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Caceres-Matos, R.; Castro-Méndez, A.; García-Domínguez, M.; Pabón-Carrasco, D.; Pabón-Carrasco, M. Influence of Ultra-Processed Food on Colorectal Cancer. Encyclopedia. Available online: (accessed on 14 April 2024).
Caceres-Matos R, Castro-Méndez A, García-Domínguez M, Pabón-Carrasco D, Pabón-Carrasco M. Influence of Ultra-Processed Food on Colorectal Cancer. Encyclopedia. Available at: Accessed April 14, 2024.
Caceres-Matos, Rocío, Aurora Castro-Méndez, Marina García-Domínguez, Daniel Pabón-Carrasco, Manuel Pabón-Carrasco. "Influence of Ultra-Processed Food on Colorectal Cancer" Encyclopedia, (accessed April 14, 2024).
Caceres-Matos, R., Castro-Méndez, A., García-Domínguez, M., Pabón-Carrasco, D., & Pabón-Carrasco, M. (2024, February 28). Influence of Ultra-Processed Food on Colorectal Cancer. In Encyclopedia.
Caceres-Matos, Rocío, et al. "Influence of Ultra-Processed Food on Colorectal Cancer." Encyclopedia. Web. 28 February, 2024.
Influence of Ultra-Processed Food on Colorectal Cancer

Colorectal cancer (CRC) is a disease characterised by the development of malignant tumours in the colon or rectum; it is considered the most common cancer in women, and up to 50% of cases can be prevented with a healthy lifestyle. Nutritional habits are related to its appearance, and the trend of an increased consumption of ultra-processed foods (UPFs) has led to a surge in the incidence of CRC.

colorectal cancer colorectal neoplasms diet food lifestyle nutrition prevention ultra-processed food

1. Introduction

Lifestyle is an important issue, and the scientific community is concerned about its influence on the occurrence of cancer [1]. Cancer stands out as one of the most prevalent diseases worldwide, positioning itself as the second leading cause of death after cardiovascular disease [2]. Diet has been identified as a risk factor for this disease; epidemiological studies show that the consumption of whole grains, fibre, fruits, and vegetables is associated with a lower risk of cancer [3][4][5][6].
The morbidity of cancer continues to grow worldwide, and among its forms, colorectal cancer (CRC) ranks third in prevalence within the disease according to data from the U.S. National Cancer Institute [3]. CRC is characterised by the appearance of malignant lesions in the epithelium of the intestinal mucosa, ranking as the second most common cancer in women and the third in men worldwide [4][5][6]. It is estimated that by 2030, the CRC rates will increase by 124.4% and 90%, respectively, in the population aged 20 to 34 years, reaching high prevalence [3][5].
The main risk factors for CRC include dietary habits, obesity, and lifestyle, among others [4][5][6][7]. Previous studies argue that dietary modifications can prevent 30 to 50% of CRC if fibre, grains, fruits, and vegetables are consumed [2][4][6]. Due to fast-paced lifestyles being common, novel dietary patterns have been adopted that favour the consumption of ultra-processed foods (UPFs). This is attributed to their ease of acquisition, consumption, and reduced cost compared to a Mediterranean diet. The consumption of UPFs is considered proportional to the level of development of a country [1][2][4].
These types of food exhibit low nutritional quality, a high glycaemic load, and insufficient fibre and micronutrients, predisposing people to an increased risk of CRC. In addition, there is an association between colorectal tumours and chronic inflammation [2][4][6][8][9][10]. Specific diet patterns can increase chronic inflammation by altering the microbiota of the body, thereby promoting the onset of tumours and precancerous lesions. Ultra-processed foods induce dysbiosis, a pro-inflammatory microbiota, where the intestinal permeability is affected, generating local chronic inflammation of the mucosa with the migration of lipopolysaccharides to the systemic level. This results in a state of chronic low inflammation, which some authors call “meta-inflammation”, that is, a state of chronic metabolic inflammation, which is behind many of today’s chronic diseases. To this, we must add data showing the epigenetic changes induced by metabolites of the microbiota that could be transmitted to the next generation [6][7][8][9].
The pathogenic effect of UPFs derives from their chemical compositions, since they contain substances such as acrylamide, polycyclic aromatic hydrocarbons, or heterocyclic amines (carcinogenic toxic products), which are generated due to the high temperatures reached during meat processing. The use of artificial sweeteners, such as sucralose, aspartame, saccharin, and others, modify the microbiota, as well as the use of colorants and emulsifiers, such as lecithin, carboxy methylcellulose, and guar gum, among others, which are widely used by the industry to improve UPFs’ organoleptic properties and appearance and extend their expiration dates [10][11][12][13].
Contaminants derived from their packaging should also be considered, such as bisphenol A (BPA), phthalates, microplastics, and nanoparticles, which can migrate into the foods, especially when they are displayed for sale for a long time [14].
On the other hand, their high sugar, refined oil, and saturated fat contents make them detrimental to people’s health, contrasting with their pleasant palatability that predisposes people to their consumption [7][8].
The WHO recommendations advise limiting the consumption of free sugars due to their associations with the onset of diabetes, obesity (a factor related to cancer spread), and hypertension [4][7]. Another category of foods that are harmful to people’s health includes trans fatty acids, which are increasingly present in industrial processing and found in high-fat foods that are unnecessary in the human diet. These are related to the development of cardiovascular diseases, diabetes, and cancer due to their pro-inflammatory properties and inhibitory effects on the metabolism of essential omega-3 and polyunsaturated omega-6 fatty acids [15][16].
Despite these concerns, few studies have evaluated the relationship between UPFs, such as sugar and others, with the onset of CRC [17]. This diet pattern modifies and disrupts the microbiota, which plays a crucial role in protecting individuals against pathogens [15][18]. The consumption of UPFs allows for the production of genotoxins and carcinogenic microbial metabolites, creating a pathological scenario that can favour the development of colorectal tumorigenesis (eubiosis) [8][10].
Although UPFs are considered nutritionally unfavourable, they have been approved for human consumption, and they have been the subject of toxicological studies and safety evaluations that have not been able to assess their possible long-term harmful effects regarding CRC [17]. Consequently, there is an emphasis on the need for studies that demonstrate the use and consumption of these foods in relation to CRC.

