Dietary patterns and cancer risk Steck, Susan E; Murphy, E Angela
Nature reviews. Cancer,
02/2020, Volume:
20, Issue:
2
Journal Article
Peer reviewed
Over the past decade, the search for dietary factors on which to base cancer prevention guidelines has led to the rapid expansion of the field of dietary patterns and cancer. Multiple systematic ...reviews and meta-analyses have reported epidemiological associations between specific cancer types and both data-driven dietary patterns determined by empirical analyses and investigator-defined dietary indexes based on a predetermined set of dietary components. New developments, such as the use of metabolomics to identify objective biomarkers of dietary patterns and novel statistical techniques, could provide further insights into the links between diet and cancer risk. Although animal models of dietary patterns are limited, progress in this area could identify the potential mechanisms underlying the disease-specific associations observed in epidemiological studies. In this Review, we summarize the current state of the field, provide a critical appraisal of new developments and identify priority areas for future research. An underlying theme that emerges is that the effectiveness of different dietary pattern recommendations in reducing risk could depend on the type of cancer or on other risk factors such as family history, sex, age and other lifestyle factors or comorbidities as well as on metabolomic signatures or gut microbiota profiles.
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FZAB, GEOZS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
To design and develop a literature-derived, population-based dietary inflammatory index (DII) to compare diverse populations on the inflammatory potential of their diets.
Peer-reviewed primary ...research articles published through December 2010 on the effect of diet on inflammation were screened for possible inclusion in the DII scoring algorithm. Qualifying articles were scored according to whether each dietary parameter increased (+1), decreased (-1) or had no (0) effect on six inflammatory biomarkers: IL-1β, IL-4, IL-6, IL-10, TNF-α and C-reactive protein.
The Dietary Inflammatory Index Development Study was conducted in the Cancer Prevention and Control Program of the University of South Carolina in Columbia, SC, USA from 2011 to 2012.
A total of ≈6500 articles published through December 2010 on the effect of dietary parameters on the six inflammatory markers were screened for inclusion in the DII scoring algorithm. Eleven food consumption data sets from countries around the world were identified that allowed individuals' intakes to be expressed relative to the range of intakes of the forty-five food parameters observed across these diverse populations. Qualifying articles (n 1943) were read and scored based on the forty-five pro- and anti-inflammatory food parameters identified in the search. When fit to this composite global database, the DII score of the maximally pro-inflammatory diet was +7·98, the maximally anti-inflammatory DII score was -8·87 and the median was +0·23.
The DII reflects both a robust literature base and standardization of individual intakes to global referent values. The success of this first-of-a-kind attempt at relating intakes of inflammation-modulating foods relative to global norms sets the stage for use of the DII in a wide variety of epidemiological and clinical studies.
Abstract Purpose Many dietary factors have either proinflammatory or anti-inflammatory properties. We previously developed a dietary inflammatory index (DII) to assess the inflammatory potential of ...diet. In this study, we conducted a construct validation of the DII based on data from a food frequency questionnaire and three inflammatory biomarkers in a subsample of 2567 postmenopausal women in the Women's Health Initiative Observational Study. Methods We used multiple linear and logistic regression models, controlling for potential confounders, to test whether baseline DII predicted concentrations of interleukin-6, high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor alpha receptor 2, or an overall biomarker score combining all three inflammatory biomarkers. Results The DII was associated with the four biomarkers with beta estimates (95% confidence interval) comparing the highest with lowest DII quintiles as follows: interleukin-6: 1.26 (1.15–1.38), Ptrend < .0001; tumor necrosis factor alpha receptor 2: 81.43 (19.15–143.71), Ptrend = .004; dichotomized hs-CRP (odds ratio for higher vs. lower hs-CRP): 1.30 (0.97–1.67), Ptrend = .34; and the combined inflammatory biomarker score: 0.26 (0.12–0.40), Ptrend = .0001. Conclusions The DII was significantly associated with inflammatory biomarkers. Construct validity of the DII indicates its utility for assessing the inflammatory potential of diet and for expanding its use to include associations with common chronic diseases in future studies.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
To perform construct validation of the population-based Dietary Inflammatory Index (DII) using dietary data from two different dietary assessments and serum high-sensitivity C-reactive protein ...(hs-CRP) as the construct validator.
