23 to <25, 25 to <27.5, 27.5 to <30, or ≥30), physical activity (levels 1–5), highest attained educational level (<high school, high school, or >high school), alcohol intake (0, 0 to <5, 5 to <10, 10 to <15, 15 to <30, 30 to <50, or ≥50 g/d), history of hypertension (yes or no), and energy-adjusted quintiles of fiber intake (g/d) and cholesterol intake (mg/d). The estimated HRs for unsaturated fatty acids and CHs can be interpreted as the estimated differences in risk of a 5% lower energy intake from SFAs and a concomitant higher energy intake from unsaturated fatty acids and CHs, respectively.
n = 327,660 for all; n = 228,150 for women; and n = 99,510 for men.