2. Sugar Consumption

Sugar is one of the main components and is significantly present in UPF, which favours hyperinsulinemia [19], chronic inflammation [19][20][21][22], and intestinal dysbiosis [19][20][22][23]. These components, according to the available scientific evidence, are mechanisms linking the diet with the CRC [19][24].
As a result, sugar intake is associated with an increased risk of CRC. Added sugars, free sugars, and sucrose are significantly present in sugary drinks such as sodas and in dairy products and desserts [25]. In this regard, some studies went further than simply associating sugar consumption with cancer in general but focused on colorectal neoplasia, demonstrating how a diet high in foods of a high glycaemic index significantly increases the risk of developing this pathology [24][25][26].
The high consumption of this substance leads to an increase in postprandial glucose responses, stimulating the production of pro-oxidant molecules that induce DNA damage, thus increasing the risk of tumours. This excessive intake can also generate advanced endogenous glycation products, which are highly reactive metabolites that trigger cytokine secretion and increased markers of oxidative stress production. Furthermore, refined sugars also result in a higher concentration of inflammatory markers (C-reactive protein) [25][27][28].
Regarding sugary drinks, a prospective cohort study involving a total of 116,429 nurses in the U.S. revealed that women who consumed two or more servings of sugary drinks per day had more than twice the risk of developing this pathology compared to those who consumed less than one serving per week, with a 16% increase in risk per serving per day. Furthermore, each increase in servings/day of sugary drinks during adolescence (13 to 18 years) was also reported to be associated with a 32% increase in the risk of developing early-onset CRC [27].
Sugary drinks contribute significantly to sugar intake in Western countries [25]. Other sweeteners, such as aspartame, have also been questioned. Although previous studies confirmed their safety, there are doubts about the possible long-term health consequences, as increased lymphomas and leukaemias have been reported in animal models [29].

