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Association of Retinol and Carotenoids Content in Diet and Serum With Risk for Colorectal Cancer: A Meta-Analysis.
Han, X, Zhao, R, Zhang, G, Jiao, Y, Wang, Y, Wang, D, Cai, H
Frontiers in nutrition. 2022;9:918777
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The incident rate of malignant tumours has been increasing, and so has colo-rectal cancer (CRC), which is now the third most frequent cancer and the second most common cause of cancer death. CRC development is influenced by environmental and genetic factors. Diet, diabetes, obesity, lack of physical activity, age, family history and history of benign adenomatous polyps and inflammatory bowel disease are all known risk factors. Modulating diet is one way to modify cancer risk. Vitamin A (retinol) and carotenoids, which are precursors to Vitamin A, are indispensable in the human body and widely occur in a range of vegetables, fruits and animal-derived foods. In some studies high dietary intake of retinol and carotenoids had been linked to a decreased risk of CRC, however, this was not consistent in all findings. To get a better understanding of this matter, the authors of this meta-analysis analysed 22 clinical studies from the last 20 years. The authors found an inverse association with carotenoids in blood serum, so higher blood serum of carotenoids seemed to decrease CRC risk. In regards to dietary intake, total carotenoid intake did not increase CRC risk and in fact the carotenoids carotenes, lycopene, and β-cryptoxanthin reduced risk, which was particularly noticeable in men. In women, high dietary intake of retinol also showed to reduce CRC risk, but it appeared to increase the risk in men. This raised the idea of gender-specific differences. Of clinical relevance are that carotenoids can be an important dietary contributors in reducing CRC risk. However the protective role of retinol appears to be gender-specific and only seems to benefit women, with the opposite effect in men.
Expert Review
Conflicts of interest:
None
Take Home Message:
The results of this study were mixed:
- Total dietary intake of carotenoids was not associated with CRC risk.
- Case control studies found that high serum carotenoids may increase CRC risk.
- There were differences in findings between males and females.
- Larger, well-controlled studies over long time frames are needed to further explore the relationship between dietary intake and serum concentrations of carotenoids and retinol with CRC. These studies should include results by sex, race and dose response.
Evidence Category:
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X
A: Meta-analyses, position-stands, randomized-controlled trials (RCTs)
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B: Systematic reviews including RCTs of limited number
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C: Non-randomized trials, observational studies, narrative reviews
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D: Case-reports, evidence-based clinical findings
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E: Opinion piece, other
Summary Review:
Colorectal cancer (CRC) is the third most common cancer worldwide, and second in terms of mortality. Diet and environmental factors may have a strong influence and causative effect. Research has linked dietary consumption and serum levels of carotenoids and retinol with CRC. However, results have been mixed.
The aim of this meta analysis was to identify a potential association between CRC and carotenoid and retinol intake. A total of 22 cohort and case control studies published between 2000-2019 from across Europe, North America and Asia were included. The number of CRC cases totalled 19,293 from a sample of more than 450,000 people.
Eligible studies reported data in either relative risk (RR) or odds ratios (OR) with 95% confidence intervals (95% CI). In the meta analysis, data were combined and expressed as OR with 95% CI.
Cases and control groups were based on high or low carotenoid intake as defined by the included studies and based on dietary intake or serum concentration. Sub-group analysis was undertaken by study type, sex and tumour type. A sensitivity analysis tested the robustness of the results.
Due to the heterogeneity between studies, adjustments were made for potential covariates and confounding factors including age, gender, a family history of CRC, smoking, alcohol consumption and levels of physical activity.
The quality of the studies was assessed against predefined inclusion and exclusion criteria and scored using the Newcastle-Ottawa Scale (NOS).
The nutrients studied included; beta-carotene, alpha-carotene, lycopene, lutein/zeaxanthin, beta-cryptoxanthin and retinol. These were assessed through dietary intake or serum concentrations.
Key Findings
- High dietary intake of beta-carotene was not associated with an increased risk of CRC in females (OR = 0.97; 95%CI 0.79-1.19), however, it may lower CRC risk in males (OR = 0.74; 95% CI 0.55-0.99).
