Skip to main content

Empirical dietary inflammatory pattern could increase the odds of breast cancer: a case-control study

Abstract

Background

It has been shown that chronic inflammation is a significant factor in cancer development and progression. The current study aimed to investigate whether a higher score on the empirical dietary inflammatory pattern (EDIP), which indicates a more pro-inflammatory diet, is related to higher odds of breast cancer in Iranian women.

Methods

In the present case-control study, subjects in the case (n = 133) and control (n = 265) groups were chosen from the hospitals in Tehran, Iran. The cases consisted of women with newly diagnosed breast cancer, while the controls were selected from other parts of the same hospital and had no history of cancer or hormone therapy. Individuals whose reported energy intake deviated by three standard deviations above or below the mean energy intake of the population were excluded from the study. A reliable and valid semi-quantitative food frequency questionnaire was used to determine the participants’ dietary intake. Additionally, the association between breast cancer and EDIP was evaluated by logistic regression analysis in both crude and adjusted models.

Results

The median scores of EDIP in the case and control groups were 0.65 and 0.61, respectively. The findings also indicated that, in the adjusted model, the odds of developing breast cancer significantly increased in the last tertile of EDIP compared to the first tertile (odds ratio (OR) = 1.859; 95% confidence interval (CI): 1.059–3.265; P = 0.031). Additionally, after adjusting for potential confounders, higher odds of breast cancer were observed in the last tertile of EDIP compared to the first tertile in postmenopausal women (OR = 2.516; 95% CI: 1.081–5.856; P = 0.033).

Conclusions

The current study indicated that individuals with a higher pro-inflammatory diet score were more likely to develop breast cancer.

Peer Review reports

Introduction

Breast cancer is the most common cancer among women worldwide and is the leading cause of cancer-related death in women. Although it is an international issue, it is often diagnosed in advanced stages due to women’s negligence in clinical and breast examinations [1]. The prevalence of this disease among Iranian women is reported to be 23.6% [2].

It has been shown that chronic inflammation is a significant factor in cancer development and progression [3]. In breast cancer, inflammation is considered a prognostic factor [4]. One study indicated that chronic inflammation contributes to tumor growth in the breast by activating innate immune cells, causing the infiltration of T helper 2 (Th2) cells, and stimulating humoral immune cells [5]. Research has reported that increased levels of C-reactive protein (CRP) are associated with tumor progression or burden in the breast [4]. Certain components of the diet have been linked to inflammation [6]. One dietary index used to assess inflammatory potential is the empirical dietary inflammatory pattern (EDIP), which measures circulating concentrations of inflammatory biomarkers [7]. It has been discovered that higher EDIP scores are significantly correlated with increased levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and CRP [8].

A positive association between EDIP and the risk of liver cancer [9], colorectal cancer [10, 11], and endometrial cancer [12] has been observed. To our knowledge, there are limited studies on the association between EDIP and breast cancer. One study indicated no relationship between EDIP and interval breast cancer risk [13]. However, a case-control study showed that a pro-inflammatory diet is associated with an increased chance of developing breast cancer [14]. Although the role of the inflammatory index of the diet in increasing breast cancer odds has been investigated in several studies, the results are contradictory [15, 16].

The association between EDIP and the odds of breast cancer in Iranian women remains unknown. Therefore, the current research aimed to evaluate whether a higher EDIP score, which indicates a more pro-inflammatory diet, is related to higher odds of breast cancer in Iranian women.

Methods

Participants

In the current study, the sample size was calculated based on an odds ratio (OR) = 0.47, α = 0.05, and β = 20%, as reported by Ching et al. [17]. This hospital-centric case-control research included 136 women in the case group who had received a histological diagnosis of breast cancer confirmed by a pathologist and were newly diagnosed (less than 6 months) at general hospitals in Tehran, Iran. The control group comprised 272 women hospitalized in the same facility as the cases. The participants were aged between 30 and 65 years. The control group encompassed individuals with various conditions such as skin disorders, acute surgical conditions, disk disorders, traumas, and orthopedic conditions. Neither the case nor the control group had a history of cancer. Data were collected simultaneously for cases and controls using standardized interview procedures in a homogeneous setting. Less than 8% of the recruited participants declined to participate during the interview process. Five controls and two cases were excluded due to their reported energy intake deviating by three standard deviations (SDs) from the population mean, and one case and two controls were excluded for incomplete EDIP items. Consequently, the final sample included 265 controls and 133 cases. This research was approved by the Ethics Committee of Shahid Beheshti University of Medical Sciences (IR.SBMURETECHREC.1398.640). All participants provided informed consent before entering the study. Some details of this study have been previously published [18, 19].

