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The advent of the Dietary Inflammatory Index (DII) provides a quantitative means to study the relationship between the pro-inflammatory diet and CRC. It allows the assessment of the inflammatory potential of individual food items using an FFQ, by which a DII score can be calculated. A higher DII score suggests a stronger inflammatory potential of a food item. The Dietary Inflammatory Index (DII) was extensively used to examine the inflammatory potential of diet related to colorectal cancer (CRC).
- Dietary Inflammatory Index
- colorectal cancer
- dietary pattern
- risk factor
1. Introduction
Colorectal cancer (CRC) is currently the second leading cause of cancer-related mortality worldwide. In 2020 alone, approximately 1.9 million people were diagnosed with CRC, and 935,000 of them died within the same year [1]. The high burden of CRC in countries with a medium to high human development index (HDI) suggested the potential role of both sedentary lifestyles and dietary patterns in the development of CRC [2].
More than 60% of the overall CRC cases were reported as sporadic, occurring in people without genetic predisposition or family history of CRC [3]. Such a trend further points to the impact of modifiable risk factors in the CRC development. It is generally believed that long-term exposure to an unhealthy diet, physical inactivity, smoking, and alcohol consumption are all likely to trigger the chronic systemic inflammation, which eventually induces the proliferation of cancer cells [4][5]. Molecular studies also demonstrated that the production of pro-inflammatory cytokines and arrays of free radicals present at cellular levels were attributable to the consumption of an unhealthy diet [6][7][8].
There were various types of dietary assessment methods frequently used for epidemiological purposes, which includes the 24 h dietary recall, the dietary record, and the food frequency questionnaire (FFQ). However, they were unable to relate the specific dietary risk factor with levels of inflammatory markers well-established in CRC. The advent of the Dietary Inflammatory Index (DII) provides a quantitative means to study the relationship between the pro-inflammatory diet and CRC. It allows the assessment of the inflammatory potential of individual food items using an FFQ, by which a DII score can be calculated. A higher DII score suggests a stronger inflammatory potential of a food item [9]. Remarkably, DII has been utilized in substantial epidemiologic studies that include different ethnicities and various health outcomes.
2. Association between Dietary Inflammatory Index and Colorectal Cancer
The association between high DII scores and the increased risk of CRC has been confirmed. It was grounded on the standardized quantification of inflammatory markers produced individual food parameters, which has long been used to predict the risk of chronic non-communicable diseases including cancer [10][11]. Instead of giving general recommendations on high-fat and low-fiber food intake, the DII enables an objective assessment of dietary patterns and the risk of cancer at an individual level [12][13][14].
There is a stronger impact of pro-inflammatory dietary patterns on the CRC development as compared with the research duration and other adjustment factors.
The most common approach used to measure the adherence to a routine healthy dietary intake is the Healthy Eating Index (HEI) or the Mediterranean diet since the indices were based on certain dietary recommendations [15]. Overall, the Mediterranean diet composed of rich, plant-based foods, including the fruits, vegetables, nuts, legumes, and whole grain products, combined with regular intake of seafood and low intake of red and processed meat [16]. Although many studies relate the practice of Mediterranean diet with less risk for CRC, in regions where plant-based foods serve as the food staple, the incidence of CRC continues to rise [17]. Future research works should consider the influencing factors concomitant to dietary pattern that could possibly contributed to the progression of CRC over time.
High intake of processed and red meat has been linked to increased risk of CRC. However, in countries like Korea where the CRC incidence rate is relatively high, with 44.5 cases per 100,000 persons per year [18], studies reported less than 20% of the population consumed processed meat products [19], indicating the presence of other factors that may influence the tumor progression. Numerous empirical studies proposed that the presence of mutagenic compounds, such as the heterocyclic amines (HCAs), polycyclic aromatic hydrocarbons (PAHs), and acrylamides formed during food preparation, raised the risk of CRC [11][20][21]. Understanding the cooking method and food processing involved provide beneficial value to explain the impact of food culture in the complex mechanism of CRC.
The intake of dietary fiber on daily basis has crucial role in the functionality of the guts to enhance transit time and stool formation. Disturbance of the physiologic system affected by the food solubility and fermentability causes tremendous effects towards the gut lining, thus potentially causing tumorigenesis. Notwithstanding that, a recently published longitudinal study revealed that consumption of dietary fiber intake improved the physical function and overall health of the CRC survivors upon completion of their treatment [22]. Changing to healthier diet pattern containing more anti-inflammatory foods had protective effect against cancer recurrence as well as prolonged survival [10][14][23][24]. Therefore, extensive health campaigns and awareness towards a healthy, balanced diet should target the average-risk groups and be initiated as early as possible.
When comparing the DII score across opposite gender, few studies suggested sex differentials pertaining to the risk of CRC [20][25]. A comparison study on Canadian populations showed that a 33% reduction in the risk of CRC in men [26] was attributable to the intake of anti-inflammatory diets, whereas no significant association was observed with similar dietary pattern among women. More studies are required to explain the role of sex differentials and dietary intake against the risk for CRC. Similarly, when accounted together with the physical activity factor, high DII score showed tendency to raise the CRC risk among individuals with sedentary lifestyle [27]. Collectively, this explained the importance of healthy lifestyle of an individual in a holistic manner whereby the modifiable risk factors are interdependent, leading to rapid progression towards CRC [28].
The interplay of modifiable risk factors, such as unhealthy dietary patterns and sedentary lifestyles, have partly contributed to the complexity of obesity to an extent [29]. Several epidemiological evidence have demonstrated that individuals with higher-than-normal BMI are likely to have a higher risk for CRC [8][29][30][31][32]. In a large, population-based cohort trial, obesity during early adulthood and a constantly increasing BMI throughout the lifespan were significantly associated with CRC [33]. Recent genetic studies suggested that for every one-unit increase in genetically predicted BMI, there is an increase in the odds ratios for CRC [34][35][36], indirectly implying the causality relationship between obesity and CRC. Future studies should consider the influence of residual confounding to delineate the true effect of BMI on CRC.
Substantial evidence supported the association between inflammatory potential of diet and the development of CRC. However, future research involving multiethnic population, such as in Asian regions, is needed to explain the climbing CRC incidence and plan for preventive intervention strategies. Concerted efforts tailored to specific-culture dietary patterns call for multisectoral engagement in program planning to ensure effective outcome. Quantitative evidence as reported by the DII score and the impact towards CRC risk helps to advocate to the public health authorities about the importance of tackling the underlying factors that shape the dietary pattern.
This entry is adapted from the peer-reviewed paper 10.3390/nu14081555
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