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Principal Investigator
Name
Alyson Haslam
Degrees
MS
Institution
University of Georgia
Position Title
PhD student
Email
About this CDAS Project
Study
PLCO (Learn more about this study)
Project ID
PLCO-104
Initial CDAS Request Approval
Sep 4, 2014
Title
The influence of inflammatory diets on the incidence of colorectal cancer, with special consideration of race and obesity
Summary
It is estimated that as many as 80% of colorectal cancer cases can be attributed to diet (Bingham, 2000), suggesting that it is a relatively modifiable disease. Yet, the American Cancer Society estimates that approximately 137,000 people will develop colorectal cancer in 2014, making it the third most commonly diagnosed cancer in both men and women (excluding basal and squamous cell skin cancers; American Cancer Society, 2014). The high incidence of colorectal cancer, in spite of the preventable nature of the disease, suggests that a greater understanding of potential etiologic factors is needed to reduce disease burden. Specifically, further research is needed to fully elucidate the dietary factors that may prevent this type of cancer. Modulating inflammation may be the critical link between diet and colorectal cancer incidence.
Studies have shown an association between diet and systemic inflammation (Schultze et al., 2005). Oxidative stress, which promotes inflammation, occurs when a high-fat and/or high-carbohydrate meal is consumed; however, foods that are high in anti-oxidants, such as fruits and vegetables, can reduce oxidative stress, and consequently inflammation (Esposito and Giugliano, 2006). Further, studies indicate an association between systemic inflammation and colorectal cancer (Gunter et al., 2006). Inflammation appears to promote an environment that increases genetic mutations, while inactivating the body’s ability to repair mutations (Grivennikov et al., 2010). Despite this body of evidence, it is unknown whether or not an inflammatory diet increases the incidence of colorectal cancer through the mechanism of systemic inflammation, particularly in sub-populations with a higher risk of developing colorectal cancer, such as those of black race and with a higher BMI . Increasing body mass index can lead to excess systemic inflammation that may put an individual at higher risk of developing colorectal cancer (Beasley et al., 2009). It remains unknown whether or not diet modifies the association between obesity and colorectal cancer incidence. Black individuals have a higher incidence of both incidence and mortality from colorectal cancer as compared to white individuals (American Cancer Society, 2014). Blacks also have less inflammation-promoting visceral fat than whites (Beasley et al., 2009), yet they have a higher incidence of colorectal cancer that is at least partially attributed to inflammation. Reasons for the disparities in colorectal cancer incidence are largely unknown, but diet may at least partially explain these differences.
Prior research has examined specific nutrients or cultural diets that may be anti-inflammatory (Conner and Grisham, 1996; Mendez et al., 2006), but it has been only recently that researchers have developed a validated and universal method of quantifying the inflammatory nature of diets (Shivappa et al., 2013). The purpose of this study, therefore, is to use a validated inflammatory index to further investigate the association between an inflammatory diet and the incidence of colorectal cancer. We will also determine whether or not this association is modified by race or body mass index.
Aims

• To determine whether an inflammatory diet, as measured by a validated dietary inflammatory index, is associated with increasing obesity in a group of adult men and women, aged 55 to 74, enrolled in the the Prostate, Lung, Colorectal, and Ovarian (PLCO) Screening Trial. We hypothesize that consumption of an inflammatory diet, as indicated by a higher inflammatory index, is more common among those that are obese as compared to those who are not obese at baseline. Further, we hypothesize that a higher dietary inflammatory index at baseline leads to greater weight gain during follow-up.
• To determine whether or not there are racial differences in the consumption of inflammatory diets, as measured by a validated dietary inflammatory index, in a group of men and women, between the ages of 55 and 74, enrolled in the PLCO Screening Trial. We hypothesize that black people consume a more inflammatory diet than people of other races.
• To determine whether or not an inflammatory diet predicts the incidence of colorectal cancer in a group of men and women, between the ages of 55 and 74, enrolled in the PLCO Screening Trial. We will also determine whether or not the potential association between dietary inflammation and colorectal cancer incidence is modified by obesity or race. We hypothesize that people who have a higher dietary inflammatory index at baseline are more likely to develop colorectal cancer during follow-up than those with a lower dietary inflammatory index. We also hypothesize that the association between inflammatory diets and colorectal cancer will be stronger in people who are obese than in those who are normal weight. Finally, we hypothesize that that the association between inflammatory diets and colorectal cancer will be stronger in blacks than in whites.
Data from the PLCO Cancer Screening Trial will be analyzed cross-sectionally to determine differences in baseline inflammatory index scores between those who are obese and those who are not obese, and also between different racial groups. Prospective analysis will then be performed to test the hypothesis that people with a higher dietary inflammatory index at baseline will have more weight gain during follow-up than those with a lower dietary inflammatory index. Further prospective analysis will test for an association between a higher dietary inflammatory index at baseline and a higher incidence of colorectal cancer during follow-up. Separate stratified analyses will test for effect modification of body mass index and race.

Collaborators

Sara Wager Robb, PhD
Ye Shen, PhD
Amara Ezeamama, PhD
Jung Sun Lee, PhD