Assessment of general characteristics of the participants

Data on established and prospective risk factors for breast cancer were collected using a checklist administered by expert dietitians. Participants provided information on their social and demographic characteristics, family history of breast cancer, use of vitamin D and omega-3 supplements, nighttime bra-wearing habits, menopause status (premenopausal and postmenopausal), and smoking status.

The level of physical activity was assessed using a validated questionnaire, and results were expressed in metabolic equivalent of tasks (METs)-hours per day [20]. Weight measurements (to the nearest 0.5 kg) were taken using a digital scale (Seca) while participants were barefoot and in light clothes. Height was measured with a precision of 0.1 cm using a wall-mounted stadiometer. Also, body mass index (BMI) was calculated by dividing the weight (kg) by the square of the height (m2).

Dietary intake assessment

Dietary records of the participants were obtained by trained dietitians using a reliable and valid semi-quantitative food frequency questionnaire (FFQ) consisting of 168 items [21]. The FFQ was used to assess the participants’ dietary intake based on their consumption frequency of food of standardized serving sizes during the year preceding the cancer diagnosis for cases and before the interviews for the control group. Participants were provided with household measurement aids (such as plates, bowls, tablespoons, teaspoons, glasses, and cups) and a validated food album to assist in estimating food types and portion sizes [22].

Participants reported the frequency of consuming each food item on an annual, monthly, weekly, or daily basis. These frequencies were converted into daily intake frequencies, and a handbook for household measures aided in converting intake frequencies to daily food intake amounts in grams. Additionally, the dietary table of the United States Department of Agriculture (USDA) was used to calculate the energy and nutrient content of the foods.

Calculation of EDIP

The EDIP score in our study was calculated based on the methodology developed by Tabung et al. [7], which originally included 18 food items associated with diagnostic biomarkers TNF-α, high-sensitivity CRP (hs-CRP), and IL-6. To adapt the score for our population, we excluded alcoholic beverages like wine and beer due to their infrequent consumption and potential underreporting influenced by religious considerations. Additionally, low-energy drinks were not included in our FFQ, leading us to remove this item from the questionnaire.

Our modified EDIP score was based on 15 dietary components: dark yellow vegetables, green leafy vegetables, fish, organ meat, processed meat, red meat, refined grains, tomato, coffee, tea, sugar-containing fruit juices, high-energy drinks (carbonated beverages containing added sugars, sugar-sweetened cola, and fruit-flavored beverages), snacks, and pizza. Each food item was assigned a weight according to its correlation with biomarker levels. We multiplied these weights by the average daily consumption of each food item and then calculated the sum of the weighted values. To prevent inflated scores, the cumulative totals were divided by 1000. A higher EDIP score indicates a diet that promotes inflammation, while a lower score suggests a less pro-inflammatory diet [23].

Statistical analysis

Firstly, the normality of the data was checked using the Kolmogorov-Smirnov test. Categorical variables were reported as frequency (percentage), while continuous variables were presented as mean (SD) or median (interquartile range [IQR]), depending on their distribution. Non-parametric variables were analyzed using the Mann-Whitney U test, and parametric continuous variables were assessed using the independent samples T-test.

The intake of EDIP components across EDIP tertiles was evaluated using the analysis of variance (ANOVA) test. Logistic regression analysis was employed to examine the relationship between breast cancer and EDIP in two models: crude and adjusted. The adjusted model included variables such as age, menopausal status, physical activity, smoking history, energy intake, family history of cancer, BMI, nighttime bra-wearing habits, and taking vitamin D supplements as covariates. Statistical analysis was conducted using SPSS (version 26.0), with a significance level set at a p-value of less than 0.05.

Results

Table 1 presents the baseline characteristics of the study subjects. Significant differences between the case and control groups were observed in age, menopausal status, cancer family history, history of abortion, use of vitamin D supplements, and intake of protein and carbohydrates (P < 0.05). However, there were no significant differences between the groups in variables such as age of marriage, breastfeeding duration, physical activity, BMI, BMI category, family history of breast cancer, nighttime bra-wearing habits, smoking, consumption of mega-3, herbal drugs, total EDIP score, energy intake, fat intake, and fiber intake (P > 0.05).