- High dietary intake of retinol was not associated with CRC risk (OR = 0.99; 95% CI 0.89-1.10). However, the findings suggested that it may reduce CRC risk in females but increase CRC risk in males.
- There was a tendency towards a slightly decreased risk of CRC with high dietary intakes of alpha-carotene), lycopene, and beta-cryptoxanthin. The results were more pronounced in males.
- No association was found between high consumption of high lutein/zeaxanthin, retinol or total carotenoids and the risk of CRC
- Case control studies found a negative association between serum carotenoids and CRC risk. This relationship was not found in cohort studies and therefore remains uncertain.
Conclusions
This was a well-conducted meta-analysis that was not subject to any conflicts of interest. Larger, well controlled prospective studies adjusting for sex and with long-term follow-up are needed to confirm the relationship between dietary intake and serum levels of carotenoids and CRC.
Notes: The authors had no conflicts of interest to disclose.
Clinical practice applications:
- Healthcare practitioners working with people with a family history of CRC or those who may be at increased risk may like to consider increasing carotenoid intake modestly.
- A modest increase in dietary intake of beta-carotene for males may be beneficial.
- A modest increase in dietary retinol may be beneficial for females.
Considerations for future research:
- Further research is needed to explore the differences between sexes for dietary intake of carotenoids and retinol and CRC risk
- Further studies are needed to investigate the relationship between serum carotenoids and CRC
- Analysis of results by race and continent may be beneficial
- Further research is needed to define dose response
- Due to heterogeneity between studies, large, well controlled studies over long time frames are needed
Abstract
Background: Colorectal cancer (CRC) risk is linked to serum and dietary retinol and carotenoids, according to clinical and epidemiological research. However, the findings are not consistent. As a result, we did this meta-analysis to determine the link between them. Methods: From 2000 through 2022, the PubMed, Web of Science, and Embase databases, as well as pertinent article references, were searched and filtered based on inclusion and exclusion criteria and literature quality ratings. High and low intake were used as controls, and OR (odds ratio) or RR (relative risk) and 95% confidence interval were extracted. The extracted data were plotted and analyzed using Stata12.0 software. Results: A total of 22 relevant studies were included, including 18 studies related to diet and 4 studies related to serum. For high and low intake or concentration controls, the pooled OR was as follows: β-carotene (OR = 0.89, 95% CI: 0.78-1.03), α-carotene (OR = 0.87, 95% CI: 0.72-1.03), lycopene (OR = 0.93, 95% CI: 0.81-1.07), lutein/zeaxanthin (OR = 0.96, 95% CI: 0.87-1.07), β-cryptoxanthin (OR = 0.70, 95% CI: 0.48-1.01), total carotenoids (OR = 0.97, 95% CI: 0.81-1.15), retinol (OR = 0.99, 95% CI: 0.89-1.10), serum carotenoids (OR = 0.73, 95% CI: 0.58-0.93), serum retinol (OR = 0.62, 95% CI: 0.26-1.49). Subgroup analysis was performed according to tumor type, study type and sex. Conclusion: Total carotenoid intake and Lutein/Zeaxanthin intake were not associated with CRC risk. High β-carotene, α-carotene, lycopene, and β-cryptoxanthin all tended to reduce CRC risk. Serum carotenoid concentrations were significantly inversely associated with CRC risk.
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Sedentary behavior and cancer-an umbrella review and meta-analysis.
Hermelink, R, Leitzmann, MF, Markozannes, G, Tsilidis, K, Pukrop, T, Berger, F, Baurecht, H, Jochem, C
European journal of epidemiology. 2022;37(5):447-460
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Globally, cancer is one of the leading causes of death. In modern day-to-day life, sedentary behaviour is prevalent, with adults spending an average of 8.2 hours without any physical activity. It is believed that sedentary behaviour plays a significant role in the increase in all-cause mortality, obesity, chronic diseases, and cancer risk. The purpose of this review and meta-analysis was to examine previous studies that reported associations between sedentary behaviour and cancer incidence and all-cancer mortality. A total of 14 meta-analyses were included in the study, and the strength of the evidence for each association was rated. A significant association was found between sedentary behaviour and cancer incidence across various cancer sites, including ovarian, endometrial, colon, breast, rectal, and prostate cancers. All-cancer mortality also showed positively significant associations with sedentary behaviour. There is a need for further research to evaluate the mechanisms associated with sedentary behaviour and the development of cancer at various sites. However, the results of this study can be used by healthcare professionals to better understand the importance of recommending physical activity and other therapeutic strategies.