Using data derived from (i) three 24 h dietary recalls (24HR) at baseline and at the end of each subsequent quarter (i.e. up to fifteen over a year) and (ii) a 7 d dietary recall (7DDR) measured at baseline and then quarterly, regression analyses were conducted to test the effect of the DII score on serum hs-CRP as dichotomous (≤3 mg/l, >3 mg/l), while controlling for important potential confounders.
Existing data from the Seasonal Variation of Blood Cholesterol Study (SEASONS), a longitudinal observational study of healthy participants recruited in Worcester, MA, USA and participants were followed for 1 year.
Participants who had at least one hs-CRP measurement over her/his 1-year participation (n 495 for 24HR, n 559 for 7DDR).
Higher DII scores were associated with values of hs-CRP >3 mg/l (OR = 1·08; 95 % CI 1·01, 1·16, P = 0·035 for the 24HR; and OR = 1·10; 95 % CI 1·02, 1·19, P = 0·015 for the 7DDR).
The population-based DII was associated with interval changes in hs-CRP using both the 24HR and 7DDR. The success of this first-of-a-kind attempt at relating individuals' intakes of inflammation-modulating foods using this refined DII, and the finding that there is virtually no drop-off in predictive capability using a structured questionnaire in comparison to the 24HR standard, sets the stage for use of the DII in a wide variety of other epidemiological and clinical studies.
Colorectal cancer, the third most common cancer in the United States, has a natural history that usually encompasses several decades. Dietary components have been implicated in the etiology of ...colorectal cancer, perhaps through their effect on inflammation.
We examined the ability of the dietary inflammatory index (DII) to predict colorectal cancer in the Iowa Women's Health Study. The DII was computed based on dietary intake assessed by a 121-item food frequency questionnaire in this cohort of 34,703 women, ages 55 to 69 years, free of any self-reported prior malignancy at enrollment in 1986. Incident colorectal cancer cases were identified through linkage with the State Health Registry of Iowa (a Surveillance, Epidemiology, and End Results program member). Cox proportional hazards regression was used to estimate HRs. Through the end of 2010, 1,636 incident colorectal cancers were identified, including 1,329 colon and 325 rectal cancers.
Multivariable analysis, adjusting for body mass index, smoking status, pack-years of smoking, hormone replacement therapy, education, diabetes, and total energy intake, revealed positive associations between higher DII and colorectal cancer risk HR for DIIcontinuous: 1.07 per unit increase in DII (corresponding to 0.5 SD unit increase); 95% confidence interval (CI), 1.01-1.13; HR for DIIquintiles: Q5 vs. Q1 = 1.20; 95% CI, 1.01-1.43. HRs for DII were similar for colon cancer and rectal cancer, though not statistically significant for rectal cancer.
These results indicate that a proinflammatory diet, as indicated by higher DII scores, was associated with higher risk of developing colorectal cancer.
Proinflammatory diets are associated with increased risk of colorectal cancer.
Ultra-processed food (UPF) intake has been positively associated with obesity and diabetes. The relationship between UPF intake and liver health has been scarcely studied.
We aimed to evaluate the ...association of UPF intake with risk of adverse liver outcomes including nonalcoholic fatty liver disease (NAFLD), liver fibrosis/cirrhosis, liver cancer, severe liver disease, and serum biomarkers of liver health.
A total of 173,889 participants aged 40 to 69 y from the UK Biobank were included. UPF intake was defined using 24-h dietary recalls and NOVA classification. Liver outcome data were obtained from cancer registry, in-hospital records, and death registries. Serum biomarkers were measured at baseline. We used Cox proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for associations between UPF and adverse liver outcomes adjusting for demographics, lifestyle factors, body mass index, and diabetes. We used multinomial logistic regression to evaluate associations between UPF and liver function biomarkers.
