Dietary inflammatory index and breast cancer risk: an updated meta-analysis of observational studies

This updated meta-analysis sought to determine whether the pro-inflammatory potential of diet is a risk factor for breast cancer (BrCa) development, for the first time focusing on the effects of design heterogeneity. The search was performed using Scopus, PubMed, and Embase databases. Data were extr...

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Published inEuropean journal of clinical nutrition Vol. 76; no. 8; pp. 1073 - 1087
Main Authors Hayati, Zahra, Jafarabadi, Mohammad Asghari, Pirouzpanah, Saeed
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.08.2022
Nature Publishing Group
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Abstract This updated meta-analysis sought to determine whether the pro-inflammatory potential of diet is a risk factor for breast cancer (BrCa) development, for the first time focusing on the effects of design heterogeneity. The search was performed using Scopus, PubMed, and Embase databases. Data were extracted from twenty-one eligible studies, including eleven cohorts (336,085 participants/20,033 incidence cases), and ten case-control studies (9,833 cases/12,752controls). The random-effect was used to calculate the relative risk (RR) using STATA 16 software. The highest dietary inflammatory index (DII) vs. the lowest category showed 16% increased risk of BrCa (95% CI: 1.06–1.26; I 2  = 62.8%, P ( I 2 ) < 0.001). This was notable in post-menopausal status (RR = 1.13, 95% CI: 1.04–1.22), women with body mass index (BMI) ≥ 30 kg/m 2 (RR = 1.35, 95% CI: 1.07–1.63), and study populations from developing countries (RR = 1.79, 95% CI: 1.12–2.47). Methodological covariates were subject to subgroup meta-analyses and showed stronger results among case-control studies (RR = 1.50, 95% CI: 1.20–1.80), studies considered age-matched controls (RR = 1.56, 95% CI: 1.19–1.93) and hospital-based controls (RR = 2.11, 95% CI: 1.58–2.64), and cohort studies identified by prolong follow-up durations (RR = 1.13, 95% CI: 1.03–1.22). This updated meta-analysis highlighted the pro-inflammatory diet as a risk factor for BrCa, especially among women in post-menopausal status, obese groups, and developing countries. Meta-analysis in methodological subgroups could improve results, less affected by heterogeneity, and suggested subclassification with important implications for future epidemiological designs and even clinical management.
AbstractList This updated meta-analysis sought to determine whether the pro-inflammatory potential of diet is a risk factor for breast cancer (BrCa) development, for the first time focusing on the effects of design heterogeneity. The search was performed using Scopus, PubMed, and Embase databases. Data were extracted from twenty-one eligible studies, including eleven cohorts (336,085 participants/20,033 incidence cases), and ten case-control studies (9,833 cases/12,752controls). The random-effect was used to calculate the relative risk (RR) using STATA 16 software. The highest dietary inflammatory index (DII) vs. the lowest category showed 16% increased risk of BrCa (95% CI: 1.06-1.26; I  = 62.8%, P (I ) < 0.001). This was notable in post-menopausal status (RR = 1.13, 95% CI: 1.04-1.22), women with body mass index (BMI) ≥ 30 kg/m (RR = 1.35, 95% CI: 1.07-1.63), and study populations from developing countries (RR = 1.79, 95% CI: 1.12-2.47). Methodological covariates were subject to subgroup meta-analyses and showed stronger results among case-control studies (RR = 1.50, 95% CI: 1.20-1.80), studies considered age-matched controls (RR = 1.56, 95% CI: 1.19-1.93) and hospital-based controls (RR = 2.11, 95% CI: 1.58-2.64), and cohort studies identified by prolong follow-up durations (RR = 1.13, 95% CI: 1.03-1.22). This updated meta-analysis highlighted the pro-inflammatory diet as a risk factor for BrCa, especially among women in post-menopausal status, obese groups, and developing countries. Meta-analysis in methodological subgroups could improve results, less affected by heterogeneity, and suggested subclassification with important implications for future epidemiological designs and even clinical management.
