Objective To explore the associations between metabolic syndrome (MetS) and its individual components and the risk of rheumatoid arthritis (RA). Methods A total of 369,065 individuals were included in the present study based on the UK Biobank. Multivariable Cox proportional hazards regression models were applied to estimate the associations between MetS and its individual components and the risk of RA. Mediation analysis was performed to further assess the potential mediating role of C-reactive protein (CRP) in the relationship between MetS and RA. Results During a median follow-up period of 12.04 years, a total of 4901 incident RA cases were documented. MetS (hazard ratio [HR] 1.22, 95% CI 1.14-1.30) and 4 of its 5 components (elevated waist circumference [WC; HR 1.21, 95% CI 1.12-1.32], elevated triglyceride [TG] level [HR 1.12, 95% CI 1.05-1.19], reduced high-density lipoprotein cholesterol [HDL-C] level [HR 1.31, 95% CI 1.23-1.39], and hyperglycemia [HR 1.15, 95% CI 1.05-1.25]) were associated with an increased risk of RA. In addition, the risk of RA increased as the number of diagnosed MetS components increased, with the highest risk in participants with all 5 components. Mediation analysis showed that CRP might mediate the association between MetS and RA, accounting for 9.27% of the total effect. Conclusion These findings indicated positive associations between MetS and 4 of its components (WC, TG, HDL-C, and hyperglycemia) and the risk of RA, highlighting the importance of MetS management in the prevention of RA.

BACKGROUND:Limited research has been conducted on the association between long-term exposure to air pollutants and the incidence of gout. OBJECTIVES:This study aims to assess the individual and combined effects of prolonged exposure to five air pollutants (NO2, NOx, PM10, PMcoarse and PM2.52) on the incidence of gout among 458,884 initially gout-free participants enrolled in the UK Biobank. METHODS:Employing a land use regression model, we utilized an estimation method to ascertain the annual concentrations of the five air pollutants. Subsequently, we devised a weighted air pollution score to facilitate a comprehensive evaluation of exposure. The Cox proportional hazards model was utilized to investigate the association between ambient air pollution and gout risk. Interaction and stratification analyses were conducted to evaluate age, sex, BMI, and genetic predisposition as potential effect modifiers in the air pollution-gout relationship. Furthermore, mediation analyses were conducted to explore the potential involvement of biomarkers in mediating the association between air pollution and gout. RESULTS:Over a median follow-up time of 12.0 years, 7,927 cases of gout were diagnosed. Significant associations were observed between the risk of gout and a per IQR increase in NO2 (HR3: 1.05, 95 % CI4: 1.02-1.08, p = 0.003), NOx (HR: 1.04, 95 % CI: 1.01-1.06, p = 0.003), and PM2.5 (HR: 1.03, 95 % CI: 1.00-1.06, p = 0.030). Per IQR increase in the air pollution score was associated with an elevated risk of gout (p = 0.005). Stratified analysis revealed a significant correlation between the air pollution score and gout risk in participants ≥60 years (HR: 1.05, 95 % CI: 1.02-1.09, p = 0.005), but not in those <60 years (p = 0.793), indicating a significant interaction effect with age (p-interaction=0.009). Mediation analyses identified five serum biomarkers (SUA:15.87 %, VITD: 5.04 %, LDLD: 3.34 %, GGT: 1.90 %, AST: 1.56 %5) with potential mediation effects on this association. CONCLUSIONS:Long-term exposure to air pollutants, particularly among the elderly population, is associated with an increased risk of gout. The underlying mechanisms of these associations may involve the participation of five serum biomarkers.