Table 1 The baseline features between the control and case participants

Table 2 presents the intake of EDIP components in servings per day across EDIP tertiles. Compared to the first tertile, the last tertile of EDIP showed a significantly higher intake of processed meats, tomatoes, high-energy beverages, and refined grains (P < 0.05). On the other hand, tea, sugar-containing fruit juices, leafy green and dark yellow vegetables were significantly lower in the last tertile (P < 0.05).

Table 2 The intake of food groups across tertiles of EDIP

Table 3 displays the ORs and 95% confidence intervals (CIs) in both crude and multivariable models across EDIP tertiles. In the crude model, there was no significant relationship between EDIP and the odds of developing breast cancer (P > 0.05). However, in the adjusted model (adjusted for age, BMI, family history of cancer, physical activity, energy intake, smoking history, menopausal status, nighttime bra-wearing habits, and vitamin D supplement use), the odds of breast cancer in the last tertile of EDIP were significantly higher than in the first tertile (OR = 1.859; 95% CI: 1.059–3.265; P = 0.031).

Table 3 Association between EDIP and breast cancer

Table 4 presents ORs and 95% CIs in both crude and multivariable models across EDIP tertiles stratified by menopausal status. In the crude model, there was no significant relationship between EDIP and the odds of developing breast cancer in both pre-and post-menopausal women (P > 0.05). However, after adjusting for potential confounders, a higher chance of breast cancer was observed in the last tertile of EDIP compared to the first tertile, especially in post-menopausal women (OR = 2.516; 95% CI: 1.081–5.856; P = 0.033).

Table 4 Association between EDIP and breast cancer based on menopausal status

Discussion

The present case-control study revealed that a high EDIP score increases the odds of breast cancer among Iranian women, particularly in post-menopausal women. These findings imply that women who follow a pro-inflammatory diet are more susceptible to breast cancer.

Breast cancer has various risk factors, including age, genetic background, smoking, vitamin D level, physical activity, and diet [24]. Among these factors, diet is a modifiable risk factor that plays a significant role. It has been demonstrated that nearly one-third of breast cancer cases can be prevented through dietary modifications [25].

The findings of this study align with previous similar research. Most case-control studies have shown a correlation between a pro-inflammatory diet and higher odds of breast cancer [16, 26,27,28], except for one study [29]. In a case-control study with a sample size of 300, the likelihood of breast cancer was found to increase with a food-based empirically derived dietary inflammation index [14]. In contrast, cohort studies have reported slightly increased odds [30] or no association [31, 32]. A thorough examination of the covariate distribution among the populations studied and their dietary patterns will help us understand this inconsistency.

Additionally, the current study indicated a positive relationship between EDIP and the chance of developing breast cancer among postmenopausal women. A study conducted on 49,258 Swedish women showed a positive correlation between the Dietary Inflammatory Index (DII) and breast cancer, which was slightly stronger in postmenopausal women [33]. Similarly, a case-control study comprising 364 breast cancer patients and 364 age-matched controls revealed that the DII had a stronger association with breast cancer in postmenopausal women compared to premenopausal women [15]. However, a population-based case-control study conducted in Germany, involving 2,887 postmenopausal breast cancer patients aged 50–74 and 5,512 age-matched healthy controls, found no significant link between energy-adjusted DII and postmenopausal breast cancer [29]. Contradictory outcomes may be attributed to variations in the studied population, study design, or differences in ethnic and socio-demographic characteristics.

Obesity or overweight, which refers to an excessive intake of energy relative to total energy expenditure, is linked to an elevated risk of various types of cancer [34]. In postmenopausal women, obesity can be considered an endocrine-related risk factor for breast cancer due to alterations in fat metabolism and the potential increase in estrogen production by aromatase activity in breast adipose tissue [35]. Furthermore, there is compelling evidence suggesting a potential preventive role of physical activity in postmenopausal breast cancer. Nevertheless, the precise mechanisms through which long-term physical activity reduces the risk of breast cancer remain uncertain [36]. However, physical activity can decrease insulin levels and consequently elevate sex hormone-binding globulin (SHBG) levels, thereby potentially decreasing the bioavailability of testosterone and estradiol [34, 37, 38]. Additionally, physical activity has been shown to be effective in reducing the risk of breast cancer by lowering body fat and decreasing inflammatory markers [15]. For this reason, these factors were taken into account as confounding factors in the adjusted model.

