Meat cooked at high temperatures may increase risk for kidney cancer
Eating meat may increase the risk for renal cell carcinoma through mechanisms related to mutagenic compounds associated with cooking at high temperatures, according to results of a study conducted at The University of Texas MD Anderson Cancer Center.
This risk also may be associated with a genetic susceptibility to renal cell carcinoma (RCC), according to researchers.
The increasing incidence of RCC in the United States and other developed nations may be linked to diets that are rich in meats, starches and processed foods, according to study background. Cooking meat at high temperatures — such as those reached when barbecuing or pan-frying — results in the formation of carcinogenic compounds such as PhIP, MeIQ and DiMeIQx.
Thus, Xifeng Wu, MD, PhD, chair of the department of epidemiology and director of the center for translational and public health genomics at The University of Texas MD Anderson Cancer Center in Houston, and colleagues sought to determine whether the intake of certain mutagens derived from high-temperature meat-cooking mechanisms appeared associated with RCC risk. Researchers also evaluated whether those associations were modified by other potential RCC risk factors such as smoking and previously identified genetic variants.
The analysis included data from 659 newly diagnosed patients with RCC (mean age, 59.27 years) and 699 healthy controls (mean age, 60.7 years) from an ongoing case-control study that was initiated in 2002.
Dietary intake — measured in mean grams per day — appeared greater in the RCC cohort for red meat (55.25 vs. 39.03; P = .001), white meat (23.03 vs. 21.21; P = .01) and all fresh meat (59.37 vs. 43.53; P = .001). Daily intake (in ng) of MeIQx (16.95 vs. 9.45; P ˂ .001), PhIP (48.65 vs. 43.94; P = .001) and DiMeIQx (1.22 vs. 0.73; P = .03) also appeared greater in the RCC cohort.
Results of age- and sex-adjusted and multivariable-adjusted models demonstrated an increased risk for RCC associated with higher intake of all red meat (P < .001), all white meat (P = .01) and all fresh meat (P < .001).
Further, increased RCC risk appeared linked to greater intake of MelQx (age- and sex-adjusted OR = 2.61; 95% CI, 1.99-3.44; multivariable-adjusted OR = 1.95; 95% CI, 1.43-2.66) and PhIP (age- and sex-adjusted OR = 1.88; 95% CI, 1.42-2.49; multivariable-adjusted OR = 1.54; 95% CI, 1.14-2.07).
Results of an analysis stratified by smoking status indicated the association between PhIP intake and RCC risk was greater in ever-smokers (P = .02) than in never-smokers.
Additionally, they found that patients with certain genetic variants were more susceptible to the effects of the cancer-causing chemicals. There appeared to be a significant interaction between PhIP and rs718314 (individuals with no minor alleles, OR = 1.14; 95% CI, 0.73-1.76; individuals with at least one copy of minor allele, OR = 2.19; 95% CI, 1.37-3.49) and rs7579899 (individuals with no minor alleles, OR = 1.25; 95% CI, 0.75-2.08; individuals with at least one copy of minor allele, OR = 1.89; 95% CI, 1.25-2.85).
“Our study provides additional evidence for the role of red meat, white meat and [PhIP] in RCC etiology and is the first study of dietary intake of mutagenic compounds and RCC risk to suggest an association with [MeLQx], one of the most abundant heterocyclic amines commonly created in grilling, barbequing and pan-frying meats at high temperatures,” Wu said in a press release. “Also, our study is the first to evaluate the impact of RCC susceptibility variants, identified via genome-wide association studies, on the association between intake of mutagenic compounds and RCC risk.”– by Anthony SanFilippo
Disclosure: The researchers report consultant/advisory roles with Pfizer and research funding from Argos, GlaxoSmithKline and Pfizer.