After a median follow-up of 8.9 y, we documented 1108 NAFLD, 350 liver fibrosis/cirrhosis, 134 liver cancer, and 550 severe liver disease cases. Higher UPF intake was associated with increased risk of NAFLD (HR
: 1.43; 95% CI: 1.21, 1.70; P
< 0.001), liver fibrosis/cirrhosis (HR: 1.18; 95% CI: 0.87, 1.59; P
= 0.009), and severe liver disease (HR: 1.50; 95% CI: 1.19, 1.90; P
< 0.001) but not with liver cancer (HR: 1.00; 95% CI: 0.63, 1.58; P
= 0.88). Higher UPF intake was associated with elevated levels of C-reactive protein, alkaline phosphatase, aspartate aminotransferase, γ-glutamyltransferase, and triglycerides and lower cholesterols (all P
< 0.001).
Higher UPF intake is associated with an increased risk of NAFLD, liver fibrosis and cirrhosis, and severe liver disease and adverse levels of multiple clinical biomarkers, suggesting the potential importance of reducing UPF intake to improve liver health.
Background
Various dietary components have been studied in relation to overall mortality; however, little is known about the relationship between the inflammatory potential of overall diet and ...mortality.
Materials and methods
We examined the association between the dietary inflammatory index (DII) and mortality in the National Health and Nutrition Examination Survey III follow-up study. The DII was computed from baseline dietary intake assessed using 24-h dietary recalls (1988–1994). Mortality was determined from the National Death Index records through 2006. Cox proportional hazards regression was used to estimate hazard ratios (HRs) and 95 % confidence interval (95 % CI). During the follow-up, 2795 deaths were identified, including 1233 due to cardiovascular disease (CVD), and 615 due to cancer, 158 of which were due to digestive-tract cancers.
Results
Multivariate Cox proportional hazards regression analyses, adjusting for age, race, diabetes status, hypertension, physical activity, body mass index, poverty index, and smoking, revealed positive associations between higher DII scores and mortality. Comparing subjects in DII tertile 3 versus tertile 1, significant associations were noted for all-cause mortality (HR
Tertile3vs1
1.34; 95 % CI 1.19–1.51,
P
trend
< 0.0001), CVD mortality (HR
Tertile3vs1
1.46; 95 % CI 1.18–1.81,
P
trend
= 0.0006), cancer mortality (HR
Tertile3vs1
1.46; 95 % CI 1.10–1.96,
P
trend
= 0.01), and digestive-tract cancer mortality (HR
Tertile3vs1
2.10; 95 % CI 1.15–3.84,
P
trend
= 0.03).
Conclusion
These results indicate that a pro-inflammatory diet, as indicated by higher DII scores, was associated with higher risk of all-cause, CVD, and cancer mortality.
