by increasing inflammation, new research suggests.
In the Jan. 18 online edition of JAMA Oncology, Fred K. Tabung, PhD, from the department of nutrition at the Harvard T.H. Chan School of Public Health, Boston, and coauthors presented analysis of data from 46,804 men in the Health Professionals Follow-up Study and 74,246 women in the Nurses’ Health Study, examining the relationship between proinflammatory diets and colorectal cancer.
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The effect was more pronounced in men with highly inflammatory diets, who had a 44% higher risk of colorectal cancer, compared with those whose diets had low inflammatory potential (95% CI, 1.19-1.74; P less than .001). Women in the highest quintile had a 22% higher risk of colorectal cancer, compared with those in lowest quintile (95% CI, 1.02-1.45; P = .007). These increases in risk were seen even after adjusting for potential confounders such as age, family history of cancer, physical activity, smoking, NSAID use, and menopause status (JAMA Oncology. 2018 Jan 18. doi: 10.1001/jamaoncol.2017.4844).
Overall, there were 2,699 cases of incident colorectal cancer over 2,571,831 person-years of follow-up. Researchers noted 38 more incidents of colorectal cancer per 100,000 person-years among men in the highest quintile, and 12 more among women in the highest quintile, compared with men and women in the lowest quintiles.
The score used in the study looks at intake of foods such as processed, red, and organ meat; fish, vegetables other than green leafy or dark yellow vegetables, refined grains, high-energy and low-energy drinks, and tomatoes, which are all positively related to concentrations of the inflammatory markers. Foods linked to low concentrations of inflammatory markers include beer, wine, tea, coffee, dark yellow vegetables, green leafy vegetables, snacks, fruit juice, and pizza.
The association between proinflammatory diet and colorectal cancer risk was found in all anatomic locations, including the proximal and distal colon. The only exception was for rectal cancer in women, where dietary inflammatory potential did not significantly change cancer risk.
“It is not entirely clear why associations for rectal cancer were stronger in men than in women but are unlikely to be due to chance given the large significant heterogeneity by sex,” wrote Dr. Tabung and coauthors. They suggested the difference in risk pattern for rectal cancer may relate to broader differences in risk patterns between sexes.
“For example, higher body weight strongly predisposes men to higher risk of proximal colon cancer, distal colon cancer, and rectal cancer, and predisposes women to mainly higher risk of distal colon cancer but not rectal cancer.”
This was also evident when the authors looked at subgroup effects based on body mass index and alcohol intake. Men who were overweight or obese and who were on the most proinflammatory diet had a significant, 48% higher risk of colorectal cancer, compared with the lowest quintile. The same effect was not seen in overweight or obese women.
When alcohol intake was examined, researchers saw a significant 62% higher risk of colorectal cancer among men who were in the highest quintile for dietary inflammatory potential, but who did not drink alcohol, compared with teetotalers in the lowest quintile. In women, there was a 33% higher risk in the highest quintile, compared with the lowest in those who did not drink.
A similar trend was evident in individuals who drank up to one alcoholic drink a day, but it was only borderline significant, and there was no significant effect seen in individuals who drank more than one alcoholic drink a day, despite the fact that a high intake of alcohol has been associated with cancer risk in both men and women.
“It is possible that the adverse effects of alcohol intake through other mechanisms may be more dominant than those of its effect on the EDIP and may partially explain the stronger associations among men and women not consuming alcohol than among alcohol consumers.”
The Health Professionals Follow-up Study and Nurses’ Health Study are supported by the National Institutes of Health. Three authors were also supported by grants from the National Institutes of Health, and one also received support from the Friends of the Dana-Farber Cancer Institute and the Dana-Farber Harvard Cancer Center. No conflicts of interest were declared.