PurposeThis study aimed to explore the clinical characteristics of male breast cancer (MBC) patients and the factors influencing their prognosis.MethodsWe conducted a retrospective case series analysis of 117 MBC cases who were treated at Zhejiang Cancer Hospital from 2009 to 2022. Cox proportional hazard model was used to identify prognostic factors of MBC. Nomogram was constructed based on these factors, which was further evaluated by C-index and calibration curves.ResultsA total of 115 MBC cases were finally included in our analyses, with median diagnosis age of 59 years. Of these cases, 80.0% were estrogen receptor (ER) positive, 79.2% were progesterone receptor (PR) positive, 48.7% were human epidermal growth factor receptor 2 (HER2) negative, and 42.6% had Ki67 levels higher than 15%. 108 (93.9%) cases underwent radical mastectomy, while only 3 (2.6%) received breast-conserving surgery. The Logrank test suggested that lymphocyte-to-monocyte ratio (LMR) was negatively associated with both overall survival (OS) and disease-free survival (DFS) of MBC, while platelet-to-lymphocyte ratio (PLR) and neutrophil-to-lymphocyte ratio (NLR) were only positively associated with OS (all P-values < 0.05). Multivariate regression analysis showed that age (HR 1.08, 95% CI 1.03-1.13) was significant prognostic factors for OS. Meanwhile, age (HR 1.06, 95% CI 1.02-1.10), histological differentiation grade (poorly differentiated/undifferentiated vs. well-differentiated: HR 2.55, 95% CI 1.05-6.17), and TNM stage (IV vs. I: HR 31.59, 95% CI 6.01-165.93) were also significant prognostic factors for DFS. Nomograms were developed for DFS, with C-indexes of 0.782, indicating good predictive performance.ConclusionIncreased age, bigger tumor size, higher TNM stage, and lower histological differentiation grade were associated with poor MBC prognosis, and LMR, PLR, and NLR might be potential predictors for MBC prognosis.

Objective To investigate the associations of sleep behaviors with the risk of rheumatoid arthritis, and whether the associations differ among individuals with low, intermediate, or high genetic risk. Methods We included participants who were free of rheumatoid arthritis at baseline based the UK Biobank. We evaluated the associations of five sleep behaviors with the risk of rheumatoid arthritis using Cox proportional hazard regression models. We then generated a sleep risk score which combined five sleep behaviors and assessed its association with the risk of rheumatoid arthritis. We finally generated a genetic risk score and examined the joint effects of sleep patterns and genetic susceptibility on the risk of rheumatoid arthritis. Results Of the 375,133 participants at baseline, 4913 incident rheumatoid arthritis cases were identified over a median follow-up of 11.73years. We found that insomnia and daytime sleepiness were associated with a 33% and a 38% increased risk of rheumatoid arthritis. A U-shaped association was observed between sleep duration and the risk of rheumatoid arthritis, with a 29% higher risk for those with short sleep and a 30% higher risk for those with long sleep. Participants with unfavorable sleep patterns had a 63% increased risk of rheumatoid arthritis compared with those with favorable sleep patterns. Participants with unfavorable sleep patterns and high genetic risk showed the highest risk of rheumatoid arthritis although no statistically significant multiplicative or additive interaction was found. Conclusions Our study suggested that insomnia, daytime sleepiness, and short or long sleep duration, as well as sleep risk score were associated with an increased risk of rheumatoid arthritis.

A proposed model for LCHF-diet alleviated ALD.

ObjectiveAlthough previous studies have explored the association of drinking with gout risk, we sought to explore the dose-response relationship and the evidence between subtypes of alcoholic beverages and gout risk.MethodsThe weekly alcoholic beverage consumption of patients in the UK Biobank was collected and calculated. The Cox regression model was applied to assess the effects of drinking alcohol in general and its subtypes on gout risk by calculating the hazard ratio (HR) and 95% CIs. Additionally, the restricted cubic splines were used to estimate the dose-response relationship between alcohol consumption and gout risk. To evaluate the robustness, we performed subgroup analysis across various demographic characteristics.ResultsDuring a mean follow-up period of 11.7 years, a total of 5728 new incident gout cases were diagnosed among 331,865 participants. We found that light alcohol consumption was linked to a slight decrease in gout incidence among female individuals (HR 0.78, 95% CI 0.65-0.94,P= 0.01), whereas there was no significant association in male individuals. Moreover, the dose-response relationship showed that drinking light red wine and fortified wine could reduce the gout risk, whereas beer or cider, champagne or white wine, and spirits increased the gout risk at any dose.ConclusionOur study suggested a J-shaped dose-response relationship between drinking and gout risk in female individuals, but not in male individuals. For specific alcoholic beverages, light consumption of red wine and fortified wine was associated with reduced gout risk. These findings offer new insights into the roles of alcoholic beverages in gout incidence risk, although further validation is warranted.