Abstract
Several systematic reviews and meta-analyses have summarized the association between sedentary behavior (SB) and cancer. However, the level of evidence and the potential for risk of bias remains unclear. This umbrella review summarized the current data on SB in relation to cancer incidence and mortality, with a particular emphasis on assessing the risk of bias. We searched PubMed, Web of Science and Cochrane Database for systematic reviews and meta-analyses on the association between SB and cancer incidence and mortality. We also searched for recent observational studies not yet included in existing meta-analyses. We re-calculated summary risk estimates for cancer incidence and mortality using random effects models. We included 14 meta-analyses covering 17 different cancer sites from 77 original studies. We found that high SB levels increase the risk for developing ovarian, endometrial, colon, breast, prostate, and rectal cancers, with relative risks of 1.29 (95% confidence interval (CI) = 1.08-1.56), 1.29 (95% CI = 1.16-1.45), 1.25 (95% CI = 1.16-1.33), 1.08 (95% CI = 1.04-1.11), 1.08 (95% CI = 1.00-1.17), and 1.07 (95% CI = 1.01-1.12), respectively. Also, we found an increased risk of cancer mortality of 1.18 (95% CI = 1.09-1.26). Most associations between SB and specific cancer sites were supported by a "suggestive" level of evidence. High levels of SB are associated with increased risk of several types of cancer and increased cancer mortality risk.
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Salmonella Infection in Chronic Inflammation and Gastrointestinal Cancer.
Zha, L, Garrett, S, Sun, J
Diseases (Basel, Switzerland). 2019;7(1)
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Salmonella is a group of bacteria that is normally associated with food poisoning. In 2% to 5% of people with Salmonella food poisoning, the bacteria remain in the body, leading to long-term infection, which has been linked to various health problems. This literature review looked at the link between Salmonella infection and the development of diseases such as inflammatory bowel disease (IBD), gall bladder cancer and colon cancer. The authors describe how long-term Salmonella infection plays a role in several biological processes, such as stem cell maintenance, host cell transformation, and gut dysbiosis. Leaky gut, dysbiosis and inflammation are induced by the bacteria and contribute to the development of cancer. The authors conclude that more studies are needed to further understand the relationship between Salmonella infections and the risk of colon cancer.
Abstract
Salmonella not only causes acute infections, but can also cause patients to become chronic "asymptomatic" carriers. Salmonella has been verified as a pathogenic factor that contributes to chronic inflammation and carcinogenesis. This review summarizes the acute and chronic Salmonella infection and describes the current research progress of Salmonella infection contributing to inflammatory bowel disease and cancer. Furthermore, this review explores the underlying biological mechanism of the host signaling pathways manipulated by Salmonella effector molecules. Using experimental animal models, researchers have shown that Salmonella infection is related to host biological processes, such as host cell transformation, stem cell maintenance, and changes of the gut microbiota (dysbiosis). Finally, this review discusses the current challenges and future directions in studying Salmonella infection and its association with human diseases.
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Coffee Consumption and Risk of Colorectal Cancer: A Systematic Review and Meta-Analysis of Prospective Studies.