Studies have demonstrated that a diet low in fiber and high in saturated fatty acids and refined carbohydrates increases inflammatory markers [39, 40]. Furthermore, a meta-analysis study has revealed a correlation between increased consumption of processed meats and red meat with a higher risk of breast cancer [41]. In the present study, the findings revealed an increase in the intake of processed meats, high-energy beverages, and refined carbohydrates, as well as a low intake of green leafy vegetables, dark yellow vegetables, sugar-containing fruit juices, and tea in the last tertile of EDIP compared to the first tertile. These findings are consistent with the results of the previous studies.

Increasing the consumption of red meat and processed meats can increase the risk of breast cancer through various mechanisms. One mechanism is the presence of heme iron and non-heme iron, which act as pro-oxidants and can increase the risk of many cancers [42]. Additionally, cooking meat at high temperatures can generate carcinogenic compounds such as heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs) [43, 44]. Studies have shown that increased intake of these compounds is associated with a higher risk of breast cancer [43, 45, 46]. Consuming refined grains with a high glycemic index (GI) can also increase the risk of cancer by affecting the modulation of insulin-like growth factor-1 (IGF-1) [47, 48]. IGF-1 can promote cell differentiation, cell proliferation, and inhibit apoptosis [49].

The present study has both limitations and strengths. Firstly, it is important to note that this is a case-control study, which means that establishing a causal relationship is not possible. Secondly, the use of FFQ to collect food data is susceptible to recall bias. Thirdly, the hormone receptor status of patients’ tumors was not considered in this research. Fourthly, because participants were selected from hospitals rather than the general population, there may be selection bias, limiting the generalizability of the findings to other populations. Fifthly, the study did not account for the potential anti-inflammatory effects of alcoholic beverages such as beer and wine due to religious beliefs, which might impact the study results.

However, the study’s strengths include controlling for various confounding factors to obtain more accurate results regarding the relationship between EDIP and breast cancer. Additionally, the use of FFQ with proven validity and reliability enhances the strength of this research.

Conclusions

The current study suggested that individuals who adhere to a pro-inflammatory diet may face higher odds of developing breast cancer. To counteract the inflammatory effects of such a diet, it is advisable to reduce the consumption of meat, processed meats, and refined grains, and instead increase the intake of green leafy vegetables and dark yellow vegetables. This dietary strategy could potentially reduce the incidence of breast cancer, especially in less developed societies. However, further studies are needed to confirm these findings.

Data availability

No datasets were generated or analyzed during the current study.

References

  1. Akram M, Iqbal M, Daniyal M, Khan AU. <ArticleTitle Language=“En”>Awareness and current knowledge of breast cancer. Biol Res. 2017;50:1–23.

    Article  Google Scholar 

  2. Kazeminia M, Salari N, Hosseinian-Far A, Akbari H, Bazrafshan M-R, Mohammadi M. The prevalence of breast cancer in Iranian women: a systematic review and meta-analysis. Indian J Gynecologic Oncol. 2022;20(1):14.

    Article  Google Scholar 

  3. Coussens LM, Werb Z. Inflammation and cancer. Nature. 2002;420(6917):860–7.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  4. Pierce BL, Ballard-Barbash R, Bernstein L, Baumgartner RN, Neuhouser ML, Wener MH, Baumgartner KB, Gilliland FD, Sorensen BE, McTiernan A. Elevated biomarkers of inflammation are associated with reduced survival among breast cancer patients. J Clin Oncol. 2009;27(21):3437.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  5. DeNardo DG, Coussens LM. Inflammation and breast cancer. Balancing immune response: crosstalk between adaptive and innate immune cells during breast cancer progression. Breast Cancer Res. 2007;9:1–10.

    Article  Google Scholar 

  6. Ricordi C, Garcia-Contreras M, Farnetti S. Diet and inflammation: possible effects on immunity, chronic diseases, and life span. J Am Coll Nutr. 2015;34(sup1):10–3.

    Article  PubMed  Google Scholar 

  7. Tabung FK, Smith-Warner SA, Chavarro JE, Wu K, Fuchs CS, Hu FB, Chan AT, Willett WC, Giovannucci EL. Development and validation of an empirical dietary inflammatory index. J Nutr. 2016;146(8):1560–70.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  8. Tabung FK, Smith-Warner SA, Chavarro JE, Fung TT, Hu FB, Willett WC, Giovannucci EL. An empirical dietary inflammatory pattern score enhances prediction of circulating inflammatory biomarkers in adults. J Nutr. 2017;147(8):1567–77.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  9. Zhang X, Zhao L, Christopher C, Tabung FK, Bao W, Garcia DO, Neuhouser ML, Shadyab AH, Saquib N, Tinker L. Association of dietary inflammatory and insulinemic potential with risk of liver cancer and chronic liver disease mortality. Cancer Res. 2023;83(7_Supplement):6456–6456.

