Whereas the mechanisms underlying the association of toxic dietary xenobiotics and cancer risk are not well established, it is plausible that dietary pattern may affect the colon environment by enhancing or reducing exposure to mutagens. This work aimed to investigate the association between xenobiotics intake and different stages of intestinal mucosal damage and colorectal cancer (CRC) screening and examine whether these associations may be mediated by altered intestinal mutagenicity. This was a case control study with 37 control subjects, 49 patients diagnosed with intestinal polyps, and 7 diagnosed with CRC. Lifestyle, dietary, and clinical information was registered after colonoscopy. For xenobiotics intake estimation the European Prospective Investigation into Cancer (EPIC) and the Computerized Heterocyclic Amines Resource for Research in Epidemiology of Disease (CHARRED) databases were used. The mutagenicity of fecal supernatants was assayed by the Ames test and light microscopy was used for the presence of aberrant crypt formation. Among all the potential carcinogens studied, the polyp group showed higher intakes of ethanol and dibenzo (a) anthracene (DiB(a)A). Besides, intakes between 0.75 and 1.29 µg/d of total polycyclic aromatic hydrocarbons (PAHs) were related with a higher risk of belonging to the polyp group. On the contrary, an intake of wholegrain cereals greater than 50 g/d was associated with a reduction in the relative risk of belonging to the polyp group. Heterocyclic amines (HAs) such as 2-amino-1-methyl-6-phenylimidazo (4,5,b) pyridine (PhIP) were associated with an increased level of mutagenicity in polyps. This study is of great interest for the identification of possible therapeutic targets for the early prevention of colon cancer through diet.

Background: Although xenobiotics from food processing have gained support as possible drivers of the relationship between diet and some types of cancer, there are still few studies characterizing the intake of these compounds among different populations. Aim: To describe the intake of heterocyclic amines (HAs), polycyclic aromatic hydrocarbons (PAHs), nitrates, nitrites, nitrosamines, and acrylamide; and to identify dietary and lifestyle related factors. Methods: This was a descriptive cross-sectional study in 70 adult volunteers. Intake was registered by means of a food frequency questionnaire, including cooking methods, temperature, and degree of browning. The European Prospective Investigation into Cancer (EPIC) and the Computerized Heterocyclic Amines Resource for Research in Epidemiology of Disease (CHARRED) databases were used for xenobiotic estimation in conjunction with data from the European Food Safety Authority (EFSA) and U.S. Food and Drug Administration (FDA). Results: Dietary HAs (amino-alpha-carboline (AαC), 2-amino-3-methylimidazo (4,5,f) quinoline (IQ), 2-amino-3,8 dimethylimidazo (4,5,f) quinoxaline (MeIQx), 2-amino-3,4,8 trime-thylimidazo (4,5,f) quinoxaline (DiMeIQx), and 2-amino-1-methyl-6-phenylimidazo (4,5,b) pyridine (PhIP)) were mainly derived from meat and meat products, while benzo (a) pyrene (B(a)P), dibenzo (a) anthracene (DiB(a)A), and total PAHs were explained by oils and fats, alcoholic beverages, and milk, respectively. Microwaved, fried, grilled, broiled, barbecued, and braised cooking methods were mainly responsible for HAs and PAHs consumption. Conclusion: Based on the wide presence and levels of intake of these compounds in different sources, more efforts should be made to adjust their intake to the levels recommended by health agencies.

Diet is a major modulator of gut microbiota, which plays a key role in the health status, including colorectal cancer (CRC) development.

