Colorectal cancer (CRC) stands as the third most prevalent cancer globally. While the overall incidence of CRC has been on a decline over the past four decades, a disturbing trend has emerged: the rise of early-onset colorectal cancer (EOCRC), defined as CRC diagnosed in individuals aged 50 years or younger. This article delves into the association between modifiable risk factors such as diet quality, excess adiposity, and chronic psychosocial stress (CPS) and the development of EOCRC.
The Increasing Incidence of Early-Onset Colorectal Cancer
EOCRC incidence has been steadily increasing in the United States, with a notable 63% surge observed between 1988 and 2015. This alarming trend is not confined to the United States alone, as similar increases in EOCRC have been reported in other Westernized countries, including Australia and Canada. The etiology of EOCRC remains largely elusive, with only a small fraction of new cases (approximately 20%) attributable to familial genetic causes.
The shifting landscape of Westernized populations, characterized by alterations in diet quality, increased stress levels, rising obesity rates, and sedentary behaviors, may play a significant role in the escalating EOCRC rates. These changes are driven by factors such as urbanization, income growth, technological advancements, and the increased availability of ultraprocessed foods. Younger generations are exposed to these risk behaviors from an early age, potentially contributing to the observed increase in EOCRC rates over the past 40 years.
The Detrimental Impact of Poor Diet Quality
A Western diet pattern, characterized by a high intake of red and processed meats, refined grains, and foods with added sugars, has been linked to various chronic diseases, including obesity, cardiovascular disease, type 2 diabetes, and several cancers. Recent studies suggest that a Western diet pattern may elevate the risk of developing CRC, particularly among young adults. The increased production and consumption of ultraprocessed foods, rich in sodium, sugar, and saturated fats, have become a significant component of Western diets.
Conversely, dietary patterns such as the Dietary Approaches to Stop Hypertension (DASH) diet, the Mediterranean Diet, and the Alternative Healthy Eating Index-2010 (AHEI-2010) diet, which promote a high intake of fruits, vegetables, whole grains, nuts, and legumes, while discouraging the consumption of red and processed meats, sugar-sweetened beverages, ultraprocessed foods, and sodium, are associated with positive health outcomes.
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Studies have shown a positive relationship between consuming a Western diet and the presence of distal colon and rectal adenomas before the age of 50 years. Additionally, a hyperinsulinemic diet and lifestyle pattern has been associated with a higher risk of EOCRC.
Mechanisms Linking Diet Quality to EOCRC
Several complex and multifactorial mechanisms may explain the link between overall aspects of diet quality and colorectal adenoma and EOCRC.
- Modulation of the Gut Microbiome: Dietary factors play a crucial role in modulating the gut microbiome, a complex ecosystem of microorganisms that maintain gut homeostasis and regulate host immune responses. A poor-quality diet can lead to an imbalance in the composition and function of the gut microbiome, potentially contributing to the development of EOCRC.
- Promotion of Chronic Inflammation: Chronic inflammation, a key driver of carcinogenesis, is considered a hallmark of cancer. A poor-quality diet can induce a proinflammatory state in the gut, potentially promoting the development of EOCRC.
- Accumulation of Adipose Tissue and Insulin Resistance: A poor-quality diet intake can lead to the accumulation of adipose tissue and insulin resistance. Adipose tissue produces inflammatory cytokines and adipokines, which can promote chronic inflammation and contribute to the development of EOCRC.
Avoiding hyperinsulinemic and Western diet patterns, as well as sugary beverages, while consuming a diet pattern emphasizing fruits, vegetables, whole grains, and lean proteins, may decrease the risk of early-onset colorectal adenoma and EOCRC.
The Role of Excess Adiposity
Obesity onset in early adulthood (around 18 years of age) that persists as an individual ages is positively associated with the risk of EOCRC. This is particularly concerning, as obesity among young adults in the United States has increased significantly in recent years. Childhood obesity rates have also tripled in the United States over the past 30 years, resulting in some of the highest obesity rates worldwide.
Obesity is associated with metabolic, hormonal, and immune perturbations, such as insulin resistance, increased systemic inflammation, and oxidative stress, which promote gene mutations that can impact EOCRC tumorigenesis. Targeting excess adiposity is crucial for preventing the development of EOCRC.
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The Association Between Obesity and EOCRC
The relationship between obesity and EOCRC has been investigated in numerous studies, with varying results. While some studies have found a significant positive association between obesity and EOCRC, others have reported no significant relationship or even a protective effect of obesity. These discrepancies may be attributed to differences in study designs, sample sizes, and BMI categorization across studies. It is important to note that BMI data are not a reliable measure of an individual’s body composition, as it only accounts for height and weight, ignoring the percentage of fat mass compared with muscle mass or body fat distribution.
Despite the inconsistencies, a significant number of studies suggest that obesity is associated with an increased risk of EOCRC or the presence of early-onset colorectal adenoma. Obesity at a young age (e.g., 20 or 30 years old) has been linked to increased odds of EOCRC. Some studies have also found a higher prevalence of EOCRC in patients who underwent bariatric weight loss surgery compared with controls with obesity.
The Impact of Chronic Psychosocial Stress
Chronic psychosocial stress (CPS) is a less investigated modifiable risk factor for EOCRC. While research examining the association between CPS and CRC/EOCRC is sparse, there are likely pathways linking CPS to tumorigenesis.
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