    Article  Google Scholar 

  10. Wang P, Song M, Eliassen AH, Wang M, Giovannucci EL. Dietary patterns and risk of colorectal cancer: a comparative analysis. Int J Epidemiol. 2023;52(1):96–106.

    Article  PubMed  CAS  Google Scholar 

  11. Liu L, Nishihara R, Qian ZR, Tabung FK, Nevo D, Zhang X, Song M, Cao Y, Mima K, Masugi Y. Association between inflammatory diet pattern and risk of colorectal carcinoma subtypes classified by immune responses to tumor. Gastroenterology. 2017;153(6):1517–30. e1514.

    Article  PubMed  Google Scholar 

  12. Romanos-Nanclares A, Tabung FK, Sinnott JA, Trabert B, De Vivo I, Playdon MC, Eliassen AH. Inflammatory and insulinemic dietary patterns and risk of endometrial cancer among US women. JNCI: J Natl Cancer Inst. 2023;115(3):311–21.

    Article  PubMed  CAS  Google Scholar 

  13. Zhang Z, Tabung FK, Jin Q, Curran G, Irvin VL, Shannon J, Velie EM, Manson JE, Simon MS, Vitolins M. Diet-Driven Inflammation and Insulinemia and Risk of Interval Breast Cancer. Nutr Cancer. 2022;74(9):3179–93.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  14. Ghanbari M, Shahinfar H, Imani H, Safabakhsh M, Shab-Bidar S. Association of empirically derived food-based inflammatory potential of the diet and breast cancer: a hospital-based case-control study. Clin Breast Cancer. 2022;22(4):e567–75.

    Article  PubMed  Google Scholar 

  15. Lee S, Quiambao AL, Lee J, Ro J, Lee E-S, Jung S-Y, Sung M-K, Kim J. Dietary inflammatory index and risk of breast cancer based on hormone receptor status: a case-control study in Korea. Nutrients. 2019;11(8):1949.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  16. Moradi S, Issah A, Mohammadi H, Mirzaei K. Associations between dietary inflammatory index and incidence of breast and prostate cancer: A systematic review and meta-analysis. Nutrition. 2018;55:168–78.

    Article  PubMed  Google Scholar 

  17. Ching S, Beilby J, Rossi E, Ingram D, Hahnel R. Serum levels of micronutrients, antioxidants and total antioxidant status predict risk of breast cancer in a case control study. J Nutr. 2002;132(2):303–6.

    Article  PubMed  CAS  Google Scholar 

  18. Hosseini Y, Hadi Sichani P, Moslemi E, Nouri M, Rajabzadeh-dehkordi M, Jalali S, Heidari Z, Shateri Z, Rashidkhani B. Pro-vegetarian dietary pattern and risk of breast cancer: a case–control study. Breast Cancer Res Treat. 2024;205(2):395–402.

    Article  PubMed  Google Scholar 

  19. Pourhabibi-Zarandi F, Kahrizsangi MA, Eskandarzadeh S, Mansouri F, Vali M, Jalali S, Heidari Z, Shateri Z, Nouri M, Rashidkhani B. Dietary quality index and the risk of breast cancer: a case-control study. BMC Womens Health. 2023;23(1):469.

    Article  PubMed  PubMed Central  Google Scholar 

  20. Aadahl M, Jørgensen T. Validation of a new self-report instrument for measuring physical activity. Med Sci Sports Exerc. 2003;35(7):1196–202.

    Article  PubMed  Google Scholar 

  21. Asghari G, Rezazadeh A, Hosseini-Esfahani F, Mehrabi Y, Mirmiran P, Azizi F. Reliability, comparative validity and stability of dietary patterns derived from an FFQ in the Tehran Lipid and Glucose Study. Br J Nutr. 2012;108(6):1109–17.

    Article  PubMed  CAS  Google Scholar 

  22. Ghaffarpour M, Houshiar-Rad A, Kianfar H. The manual for household measures, cooking yields factors and edible portion of foods. Tehran: Nashre Olume Keshavarzy. 1999;7(213):42–58.