Objectives: Although xenobiotics derived from food processing may cause modifications in the composition of the gut microbiota (GM) evidence is scarce. The aim of this study is to evaluate the impact of potential dietary carcinogens as heterocyclic amines (HAs), polycyclic aromatic hydrocarbons (PAHs), nitrates, nitrites, nitroso compounds and acrylamide, in combination to fibers (poly)phenols on the GM composition in a group of materially deprived subjects.Study design: Transversal observational study in a sample of 19 subjects recipients of Red Cross food aid. Dietary information was recorded by means of 3 non-consecutive 24 h recalls. Questions focused on the type of cooking and the extent of cooking and roasting were included. Information on potential carcinogens was mainly obtained from the European Prospective Investigation into Cancer and Nutrition (EPIC) and Computerized Heterocyclic Amines Resource for Research in Epidemiology of Disease (CHARRED) Carcinogen Databases. Microbial composition was determined by 16S ribosomal RNA gene sequencing in fecal samples.Results: Higher levels of Lachnospiraceae and Eggerthellaceae families were found in individuals consuming less than 50 ng/day of 2-amino-3,8 dimethylimidazo (4,5,f) quinoxaline (MeIQx) (considered as lower risk dose for colorectal adenoma) while those consuming more than 40 ng/day of 2-amino-1-methyl-6-phenylimidazo (4,5,b) pyridine (PhIP) (higher risk for colorectal adenoma) showed lower relative abundance of Muribaculaceae and greater presence of Streptococcaceae and Eubacterium coprostanoligenes group.Conclusion: The associations identified between diet and processing by-products on GM in this study could be used as potential targets for the designing of dietary interventions tailored to this collective.

Colorectal cancer (CRC) is among the leading causes of mortality in adults of both sexes worldwide, while breast cancer (BC) is among the leading causes of death in women. In addition to age, gender, and genetic predisposition, environmental and lifestyle factors exert a strong influence. Global diet, including alcohol consumption, is one of the most important modifiable factors affecting the risk of CRC and BC. Western dietary patterns promoting high intakes of xenobiotics from food processing and ethanol have been associated with increased cancer risk, whereas the Mediterranean diet, generally leading to a higher intake of polyphenols and fibre, has been associated with a protective effect. Gut dysbiosis is a common feature in CRC, where the usual microbiota is progressively replaced by opportunistic pathogens and the gut metabolome is altered. The relationship between microbiota and BC has been less studied. The estrobolome is the collection of genes from intestinal bacteria that can metabolize oestrogens. In a dysbiosis condition, microbial deconjugating enzymes can reactivate conjugated-deactivated oestrogens, increasing the risk of BC. In contrast, intestinal microorganisms can increase the biological activity and bioavailability of dietary phytochemicals through diverse microbial metabolic transformations, potentiating their anticancer activity. Members of the intestinal microbiota can increase the toxicity of xenobiotics through metabolic transformations. However, most of the microorganisms involved in diet-microbiota interactions remain poorly characterized. Here, we provide an overview of the associations between microbiota and diet in BC and CRC, considering the diverse types and heterogeneity of these cancers and their relationship between them and with gut microbiota.

Non-communicable diseases are particularly prevalent among low-income individuals and are associated with the consumption of processed foods, fat, and sugars. This work aims to evaluate the impacts of a nutrition education intervention for low socio-economic individuals on sensory perception, health-related parameters and gut microbiota. Twenty low-income adults underwent a 4-week intervention. Dietary information (three 24 h recalls), detection thresholds and discrimination scores (salty and sweet), and severity of depressive symptoms (Beck Depression Inventory-II (BDI-II)) were collected. Fecal microbial composition and short chain fatty acids were determined by 16S ribosomal RNA-gene sequencing and gas chromatography, respectively. After the intervention, 35% of subjects presented higher compliance with dietary recommendations, increased consumption of vegetables and lignans and reduced consumption of processed meats and nitrosamines, together with depleted levels of Actinomycetota. Higher discrimination for salty and sweet and lower BDI-II scores were also obtained. This nutrition education intervention entailed changes in dietary intake towards healthier food options, reduced potentially carcinogenic compounds and improved scores for discrimination and severity of depressive symptoms. The confirmation of these results in future studies would enable the design of strategic policies contributing to the optimal nutrition of materially deprived families through affordable healthy plant-based interventions.