This updated meta-analysis sought to determine whether the pro-inflammatory potential of diet is a risk factor for breast cancer (BrCa) development, for the first time focusing on the effects of design heterogeneity. The search was performed using Scopus, PubMed, and Embase databases. Data were extracted from twenty-one eligible studies, including eleven cohorts (336,085 participants/20,033 incidence cases), and ten case-control studies (9,833 cases/12,752controls). The random-effect was used to calculate the relative risk (RR) using STATA 16 software. The highest dietary inflammatory index (DII) vs. the lowest category showed 16% increased risk of BrCa (95% CI: 1.06–1.26; I2 = 62.8%, P (I2) < 0.001). This was notable in post-menopausal status (RR = 1.13, 95% CI: 1.04–1.22), women with body mass index (BMI) ≥ 30 kg/m2 (RR = 1.35, 95% CI: 1.07–1.63), and study populations from developing countries (RR = 1.79, 95% CI: 1.12–2.47). Methodological covariates were subject to subgroup meta-analyses and showed stronger results among case-control studies (RR = 1.50, 95% CI: 1.20–1.80), studies considered age-matched controls (RR = 1.56, 95% CI: 1.19–1.93) and hospital-based controls (RR = 2.11, 95% CI: 1.58–2.64), and cohort studies identified by prolong follow-up durations (RR = 1.13, 95% CI: 1.03–1.22). This updated meta-analysis highlighted the pro-inflammatory diet as a risk factor for BrCa, especially among women in post-menopausal status, obese groups, and developing countries. Meta-analysis in methodological subgroups could improve results, less affected by heterogeneity, and suggested subclassification with important implications for future epidemiological designs and even clinical management.
This updated meta-analysis sought to determine whether the pro-inflammatory potential of diet is a risk factor for breast cancer (BrCa) development, for the first time focusing on the effects of design heterogeneity. The search was performed using Scopus, PubMed, and Embase databases. Data were extracted from twenty-one eligible studies, including eleven cohorts (336,085 participants/20,033 incidence cases), and ten case-control studies (9,833 cases/12,752controls). The random-effect was used to calculate the relative risk (RR) using STATA 16 software. The highest dietary inflammatory index (DII) vs. the lowest category showed 16% increased risk of BrCa (95% CI: 1.06–1.26; I 2  = 62.8%, P ( I 2 ) < 0.001). This was notable in post-menopausal status (RR = 1.13, 95% CI: 1.04–1.22), women with body mass index (BMI) ≥ 30 kg/m 2 (RR = 1.35, 95% CI: 1.07–1.63), and study populations from developing countries (RR = 1.79, 95% CI: 1.12–2.47). Methodological covariates were subject to subgroup meta-analyses and showed stronger results among case-control studies (RR = 1.50, 95% CI: 1.20–1.80), studies considered age-matched controls (RR = 1.56, 95% CI: 1.19–1.93) and hospital-based controls (RR = 2.11, 95% CI: 1.58–2.64), and cohort studies identified by prolong follow-up durations (RR = 1.13, 95% CI: 1.03–1.22). This updated meta-analysis highlighted the pro-inflammatory diet as a risk factor for BrCa, especially among women in post-menopausal status, obese groups, and developing countries. Meta-analysis in methodological subgroups could improve results, less affected by heterogeneity, and suggested subclassification with important implications for future epidemiological designs and even clinical management.