This study aimed to investigate the associations between carbohydrate intake and gout risk, along with interactions between genetic susceptibility and carbohydrates, and the mediating roles of biomarkers. We included 187,387 participants who were free of gout at baseline and completed at least one dietary assessment in the UK Biobank. Cox proportional hazard models were used to estimate the associations between carbohydrate intake and gout risk. Over a median follow-up of 11.69 years, 2548 incident cases of gout were recorded. Total carbohydrate intake was associated with a reduced gout risk (Q4 vs. Q1: HR 0.67, 95% CI 0.60–0.74), as were total sugars (0.89, 0.80–0.99), non-free sugars (0.70, 0.63–0.78), total starch (0.70, 0.63–0.78), refined grain starch (0.85, 0.76–0.95), wholegrain starch (0.73, 0.65–0.82), and fiber (0.72, 0.64–0.80), whereas free sugars (1.15, 1.04–1.28) were associated with an increased risk. Significant additive interactions were found between total carbohydrates and genetic risk, as well as between total starch and genetic risk. Serum urate was identified as a significant mediator in all associations between carbohydrate intake (total, different types, and sources) and gout risk. In conclusion, total carbohydrate and different types and sources of carbohydrate (excluding free sugars) intake were associated with a reduced risk of gout.

Background Though accumulated evidence has indicated an inverse relationship between alcohol intake and rheumatoid arthritis (RA) risk, it remained uncertain whether such association was causal or biased by confounding. We aimed to explore the dose-response relationship and the potential causality between alcohol consumption and RA risk by using both prospective study and Mendelian randomization (MR). Methods We first performed an updated meta-analysis on the association between alcohol consumption and the RA risk in PubMed and Web of Science database. Then we assessed the association of alcohol intake-related phenotypes with RA risk based on UK Biobank. The association was examined using Cox regression, while the potential non-linear relationship was modeled by restricted cubic splines (RCS). Stratification analyses based on sex, age, and ethnicity, as well as a series of sensitivity analyses were further performed. In addition, linkage disequilibrium score regression (LDSC) was used to calculate the heritability and genetic correlation between these traits, and two-sample MR was employed to assess the association of genetically predicted alcohol consumption with the risk of RA. Results Findings from the meta-analysis suggested an inverse association between alcohol intake and RA (relative risk (RR): 0.85; 95% confidence interval (CI): 0.78, 0.83). Similarly, in UK Biobank cohort, one standard deviation increases of alcohol intake per day was related to a 6% lower risk of RA (hazard ratio (HR): 0.94; 95% CI: 0.91, 0.97). RCS models revealed a J-shaped dose-response association between alcohol consumption and RA, with moderate intake associated with a reduced risk. However, alcohol use disorder (AUD) was associated with a 30% higher risk of RA (HR: 1.30; 95% CI: 1.08, 1.56). A sex- and age-dependent association of alcohol intake and RA was observed in stratification analysis. Findings from LDSC and MR both suggested AUD as a potential risk factor for RA, while no statistically significant association between alcohol consumption and RA was observed. Conclusion Our study revealed a dose- and sex- dependent pattern of alcohol consumption on RA risk. Though a slightly protective effect was observed during a specific range of alcohol consumption, it should not be recommended as a prevention strategy for RA.

A comprehensive overview of the associations between air pollution and the risk of gastrointestinal (GI) diseases has been lacking. We aimed to examine the relationships of long-term exposure to ambient particulate matter (PM) with aerodynamic diameter ≤2.5 μm (PM2.5), 2.5-10 μm (PMcoarse), ≤10 μm (PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOx), with the risk of incident GI diseases, and to explore the interplay between air pollution and genetic susceptibility. A total of 465,703 participants free of GI diseases in the UK Biobank were included at baseline. Land use regression models were employed to calculate the residential air pollutants concentrations. Cox proportional hazard models were used to evaluate the associations of air pollutants with the risk of GI diseases. The dose-response relationships of air pollutants with the risk of GI diseases were evaluated by restricted cubic spline curves. We found that long-term exposure to ambient air pollutants was positively associated with the risk of peptic ulcer (PM2.5 : Q4 vs. Q1: hazard ratio (HR) 1.272, 95% confidence interval (CI) 1.179-1.372, NO2: 1.220, 1.131-1.316, and NOx: 1.277, 1.184-1.376) and chronic gastritis (PM2.5: 1.454, 1.309-1.616, PM10 : 1.232, 1.112-1.366, NO2: 1.456, 1.311-1.617, and NOx: 1.419, 1.280-1.574) after Bonferroni correction. Participants with high genetic risk and high air pollution exposure had the highest risk of peptic ulcer, compared to those with low genetic risk and low air pollution exposure (PM2.5: HR 1.558, 95%CI 1.384-1.754, NO2: 1.762, 1.395-2.227, and NOx: 1.575, 1.403-1.769). However, no significant additive or multiplicative interaction between air pollution and genetic risk was found. In conclusion, long-term exposure to ambient air pollutants was associated with increased risk of peptic ulcer and chronic gastritis.