    Google Scholar 

  23. Farhadnejad H, Tehrani AN, Jahromi MK, Teymoori F, Mokhtari E, Salehi-Sahlabadi A, Mirmiran P. The association between dietary inflammation scores and non-alcoholic fatty liver diseases in Iranian adults. BMC Gastroenterol. 2022;22(1):1–9.

    Article  Google Scholar 

  24. Momenimovahed Z, Salehiniya H. Epidemiological characteristics of and risk factors for breast cancer in the world. Breast Cancer: Targets Therapy 2019:151–64.

  25. Brennan SF, Cantwell MM, Cardwell CR, Velentzis LS, Woodside JV. Dietary patterns and breast cancer risk: a systematic review and meta-analysis. Am J Clin Nutr. 2010;91(5):1294–302.

    Article  PubMed  CAS  Google Scholar 

  26. Huang W-Q, Mo X-F, Ye Y-B, Shivappa N, Lin F-Y, Huang J, Hébert JR, Yan B, Zhang C-X. A higher Dietary Inflammatory Index score is associated with a higher risk of breast cancer among Chinese women: a case–control study. Br J Nutr. 2017;117(10):1358–67.

    Article  PubMed  CAS  Google Scholar 

  27. Wang L, Liu C, Zhou C, Zhuang J, Tang S, Yu J, Tian J, Feng F, Liu L, Zhang T. Meta-analysis of the association between the dietary inflammatory index (DII) and breast cancer risk. Eur J Clin Nutr. 2019;73(4):509–17.

    Article  PubMed  Google Scholar 

  28. Shivappa N, Hébert JR, Rosato V, Montella M, Serraino D, La Vecchia C. Association between the dietary inflammatory index and breast cancer in a large Italian case–control study. Mol Nutr Food Res. 2017;61(3):1600500.

    Article  Google Scholar 

  29. Ge I, Rudolph A, Shivappa N, Flesch-Janys D, Hébert JR, Chang-Claude J. Dietary inflammation potential and postmenopausal breast cancer risk in a German case-control study. Breast. 2015;24(4):491–6.

    Article  PubMed  Google Scholar 

  30. Shivappa N, Blair CK, Prizment AE, Jacobs DR, Hébert JR. Prospective study of the dietary inflammatory index and risk of breast cancer in postmenopausal women. Mol Nutr Food Res. 2017;61(5):1600592.

    Article  Google Scholar 

  31. Gardeazabal I, Ruiz-Canela M, Sánchez-Bayona R, Romanos-Nanclares A, Aramendía-Beitia J, Shivappa N, Hébert J, Martínez-González M, Toledo E. Dietary inflammatory index and incidence of breast cancer in the SUN project. Clin Nutr. 2019;38(5):2259–68.

    Article  PubMed  CAS  Google Scholar 

  32. Tabung FK, Steck SE, Liese AD, Zhang J, Ma Y, Caan B, Chlebowski RT, Freudenheim JL, Hou L, Mossavar-Rahmani Y. Association between dietary inflammatory potential and breast cancer incidence and death: results from the Women’s Health Initiative. Br J Cancer. 2016;114(11):1277–85.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  33. Shivappa N, Sandin S, Löf M, Hébert JR, Adami H-O, Weiderpass E. Prospective study of dietary inflammatory index and risk of breast cancer in Swedish women. Br J Cancer. 2015;113(7):1099–103.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  34. Kaaks R. A Lukanova Energy balance and cancer: the role of insulin and insulin-like growth factor-I. Proc Nutr Soc 2001;60(1):91–106.

    Article  PubMed  CAS  Google Scholar 

  35. Group EHBCC. Body mass index, serum sex hormones, and breast cancer risk in postmenopausal women. J Natl Cancer Inst. 2003;95(16):1218–26.

    Article  Google Scholar 

  36. Neilson HK, Friedenreich CM, Brockton NT, Millikan RC. Physical activity and postmenopausal breast cancer: proposed biologic mechanisms and areas for future research. Cancer Epidemiol Biomarkers Prev. 2009;18(1):11–27.