Sartini, M, Bragazzi, NL, Spagnolo, AM, Schinca, E, Ottria, G, Dupont, C, Cristina, ML
Nutrients. 2019;11(3)
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Coffee is the second most widely consumed drink worldwide, after water. It contains many active compounds that affect the health and functioning of the digestive tract. Previous population studies on the relationship between coffee consumption and cancer prevention have had mixed results. The aim of this systematic review and meta-analysis was to provide an up to date summary of the relationship between coffee consumption and the risk of colorectal cancer. The authors looked at 26 prospective studies. When results from the 26 studies were pooled, no significant relationship between coffee consumption and colorectal cancer was found. The researchers then looked at the results by ethnicity and found a protective effect for coffee on colorectal cancer in people from the US. For colon cancer, coffee was protective in men and women combined and in men alone, regardless of ethnicity. When the results were separated according to ethnicity, a significant protective effect was noted in European men and in Asian women. There was no association between coffee consumption and rectal cancer. Decaffeinated coffee demonstrated a protective effect against colorectal cancer in both men and women. The authors concluded that ethnicity could explain the mixed results of previous studies. Further research is needed into the relationship between a person’s genetic make-up and the risk of colorectal cancer associated with coffee.
Abstract
Coffee is a blend of compounds related to gastrointestinal physiology. Given its popularity and the epidemiology of colorectal cancer, the impact of this beverage on public health could be considerable. Our aim was to provide an updated synthesis of the relationship between coffee consumption and the risk of colorectal cancer. We conducted a systematic review and meta-analysis of 26 prospective studies. Regarding colorectal cancer, no significant relationship was detected. Stratifying for ethnicity, a protective effect emerged in US subjects. Concerning colon cancer, coffee proved to exert a protective effect in men and women combined and in men alone. Stratifying for ethnicity, a significant protective effect was noted in European men only and in Asian women only. Concerning rectal cancer, no association was found. Decaffeinated coffee exhibited a protective effect against colorectal cancer in men and women combined. Studies were appraised for their quality by means of the Newcastle-Ottawa Quality Assessment Scale for Cohort studies. Only one study proved to be of low quality. Ethnicity could explain the heterogeneity of the studies. However, little is known about the relationship between the genetic make-up and the risk of colorectal cancer associated with coffee. Further research is warranted.
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Dietary Inflammatory Index, Dietary Non-Enzymatic Antioxidant Capacity, and Colorectal and Breast Cancer Risk (MCC-Spain Study).
Obón-Santacana, M, Romaguera, D, Gracia-Lavedan, E, Molinuevo, A, Molina-Montes, E, Shivappa, N, Hebert, JR, Tardón, A, Castaño-Vinyals, G, Moratalla, F, et al
Nutrients. 2019;11(6)
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This study aims to correlate the risk factors of inflammation and antioxidant capacity in cases of colon and breast cancer, using data from a large Spanish case-controlled study (1852 colon cancer subjects, 1567 breast cancer subjects and a total 4933 controls). The role of diet in colon cancer is widely accepted, however it is more controversial with breast cancer where genetic mutations and other lifestyle factors are cited as primary risk factors. What unites these cancers is the inter-related presence of both inflammation and oxidative stress. The dietary inflammatory index (DII®) and non-enzymatic antioxidant capacity (NEAC) were used to evaluate inflammation and oxidative stress using 30 nutrient parameters and 6 inflammatory blood markers. The results showed that colon cancer subjects typically ate a more pro-inflammatory diet compared to controls, with a higher odds ratio of men to women, and tended to be older, heavier and less physically active. The breast cancer subjects also had higher inflammatory scores versus controls but demographically were younger, premenopausal, frequently with a first-degree family link to breast cancer, and including a higher percentage of smokers. For both cancers, inflammation significantly and statistically increased risk factors. Adding in oxidative stress results showed a statistically higher risk of developing colon cancer whilst in breast cancer subjects the risk was increased but non-statistically valid. They did report that meat-eaters had a relative 9% increased risk of Breast cancer. Overall the study concluded that dietary components of inflammation and oxidative stress increased risk of colon cancer but were not statistically valid for breast cancer.