This updated meta-analysis sought to determine whether the pro-inflammatory potential of diet is a risk factor for breast cancer (BrCa) development, for the first time focusing on the effects of design heterogeneity. The search was performed using Scopus, PubMed, and Embase databases. Data were extracted from twenty-one eligible studies, including eleven cohorts (336,085 participants/20,033 incidence cases), and ten case-control studies (9,833 cases/12,752controls). The random-effect was used to calculate the relative risk (RR) using STATA 16 software. The highest dietary inflammatory index (DII) vs. the lowest category showed 16% increased risk of BrCa (95% CI: 1.06-1.26; I2 = 62.8%, P (I2) < 0.001). This was notable in post-menopausal status (RR = 1.13, 95% CI: 1.04-1.22), women with body mass index (BMI) ≥ 30 kg/m2 (RR = 1.35, 95% CI: 1.07-1.63), and study populations from developing countries (RR = 1.79, 95% CI: 1.12-2.47). Methodological covariates were subject to subgroup meta-analyses and showed stronger results among case-control studies (RR = 1.50, 95% CI: 1.20-1.80), studies considered age-matched controls (RR = 1.56, 95% CI: 1.19-1.93) and hospital-based controls (RR = 2.11, 95% CI: 1.58-2.64), and cohort studies identified by prolong follow-up durations (RR = 1.13, 95% CI: 1.03-1.22). This updated meta-analysis highlighted the pro-inflammatory diet as a risk factor for BrCa, especially among women in post-menopausal status, obese groups, and developing countries. Meta-analysis in methodological subgroups could improve results, less affected by heterogeneity, and suggested subclassification with important implications for future epidemiological designs and even clinical management.This updated meta-analysis sought to determine whether the pro-inflammatory potential of diet is a risk factor for breast cancer (BrCa) development, for the first time focusing on the effects of design heterogeneity. The search was performed using Scopus, PubMed, and Embase databases. Data were extracted from twenty-one eligible studies, including eleven cohorts (336,085 participants/20,033 incidence cases), and ten case-control studies (9,833 cases/12,752controls). The random-effect was used to calculate the relative risk (RR) using STATA 16 software. The highest dietary inflammatory index (DII) vs. the lowest category showed 16% increased risk of BrCa (95% CI: 1.06-1.26; I2 = 62.8%, P (I2) < 0.001). This was notable in post-menopausal status (RR = 1.13, 95% CI: 1.04-1.22), women with body mass index (BMI) ≥ 30 kg/m2 (RR = 1.35, 95% CI: 1.07-1.63), and study populations from developing countries (RR = 1.79, 95% CI: 1.12-2.47). Methodological covariates were subject to subgroup meta-analyses and showed stronger results among case-control studies (RR = 1.50, 95% CI: 1.20-1.80), studies considered age-matched controls (RR = 1.56, 95% CI: 1.19-1.93) and hospital-based controls (RR = 2.11, 95% CI: 1.58-2.64), and cohort studies identified by prolong follow-up durations (RR = 1.13, 95% CI: 1.03-1.22). This updated meta-analysis highlighted the pro-inflammatory diet as a risk factor for BrCa, especially among women in post-menopausal status, obese groups, and developing countries. Meta-analysis in methodological subgroups could improve results, less affected by heterogeneity, and suggested subclassification with important implications for future epidemiological designs and even clinical management.
Author Jafarabadi, Mohammad Asghari
Hayati, Zahra
Pirouzpanah, Saeed
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PublicationDate 2022-08-01
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  year: 2022
  text: 2022-08-01
  day: 01
PublicationDecade 2020
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PublicationTitle European journal of clinical nutrition
PublicationTitleAbbrev Eur J Clin Nutr
PublicationTitleAlternate Eur J Clin Nutr
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Publisher Nature Publishing Group UK
Nature Publishing Group
Publisher_xml – name: Nature Publishing Group UK
– name: Nature Publishing Group
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Snippet This updated meta-analysis sought to determine whether the pro-inflammatory potential of diet is a risk factor for breast cancer (BrCa) development, for the...
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SubjectTerms 692/499
692/699/67/1347
Body mass index
Body size
Breast cancer
Breast Neoplasms - epidemiology
Breast Neoplasms - etiology
Case studies
Case-Control Studies
Clinical Nutrition
Developing countries
Diet
Diet - adverse effects
Epidemiology
Female
Health risks
Heterogeneity
Humans
Incidence
Inflammation
Internal Medicine
LDCs
Medicine
Medicine & Public Health
Menopause
Meta-analysis
Metabolic Diseases
Observational studies
Population studies
Post-menopause
Public Health
Review Article
Risk analysis
Risk Factors
Subgroups
Title Dietary inflammatory index and breast cancer risk: an updated meta-analysis of observational studies
URI https://link.springer.com/article/10.1038/s41430-021-01039-5
https://www.ncbi.nlm.nih.gov/pubmed/34728816
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