Table 2. Overall and stratified analyses on the association between DII and the risk of gynecological carcinoma.
| Subgroup | No. of included studies | Pooled RR (95% CIs) | p for Z test | Heterogeneity | p for interaction | ||
|---|---|---|---|---|---|---|---|
| I2 (%) | p* | ||||||
| Overall† | 18 | 1.38 (1.21–1.56) | <0.001 | 85.8 | <0.001 | ||
| Overall‡ | 18 | 1.36 (1.20–1.54) | <0.001 | 85.4 | <0.001 | ||
| Subgroup analyses§ | |||||||
| Study design | <0.001 | ||||||
| Case-control | 12 | 1.48 (1.38–1.58) | <0.001 | 80.6 | <0.001 | ||
| Prospective cohort | 6 | 1.07 (1.02–1.13) | 0.010 | 36.1 | 0.166 | ||
| Age (yr) | 0.126 | ||||||
| <50 | 6 | 1.86 (1.21–2.85) | 0.001 | 27.9 | 0.005 | ||
| ≥50 | 10 | 1.21 (1.08–1.35) | <0.001 | 72.1 | 0.001 | ||
| BMI (kg/m2) | 0.026 | ||||||
| <25 | 7 | 1.23 (1.08–1.40) | 0.002 | 38.9 | 0.132 | ||
| ≥25 | 7 | 1.52 (1.33–1.75) | <0.001 | 7.4 | 0.372 | ||
| Family history of hormone-related cancers | 0.769 | ||||||
| No | 2 | 1.66 (1.36–2.03) | <0.001 | 0.0 | 0.541 | ||
| Yes | 2 | 1.51 (0.81–2.80) | 0.192 | 8.1 | 0.297 | ||
| Menopausal status | 0.975 | ||||||
| Pre | 8 | 1.50 (1.25–1.80) | <0.001 | 70.6 | 0.001 | ||
| Post | 8 | 1.49 (1.32–1.68) | <0.001 | 27.0 | 0.213 | ||
| Parity | 0.784 | ||||||
| 0 | 3 | 1.53 (0.99–2.37) | 0.058 | 0.0 | 0.444 | ||
| ≥1 | 3 | 1.63 (1.36–1.96) | <0.001 | 0.0 | 0.574 | ||
| Cancer type | 0.038 | ||||||
| Breast cancer | 12 | 1.19 (1.14–1.24) | <0.001 | 89.9 | <0.001 | ||
| Ovarian cancer | 4 | 1.42 (1.21–1.65) | <0.001 | 0.0 | 0.664 | ||
| Endometrial cancer | 2 | 1.49 (1.09–2.03) | 0.013 | 68.6 | 0.074 | ||
| Influence analyses∥ | |||||||
| Minimal | - | 1.32 (1.17–1.50) | <0.001 | 84.1 | <0.001 | ||
| Maximal | - | 1.41 (1.24–1.61) | <0.001 | 82.2 | <0.001 | ||
BMI, body mass index; CI, confidence interval; DII, dietary inflammation index; RR, relative risk.
*Each foot-note is presented as for p value of Q-test for between study heterogeneity test; †for DII calculated with consideration of dietary supplements; RRs and 95% CIs were pooled by using the random effects model (the DerSimonian and Laird method); ‡for DII calculated without consideration of dietary supplements; RRs and 95% CIs were pooled by using the random effects model (the DerSimonian and Laird method); §for RRs and 95% CIs were pooled by using the fixed effects model; ‖Influence analysis was conducted by eliminating one study at a time; for overall, the excluded study was the study by Huang et al. [47] for minimal pooled RRs, and the study by Tabung et al. [48] for the maximal pooled RRs.