Abstract
Inflammation and antioxidant capacity have been associated with colorectal and breast cancer. We computed the dietary inflammatory index (DII®), and the total dietary non-enzymatic antioxidant capacity (NEAC) and associated them with colorectal and breast cancer risk in the population-based multi case-control study in Spain (MCC-Spain). We included 1852 colorectal cancer and 1567 breast cancer cases, and 3447 and 1486 population controls, respectively. DII score and NEAC were derived using data from a semi-quantitative validated food frequency questionnaire. Unconditional logistic regression models were used to estimate odds ratios (OR) and 95% confidence intervals (95%CI) for energy-adjusted DII (E-DII), and a score combining E-DII and NEAC. E-DII was associated with colorectal cancer risk (OR = 1.93, highest quartile versus lowest, 95%CI:1.60-2.32; p-trend: <0.001); this increase was observed for both colon and rectal cancer. Less pronounced increased risks were observed for breast cancer (OR = 1.22, highest quartile versus lowest, 95%CI:0.99-1.52, p-trend: >0.10). The combined score of high E-DII scores and low antioxidant values were associated with colorectal cancer risk (OR = 1.48, highest quartile versus lowest, 95%CI: 1.26-1.74; p-trend: <0.001), but not breast cancer. This study provides evidence that a pro-inflammatory diet is associated with increased colorectal cancer risk while findings for breast cancer were less consistent.
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Effect of ω-3 polyunsaturated fatty acid-supplemented parenteral nutrition on inflammatory and immune function in postoperative patients with gastrointestinal malignancy: A meta-analysis of randomized control trials in China.
Zhao, Y, Wang, C
Medicine. 2018;97(16):e0472
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Omega-3 polyunsaturated fatty acids (PUFAs) can have a beneficial effect on inflammation and immune function. This meta-analysis looked at the effectiveness of omega-3 PUFAs on inflammatory and immune function in patients with stomach or colorectal cancers, following surgery. 16 Chinese randomised controlled trials with over 1000 patients carried out between 2000 and 2017 were included in the analysis. The researchers found that the numbers of immune cells in the omega-3 group were significantly higher than those in the control group. The levels of antibodies in people given omega-3 were significantly higher than those in the control group. Inflammatory markers in the omega-3 group were significantly lower. Those given omega-3 were 64% less likely to experience post-surgical infections. The result of this meta-analysis confirmed that supplementing gastrointestinal cancer patients with omega-3 improves post-surgery indicators of immune function, reduces inflammation, and reduces infections related to surgery. The authors recommend that omega-3 should be added to the nutrition formula given to gastrointestinal cancer patients following surgery.
Abstract
BACKGROUND There are no consensus regarding the efficacy of omega-3polyunsaturated fatty acids (PUFAs) on inflammatory and immune function in postoperative patients with gastrointestinal malignancy. METHODS The literatures published randomized control trials (RCT) were searched in PubMed, Embase, Scopus, Cochrane Library, CNKI, Weipu, and Wanfang Databases. The immune efficacy outcomes of ω-3 polyunsaturated fatty acid-supplemented parenteral nutrition in patients with gastrointestinal malignancy were compared. RESULTS Sixteen RCTs involving 1008 patients (506 in the omega-3 group, 502 in the control group) were enrolled into the analysis. The results of meta-analysis: the cell immunity: The proportions of CD3, CD4, CD4/CD8 in the omega-3 group were significantly higher than those in the control group (CD3: WMD = 4.48; 95% CI, 3.34-5.62; P < .00001; I = 0%; CD4: WMD = 5.55; 95% CI, 4.75-6.34; P < .00001; I = 0%; CD4/CD8: WMD = .28; 95% CI, 0.13-0.44; P = .0004; I = 81%). In the humoral immunity: The levels of IgA, IgM and IgG in the omega-3 group were significantly higher than those in the control group (IgA: WMD = 0.31; 95% CI, 0.25-0.37; P < .00001; I = 0%; IgM: WMD = 0.12; 95% CI, 0.06-1.81; P < .00001; I = 0%; IgG: WMD = 1.19; 95% CI, 0.80-1.58; P < .00001; I = 0%). The count of lymphocyte in the omega-3 group was significantly higher than that in the control group (WMD = 0.22; 95% CI, 0.12-0.33; P < .0001; I = 40%). In the postoperative inflammatory cytokine: The levels of interleukin-6, tumor necrosis factor (TNF)-α and C-reactive protein in the omega-3 group were significantly lower than those in the control group (IL-6: WMD = -3.09; 95% CI, -3.91 to 2.27; P < .00001; I = 45%; TNF-α: WMD = -1.65; 95% CI, -2.05 to 1.25; P < .00001; I = 28%; CRP: WMD = -4.28; 95% CI, -5.26 to 3.30; P < .00001; I = 37%). The rate of postoperative infective complications in the omega-3 group was significantly lower than that in the control group (OR = 0.36; 95% CI, 0.20-0.66; P = .0008; I = 0%). CONCLUSION This meta-kanalysis confirmed that early intervention with Omega -3 fatty acid emulsion in gastrointestinal cancer can not only improve the postoperative indicators of immune function, reduce inflammatory reaction, and improve the postoperative curative effect but also improve the immune suppression induced by conventional PN or tumor. Therefore, postoperative patients with gastrointestinal cancer should add omega-3 unsaturated fatty acids in their PN formula. Further high-quality RCTs are needed to verify its efficacy.