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DOBA, EMUNI, FIS, FSPLJ, FZAB, GEOZS, GIS, IJS, IMTLJ, IZUM, KILJ, KISLJ, MFDPS, NLZOH, NUK, OBVAL, OILJ, PILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, SIK, UILJ, UKNU, UL, UM, UPUK, VKSCE, VSZLJ, ZAGLJ
Abstract Studies have shown an association between depression and both antioxidant levels and oxidant stress, but generally have not included intakes of antioxidants and antioxidant-rich fruits and ...vegetables. This study examined the cross-sectional associations between clinically diagnosed depression and intakes of antioxidants, fruits, and vegetables in a cohort of older adults. Antioxidant, fruit, and vegetable intakes were assessed in 278 elderly participants (144 with depression, 134 without depression) using a Block 1998 food frequency questionnaire that was administered between 1999 and 2007. All participants were aged 60 years or older. Vitamin C, lutein, and beta cryptoxanthin intakes were significantly lower among individuals with depression than in comparison participants ( P <0.05). In addition, fruit and vegetable consumption, a primary determinant of antioxidant intake, was lower in individuals with depression. In multivariable models controlling for age, sex, education, vascular comorbidity score, body mass index, total dietary fat, and alcohol; vitamin C, beta cryptoxanthin, fruits, and vegetables remained significant. Antioxidants from dietary supplements were not associated with depression. Antioxidant, fruit, and vegetable intakes were lower in individuals with late-life depression than in comparison participants. These associations may partially explain the elevated risk of cardiovascular disease among older individuals with depression. In addition, these findings point to the importance of antioxidant food sources rather than dietary supplements.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Purpose: Inflammation is a process central to carcinogenesis and in particular to colorectal cancer (CRC). Previously, we developed a dietary inflammatory index (DII) from extensive literature review ...to assess the inflammatory potential of diet. In the current study, we utilized this novel index in the Women's Health Initiative to prospectively evaluate its association with risk of CRC in postmenopausal women. Methods: The DII was calculated from baseline food frequency questionnaires administered to 152,536 women aged 50–79 years without CRC at baseline between 1993 and 1998 and followed through 30 September 2010. Incident CRC cases were ascertained through a central physician adjudication process. Multiple covariate-adjusted Cox proportional hazards regression models were used to estimate hazard ratios (HR) and 95 % confidence intervals (95 % CI) for colorectal, colon (proximal/distal locations), and rectal cancer risk, by DII quintiles (Q). Results: During an average 11.3 years of follow-up, a total of 1,920 cases of CRC (1,559 colon and 361 rectal) were identified. Higher DII scores (representing a more pro-inflammatory diet) were associated with an increased incidence of CRC (HRQ5-Q1 1.22; 95 % CI 1.05, 1.43; Ptrend = 0.02) and colon cancer, specifically proximal colon cancer (HRQ5-Q1 1.35; 95 % CI 1.05, 1.67; Ptrend 0.01) but not distal colon cancer (HRQ5-Q1 0.84; 95 % CI 0.61, 1.18; Ptrend = 0.63) or rectal cancer (HRQ5-Q1 1.20; 95 % CI 0.84, 1.72; Ptrend = 0.65). Conclusion: Consumption of pro-inflammatory diets is associated with an increased risk of CRC, especially cancers located in the proximal colon. The absence of a significant association for distal colon cancer and rectal cancer may be due to the small number of incident cases for these sites. Interventions that may reduce the inflammatory potential of the diet are warranted to test our findings, thus providing more information for colon cancer prevention.
Context
Pancreatic cancer has the highest case fatality rate of all major cancers.
Objective
A systematic review using PRISMA guidelines was conducted to summarize the associations between dietary ...patterns and risk of pancreatic cancer.
Data Sources
PubMed and Web of Science databases were searched for case–control and cohort studies published up to June 15, 2016.
Study Selection
Eligible studies included a dietary pattern as exposure and pancreatic cancer incidence or mortality as outcome and reported odds ratios, hazard ratios, or relative risks, along with corresponding 95%CIs.
Data Extraction
Important characteristics of each study, along with the dietary assessment instrument, the component foods or nutrients included in each dietary pattern or the scoring algorithm of a priori dietary patterns, were presented. For each dietary pattern identified, the estimate of association and the 95%CI comparing the highest versus the lowest category from the model with the most covariate adjustment were reported.
Results
A total of 16 studies were identified. Among the 8 studies that examined data-driven dietary patterns, significant positive associations were found between pancreatic cancer risk and the Animal Products, Starch Rich, and Western dietary patterns, with effect estimates ranging from 1.69 to 2.40. Significant inverse relationships were found between risk of pancreatic cancer and dietary patterns designated as Fruits and Vegetables, Vitamins and Fiber, and Prudent, with effect estimates ranging from 0.51 to 0.55. Eight studies of a priori dietary patterns consistently suggested that improved dietary quality was associated with reduced risk of pancreatic cancer.
Conclusions
Better diet quality is associated with reduced risk of pancreatic cancer. The associations between dietary patterns and pancreatic cancer were stronger in case–control studies than in cohort studies and were stronger among men than among women.
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