Dietary Inflammatory Index and Site-Specific Cancer Risk: A Systematic Review and Dose-Response  Meta-Analysis

Abstract

Existing evidence suggests a link between the inflammatory potential of diet and risk of cancer. This study aimed to test the linear and potential nonlinear dose-response associations of the Dietary Inflammatory Index (DII), as being representative of inflammatory features of the diet, and site-specific cancer risk. A systematic search was conducted with the use of PubMed and Scopus from 2014 to November 2017. Prospective cohort or case-control studies reporting the risk estimates of any cancer type for ≥3 categories of the DII were selected. Studies that reported the association between continuous DII score and cancer risk were also included. Pooled RRs were calculated by using a random-effects model. Eleven prospective cohort studies (total n = 1,187,474) with 28,614 incident cases and 29 case-control studies with 19,718 cases and 33,229 controls were identified. The pooled RRs for a 1-unit increment in the DII were as follows: colorectal cancer, 1.06 (95% CI: 1.04, 1.08; I2 = 72.5%; n = 9); breast cancer, 1.03 (95% CI: 1.00, 1.07; I2 = 84.0%; n = 7); prostate cancer, 1.06 (95% CI: 0.97, 1.15; I2 = 56.2%; n = 6); pancreatic cancer, 1.16 (95% CI: 1.05, 1.28; I2 = 61.6%; n = 2); ovarian cancer, 1.08 (95% CI: 1.03, 1.13; I2 = 0%; n = 2); esophageal squamous cell carcinoma, 1.24 (95% CI: 1.10, 1.38; I2 = 64.3%; n = 2); renal cell carcinoma, 1.08 (95% CI: 1.02, 1.13; I2 = 0%; n = 2); and esophageal adenocarcinoma, 1.26 (95% CI: 1.13, 1.39; I2 = 0%; n = 2). A nonlinear dose-response meta-analysis showed that, after a somewhat unchanged risk within initial scores of the DII, the risk of colorectal cancer increased linearly with increasing DII score. In the analyses of breast and prostate cancers, the risk increased with a very slight trend with increasing DII score. In conclusion, the results showed that dietary habits with high inflammatory features might increase the risk of site-specific cancers.

Effect of proinflammatory diet before pregnancy on gestational age and birthweight: The Japan Environment and Children's Study

“…The dietary inflammatory index (DII) is a method to assess the inflammatory potential of an individual's diet (Shivappa, Steck, Hurley, Hussey, & Hébert, ). The DII has been proved to associate with well‐known inflammation related condition such as obesity (Ruiz‐Canela et al, ), asthma (Wood, Shivappa, Berthon, Gibson, & Hebert, ), and colorectal cancer (Jayedi, Emadi, & Shab‐Bidar, ).…”

“…The DII has been proved to associate with well-known inflammation related condition such as obesity (Ruiz-Canela et al, 2015), asthma (Wood, Shivappa, Berthon, Gibson, & Hebert, 2015), and colorectal cancer (Jayedi, Emadi, & Shab-Bidar, 2018).…”

The Dietary Inflammatory Index and Chronic Lymphocytic Leukaemia in the MCC Spain Study

“…There is mounting evidence regarding the association between DII and solid neoplasms. Clear associations have been reported for colorectal cancers [51,52] and gastric cancers [53], whereas the association with breast cancer is still inconclusive [54][55][56]. Regarding haematological cancers, other case-control studies looking into the association of DII (and DII-like tools) and other types of haematological cancers have been carried out [37,38], reporting positive associations between a pro-inflammatory diet and NHL and B-cell lymphoma subtypes.…”

The Biological Role of Intestine: Overall Inflammation

“…BG elevation and long persistence of nutrients in the bowel are frequent events during changes in climate or in home heating and during emotions [7][8][9][10][11][12]. These events (of no metabolic adaptation) prevail more and more in the evolution from insulin resistance to diabetes [13][14][15][16][17][18][19]. Fattening is a way to slow and delay the development of diabetes, but has own limits.…”

“…Overall inflammation is transient, few days in children with diarrhea, and it shows spontaneous regression. Decades of maintenance are possible [18,19], but DNA may remain damaged (oncogene) in the site of Inflammatory persistence.…”