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Associations between genes in the one-carbon metabolism pathway and advanced colorectal adenoma risk in individuals with low folate intake.
Han, SS, Sue, LY, Berndt, SI, Selhub, J, Burdette, LA, Rosenberg, PS, Ziegler, RG
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. 2012;21(3):417-27
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Colorectal cancer is the third most common cancer and third leading cause of cancer-related death in the US. Folate is essential for one-carbon metabolism, a pathway required by DNA synthesis, methylation, and repair. The aim of this study was to investigate associations between the risk of colorectal cancer and genes involved in one-carbon metabolism. Scientists looked at the folate intake, folate levels and genes of 500 people with advanced colorectal adenomas (benign tumours that have a high risk of becoming cancerous), and compared them to 500 healthy controls. Estimates of folate intake were based on a food frequency questionnaire which was completed by participants at the baseline of the study. Blood folate levels were also measured. People with the lowest intake of folate in their diets (0 to 262 micrograms/day) were at a 46% increased risk of advanced colorectal adenoma compared to people with the highest intakes (more than 466 micrograms/day). For those with the lowest intakes only, variations in several genes including adenosine deaminase (ADA) and cysteine dioxygenase (CDO1) were associated with adenoma risk. There were no associations between gene variations and adenoma risk in people with higher intakes of folate. The authors concluded that folate intake may interact with variations in one-carbon metabolism genes to modify colorectal adenoma risk.
Abstract
BACKGROUND Folate is essential for one-carbon metabolism, a pathway required by DNA synthesis, methylation, and repair. Low dietary and circulating folate and polymorphic variation in this pathway are associated with increased risk of colorectal adenoma and cancer. METHODS We genotyped 882 single nucleotide polymorphisms (SNP) in 82 one-carbon metabolism genes for 1,331 cases of advanced colorectal adenoma, identified by sigmoidoscopy at baseline, and 1,501 controls from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO). We evaluated associations between one-carbon genes and adenoma risk in all subjects and stratified by folate intake. We applied the Adaptive Rank Truncated Product (ARTP) method to assess statistical significance at the gene and pathway levels. RESULTS Folate intake was inversely associated with advanced colorectal adenoma risk [odds ratio (OR) by quartile = 0.85, P = 1.9 × 10(-5)]. We found no statistically significant associations between one-carbon genes and adenoma risk in all subjects. As hypothesized, we observed a statistically significant pathway-level association (P = 0.038) in the lowest quartile of folate; no significant associations were found in higher quartiles. Several genes including adenosine deaminase (ADA) and cysteine dioxygenase (CDO1) contributed to this signal (gene-level P = 0.001 and 0.0073, respectively). The most statistically significant SNP was rs244072 in ADA (P = 2.37 × 10(-5)). CONCLUSIONS AND IMPACT Stratification by dietary folate and application of the ARTP method revealed statistically significant pathway- and gene-level associations between one-carbon metabolism genes and risk of advanced colorectal adenoma, which were not apparent in analysis of the entire population. Folate intake may interact with associations between common variants in one-carbon metabolism genes and colorectal adenoma risk.