Polycyclic aromatic hydrocarbons (PAHs) and heterocyclic amines (HCAs) are carcinogens formed in or on the surface of well-done meat, cooked at high temperature.We estimated breast cancer risk in relation to intake of cooked meat in a population-based, case-control study (1508 cases and 1556 controls) conducted in Long Island, NY from 1996 to 1997. Lifetime intakes of grilled or barbecued and smoked meats were derived from the interviewer-administered questionnaire data. Dietary intakes of PAH and HCA were derived from the self-administered modified Block food frequency questionnaire of intake 1 year before reference date. Unconditional logistic regression was used to estimate adjusted odds ratios (ORs) and 95% confidence intervals (CIs).Modest increased risk was observed among postmenopausal, but not premenopausal, women consuming the most grilled or barbecued and smoked meats over the life course (OR = 1.47; CI = 1.12-1.92 for highest vs. lowest tertile of intake). Postmenopausal women with low fruit and vegetable intake, but high lifetime intake of grilled or barbecued and smoked meats, had a higher OR of 1.74 (CI = 1.20-2.50). No associations were observed with the food frequency questionnaire-derived intake measures of PAHs and HCAs, with the possible exception of benzo(alpha)pyrene from meat among postmenopausal women whose tumors were positive for both estrogen receptors and progesterone receptors (OR = 1.47; CI = 0.99-2.19).These results support the accumulating evidence that consumption of meats cooked by methods that promote carcinogen formation may increase risk of postmenopausal breast cancer.
Colorectal cancer (CRC) is the third most common cancer in both men and women in the United States. Various a priori dietary patterns that take into account diet complexity have been associated with CRC risk. This systematic review augments the evidence for an association between CRC risk and the Mediterranean Diet Score (MDS) and the Healthy Eating Index (HEI), and provides new evidence for a novel Dietary Inflammatory Index (DII). Human studies published in English after 31 December 2008 were reviewed. Five case-control studies and 7 prospective cohort studies conducted in the United States and Europe were identified. Five of the studies examined the MDS, 4 examined the HEI, and 4 examined the DII. Comparing highest to lowest score groups, higher MDSs were associated with an 8–54% lower CRC risk, and higher HEI scores were associated with a 20–56% lower CRC risk. More proinflammatory diet scores were associated with a 12–65% higher CRC risk compared with more anti-inflammatory diets in studies that used the DII. The results reported by sex suggested similar associations for men and women. This review builds upon the evidence supporting the association between higher overall diet quality and lower risk of CRC. Increasing scores of MDS and HEI and anti-inflammatory DII scores are characterized by high intake of plant-based foods and low intake of animal products. Future studies in more diverse populations and with consistent scoring calculations are recommended.
<div>Abstract<p>Advanced glycation end-products (AGEs) are implicated in the pathogenesis of several chronic diseases including cancer. AGEs are produced endogenously but can also be consumed from foods. AGE formation in food is accelerated during cooking at high temperatures. Certain high fat or highly processed foods have high AGE values. The objective of the study was to assign and quantify N<sup>ε</sup>-carboxymethyl-lysine (CML)-AGE content in food and investigate the association between dietary AGE intake and breast cancer risk in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. The study included women enrolled in the intervention arm who were cancer-free at baseline and completed a baseline questionnaire and food frequency questionnaire (DQX). CML-AGE values were assigned and quantified to foods in the DQX using a published AGE database. Cox proportional hazards models were used to estimate the hazard ratios (HR) and 95% confidence intervals (CI) of breast cancer among all women, and stratified by race/ethnicity, invasiveness of disease, and hormone receptor status. After a median 11.5 years of follow-up, 1,592 women were diagnosed with breast cancer. Higher CML-AGE intake was associated with increased risk of breast cancer among all women (HR<sub>Q5VSQ1</sub>, 1.30; 95% CI, 1.04–1.62; <i>P</i><sub>trend</sub> = 0.04) and in non-Hispanic white women (HR<sub>T3VST1</sub>, 1.21; 95% CI, 1.02–1.44). Increased CML-AGE intake was associated with increased risk of <i>in situ</i> (HR<sub>T3VST1</sub>, 1.49; 95% CI, 1.11–2.01) and hormone receptor–positive (HR<sub>T3VST1</sub>, 1.24; 95% CI, 1.01–1.53) breast cancers. In conclusion, high intake of dietary AGE may contribute to increased breast cancer.</p></div>
Abstract Advanced glycation end-products (AGEs) are implicated in the pathogenesis of several chronic diseases including cancer. AGEs are produced endogenously but can also be consumed from foods. AGE formation in food is accelerated during cooking at high temperatures. Certain high fat or highly processed foods have high AGE values. The objective of the study was to assign and quantify Nε-carboxymethyl-lysine (CML)-AGE content in food and investigate the association between dietary AGE intake and breast cancer risk in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. The study included women enrolled in the intervention arm who were cancer-free at baseline and completed a baseline questionnaire and food frequency questionnaire (DQX). CML-AGE values were assigned and quantified to foods in the DQX using a published AGE database. Cox proportional hazards models were used to estimate the hazard ratios (HR) and 95% confidence intervals (CI) of breast cancer among all women, and stratified by race/ethnicity, invasiveness of disease, and hormone receptor status. After a median 11.5 years of follow-up, 1,592 women were diagnosed with breast cancer. Higher CML-AGE intake was associated with increased risk of breast cancer among all women (HRQ5VSQ1, 1.30; 95% CI, 1.04–1.62; Ptrend = 0.04) and in non-Hispanic white women (HRT3VST1, 1.21; 95% CI, 1.02–1.44). Increased CML-AGE intake was associated with increased risk of in situ (HRT3VST1, 1.49; 95% CI, 1.11–2.01) and hormone receptor–positive (HRT3VST1, 1.24; 95% CI, 1.01–1.53) breast cancers. In conclusion, high intake of dietary AGE may contribute to increased breast cancer.
We examined the associations between changes in dietary inflammatory potential and risk of colorectal cancer (CRC) in 87,042 postmenopausal women recruited from 1993-1998 by the Women's Health Initiative, conducted in the United States. Food frequency questionnaire data were used to compute patterns of change in dietary inflammatory index (DII) scores and cumulative average DII scores over 3 years. Cox regression models were used to estimate hazard ratios for CRC risk. After a median of 16.2 years of follow-up, 1,038 CRC cases were diagnosed. DII changes were not substantially associated with overall CRC, but proximal colon cancer risk was higher in the proinflammatory-change DII group than in the antiinflammatory-stable DII group (hazard ratio = 1.32, 95% confidence interval: 1.01, 1.74). Among nonusers of nonsteroidal antiinflammatory drugs (NSAIDs) (Pinteraction = 0.055), the proinflammatory-stable DII group was at increased risk of overall CRC and proximal colon cancer. Also among nonusers of NSAIDs, risks of overall CRC, colon cancer, and proximal colon cancer were higher in the highest quintile compared with the lowest cumulative average DII quintile (65%, 61%, and 91% higher risk, respectively). Dietary changes toward, or a history of, proinflammatory diets are associated with an elevated risk of colon cancer, particularly for proximal colon cancer and among nonusers of NSAIDs.
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