3. Consumption of Red and/or Processed Meats

Various epidemiological studies have identified the consumption of processed and/or red meat as one of the risk factors for the development of CRC [19][20][24][30][31]. According to the WHO, it is the method of processing meat products that acts as a precursor to CRC. In this regard, the high-temperature processing of meat produces carcinogens such as N-nitroso or polycyclic aromatic hydrocarbons that are involved in the occurrence of malignant tumours, present in smoked, fried, or grilled meat (bacon, ham, hot dogs, etc.) [30].
However, another factor involved in the development of CRC is the method of preserving processed meat. Sodium nitrite, a preservative and colouring substance used in processed meats, could initiate or promote the development of preneoplastic lesions in the colon, as well as chronic intestinal inflammation [22][29][32]. In a study that followed 475,581 participants, those who consumed an average of 76 grammes of red and processed meat per day had a 20% higher risk of CRC compared to those who consumed 21 grammes in the same period [19].
On the contrary, Chang, Cotterchio, and Tinmouth (2021) did not obtain statistically significant results for the association between processed meat consumption and CRC. The study sample size could have been small, which could affect the results and consequently was lacking sufficient power to detect associations between these factors [24].

4. Fats Consumption

Regarding fat consumption, studies show a positive correlation between fat intake and increased proliferation of colon cells and associated risks [26][33]. In a clinical trial, a low-fat diet (20% of the energy from fat), a moderate-fat diet (30% of the energy from fat), and a high-fat diet (40% of the energy from fat) were compared. The result was an increase in intestinal flora associated with CRC in the high-fat diet group [19].
The type of fat ingested also plays a relevant role in the development of CRC. Fats known as healthy fats, such as polyunsaturated omega-3 fatty acids (PUFA), including alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), can act as protective agents against CRC due to their anti-inflammatory effect. EPA and DHA intake was inversely associated with an 11% and 12% lower risk of developing this pathology, respectively [19].
In contrast, saturated fatty acids were associated with tumorigenesis, and VLDL cholesterol, LDL cholesterol, triglycerides, and total cholesterol were positively correlated with the frequency of colon adenomas [22]. Furthermore, a positive association was found between industrial trans fatty acids (iTFA) and CRC, as they can play a mutagenic role, although meat trans fatty acids appear not to have an influence [20][23].

5. Alcohol Consumption

A study investigating the relationship between alcohol consumption and CRC showed that excessive alcohol consumption can increase the risk of developing it [34]. The data obtained in this study are consistent with those of other researchers such as Chang et al. or Xingcun et al. [24][34]. In the prospective cohort study conducted by Bradbury, Murphy, and Key (2020), each increase of 10 g/day in alcohol intake (equivalent to approximately half a pint of beer with 4.5% alcohol) was associated with an 8% increase in the risk of developing CRC [16].
Consumption of this substance diminishes the protection of the intestinal mucosa and alters the immune system. When ethanol reaches the intestine, it is converted into acetaldehyde, damaging cells. Additionally, it stimulates the secretion and synthesis of highly reactive oxygen species, damaging DNA and altering its methylation. This compound can also promote tumour growth through angiogenesis and immunosuppression, reducing the therapeutic effect of chemotherapy drugs. However, Mehrzad et al. (2020) did not find a statistically significant relationship between alcohol consumption and the risk of CRC, although the sample size was relatively small, so the results may not be very precise [31].

6. Other Related Factors

Regarding the impact of UPF on the microbiota and inflammation, additives such as saccharin and maltodextrin, commonly used in UPF, interact with the microbiota, promoting chronic intestinal inflammation or increasing bacteria, as argued previously. Nguyen et al. (2021) concluded that an increase in the sulphur microbial diet is associated with a higher risk of early onset adenomas in the colon and rectum [35].
Obesity is another risk factor, as this health condition is influenced by the type of diet and the patterns of physical activity. Authors like Zheng et al. (2020) and Mehrzad et al. (2020) showed that the BMI of individuals with CRC before their illness was significantly higher than that of those who did not have the disease [19][31]. Higher levels of BMI and waist circumference in adulthood are positively associated with the risk of CRC [19][20][21][22]. The overall risk of cancer death is 1.5 to 1.6 times higher in men and women with a BMI > 40 kg/m [34]. Furthermore, a correlation has been observed between a country’s development and the risk of CRC, the consumption of a fibre-rich diet, or age [32][35].


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