A diet rich in foods known to cause inflammation may increase the risk for colorectal cancer by about one-third, according to the results of a newly published study.
A diet rich in foods known to cause inflammation may increase the risk for colorectal cancer by about one-third, according to the results of a study published in JAMA Oncology.
“Findings from this large prospective study support a role for the inflammatory potential of diet in colorectal cancer development, suggesting inflammation as a potential mechanism linking dietary patterns and colorectal cancer development,” wrote Fred K. Tabung, MSPH, PhD of the Harvard T.H. Chan School of Public Health in Boston, and colleagues. “Strategies to reduce the adverse role of a proinflammatory dietary pattern in colorectal cancer development may have higher benefits among overweight or obese men and among lean women or among men and women not consuming alcohol.”
According to the study, inflammation is thought to play a role in the development of many solid tumors. Diet can influence inflammation in the body as measured by inflammatory biomarkers, making diet a modifiable risk factor to prevent colorectal cancer.
To research this, Tabung and colleagues conducted a cohort study of 46,804 men from the Health Professionals Follow-Up Study, and 74,246 women from the Nurses’ Health Study who were followed for 26 years. They examined whether proinflammatory diets were associated with increased colorectal cancer risk using an empirical dietary inflammatory pattern (EDIP) score based on a weighted sum of 18 food groups that characterizes dietary inflammatory potential based on circulating levels of inflammation biomarkers.
During the follow-up period, 2,699 cases of incident colorectal cancer were documented. The researchers grouped participants into quintile based on EDIP score. Those participants in the highest EDIP quintile had an unadjusted rate difference of 38 (men) and 12 (women) more colorectal cancer cases compared with those in the lowest EDIP quintile.
In multivariable-adjusted analyses, higher EDIP scores were associated with a 44% higher risk for developing colorectal cancer among men (hazard ratio [HR], 1.44; 95% CI, 1.19–1.74; P < .001), and a 22% higher risk among women (HR, 1.22; 95% CI, 1.02–1.45; P = .007). Overall, for both men and women, higher EDIP scores resulted in a 32% higher risk for developing colorectal cancer (HR, 1.32; 95% CI, 1.12–1.55; P < .001).
“In both men and women, associations were observed in all anatomic sites, except for the rectum in women,” the researchers wrote.
The researchers also conducted a subgroup analysis and found that there were significant differences (P < .02 for all interactions) in the association between dietary inflammation potential and colorectal cancer risk for men and women based on defined body mass index categories and alcohol intake. For example, among overweight or obese men in the highest EDIP quintile there was a 48% increased risk for colorectal cancer (HR, 1.48; 95% CI, 1.12–1.94; P = .004). In addition, there was a 62% higher risk for colorectal cancer among lean men in the highest EDIP quintile not consuming alcohol and a 33% higher risk among lean women in the highest EDIP quintile not consuming alcohol compared with men and women in the lowest EDIP quintile.
“The differences by body weight category may partly underlie the differences by sex observed for rectal cancer risk; whereas the differences by alcohol intake category may indicate that the influence of alcohol on colorectal cancer risk through mechanisms other than inflammation, may be stronger than that of its effects on the EDIP,” the researchers wrote.