    Article  PubMed  CAS  Google Scholar 

  37. Kaaks R. Nutrition, hormones, and breast cancer: is insulin the missing link? Cancer Causes Control. 1996;7:605–25.

    Article  PubMed  CAS  Google Scholar 

  38. Stephenson GD, Rose DP. Breast cancer and obesity: an update. Nutr Cancer. 2003;45(1):1–16.

    Article  PubMed  CAS  Google Scholar 

  39. Esmaillzadeh A, Kimiagar M, Mehrabi Y, Azadbakht L, Hu FB, Willett WC. Dietary patterns and markers of systemic inflammation among Iranian women. J Nutr. 2007;137(4):992–8.

    Article  PubMed  CAS  Google Scholar 

  40. Giugliano D, Ceriello A, Esposito K. The effects of diet on inflammation: emphasis on the metabolic syndrome. J Am Coll Cardiol. 2006;48(4):677–85.

    Article  PubMed  CAS  Google Scholar 

  41. Guo J, Wei W, Zhan L. Red and processed meat intake and risk of breast cancer: a meta-analysis of prospective studies. Breast Cancer Res Treat. 2015;151:191–8.

    Article  PubMed  CAS  Google Scholar 

  42. Fonseca-Nunes A, Jakszyn P, Agudo A. Iron and Cancer Risk—A Systematic Review and Meta-analysis of the Epidemiological EvidenceA Systematic Review and Meta-analysis on Iron and Cancer Risk. Cancer Epidemiol Biomarkers Prev. 2014;23(1):12–31.

    Article  PubMed  CAS  Google Scholar 

  43. Kazerouni N, Sinha R, Hsu C-H, Greenberg A, Rothman N. Analysis of 200 food items for benzo [a] pyrene and estimation of its intake in an epidemiologic study. Food Chem Toxicol. 2001;39(5):423–36.

    Article  PubMed  CAS  Google Scholar 

  44. Knize MG, Salmon CP, Pais P, Felton JS. Food heating and the formation of heterocyclic aromatic amine and polycyclic aromatic hydrocarbon mutagens/carcinogens. Impact Process food Saf 1999:179–93.

  45. Rundle A, Tang D, Hibshoosh H, Estabrook A, Schnabel F, Cao W, Grumet S, Perera FP. The relationship between genetic damage from polycyclic aromatic hydrocarbons in breast tissue and breast cancer. Carcinogenesis. 2000;21(7):1281–9.

    Article  PubMed  CAS  Google Scholar 

  46. Bonner MR, Han D, Nie J, Rogerson P, Vena JE, Muti P, Trevisan M, Edge SB, Freudenheim JL. Breast cancer risk and exposure in early life to polycyclic aromatic hydrocarbons using total suspended particulates as a proxy measure. Cancer Epidemiol Biomarkers Prev. 2005;14(1):53–60.

    Article  PubMed  CAS  Google Scholar 

  47. Foster-Powell K, Holt SH, Brand-Miller JC. International table of glycemic index and glycemic load values: 2002. Am J Clin Nutr. 2002;76(1):5–56.

    Article  PubMed  CAS  Google Scholar 

  48. Brand-Miller JC, Liu V, Petocz P, Baxter RC. The glycemic index of foods influences postprandial insulin-like growth factor–binding protein responses in lean young subjects. Am J Clin Nutr. 2005;82(2):350–4.

    Article  PubMed  CAS  Google Scholar 

  49. Biddinger SB, Ludwig DS. The insulin-like growth factor axis: a potential link between glycemic index and cancer. In., vol. 82: Oxford University Press; 2005: 277–278.

Download references

Acknowledgements

We sincerely thank all field investigators, staff, and participants in the present study.

Funding

No funding.

Author information

Authors and Affiliations

Authors

Contributions

M.A.K, P.H.S, Z.S, A.M, M.N and H.F; Contributed to writing the first draft. Z.S, M.N and B.R; Contributed to all data and statistical analysis and interpretation of data. M.N and B.R.; Contributed to the research concept, supervised the work, and revised the manuscript. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Zainab Shateri.

Ethics declarations

Ethics approval and consent to participate

This study was conducted in accordance with the ethical standards of the Declaration of Helsinki and was approved by the Medical Research and Ethics Committee of Shahid Beheshti University of Medical Sciences. All participants read and signed the informed consent form.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.

Additional information

Publisher’s note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Amini Kahrizsangi, M., Hadi Sichani, P., Shateri, Z. et al. Empirical dietary inflammatory pattern could increase the odds of breast cancer: a case-control study. BMC Res Notes 17, 325 (2024). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s13104-024-06985-4

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s13104-024-06985-4

Keywords