Background: The investigation of dietary micronutrient intakes and risk of alcoholic liver disease (ALD) based on observational studies was limited. Objectives: Our study aimed to explore the associations of 30 dietary micronutrients intakes with risk of ALD, interactions between dietary micronutrients and genetic variation, and mediation effects of blood and urinary biomarkers on the associations between dietary micro- nutrients and risk of ALD. Methods: A case-control study was conducted within the UK Biobank cohort, with 231 incident ALD cases and 1386 controls. Dietary data were collected using a dietary questionnaire that relied on a 24-h dietary recall of the previous day. Logistic regression models were employed to assess the associations of dietary micronutrient intakes with risk of ALD. We conducted stratified fi ed analyses on the associations between dietary micronutrient intakes and risk of ALD by PNPLA3 rs738409 and tested the interactions between dietary micronutrients and genetic variation. In addition, we conducted mediation analyses to investigate the mediating effects of biomarkers on the associations between dietary micronutrients and risk of ALD. Results: Our fi ndings indicated significant fi cant inverse associations of thiamin, riboflavin, fl avin, niacin equivalent, pantothenic acid, vitamin B-6, folate, vitamin E, calcium, magnesium, phosphorus, potassium, copper, iodine, and manganese with risk of ALD (all false discovery rateP trend < 0.050). We also found a significant fi cant interaction between PNPLA3 rs738409 and magnesium ( P interaction 1 / 4 0.028). Creatinine (enzymatic) in urine, aspartate aminotransferase, and insulin-like growth factor 1 were the top 3 biomarkers with the highest number of significant fi cant mediation effects on the associations between the dietary micronutrients and risk of ALD. Conclusions: Dietary intakes of thiamin, riboflavin, fl avin, niacin equivalent, pantothenic acid, vitamin B-6, folate, vitamin E, calcium, magnesium, phosphorus, potassium, copper, iodine, and manganese were inversely associated with risk of ALD.

We aimed to probe the association of serum 25-hydroxyvitamin D [25(OH)D] concentrations with all-cause and cause-specific mortality among patients with gout and hyperuricemia (HUA). The study included 1169 gout patients and 7029 HUA patients from the National Health and Nutrition Examination Survey (NHANES) 2007–2018 and 2001–2018, respectively. The association between serum 25(OH)D and mortality was evaluated by Cox proportional hazard and restricted cubic spline models. Among participants with gout and HUA, the weighted mean concentrations of serum 25(OH)D were 71.49 ± 30.09 nmol/L and 64.81 ± 26.92 nmol/L, respectively. Vitamin D deficiency occurred in 29.68

INTRODUCTION:Although there is enough pooled evidence supporting the positive association between family history of colorectal cancer (CRC) in first-degree relatives (FDRs) and the risk of CRC, synthesized data on its association with the risk of other colorectal neoplasia are lacking. Therefore, we aimed to systematically assess this issue. METHODS:We searched PubMed, Web of Science, and Embase from database inception through May 9, 2024, to identify observational studies investigating the association between family history of CRC in FDRs and the risk of colorectal neoplasia (excepting CRC). Adenoma, nonadvanced adenoma (NAA), advanced adenoma (AA), and advanced neoplasia (AN) were further chosen as main outcomes because of data availability. Random-effects model was used for data synthesis. Subgroup meta-analyses were performed to evaluate the robustness of results. RESULTS:Of 5,172 initial records screened, 75 studies (with 931,515 participants) were identified for analysis. Family history of CRC in FDRs was associated with increased risk of adenoma (pooled odds ratio [OR] 1.67, 95% confidence interval [CI] 1.46-1.91), NAA (pooled OR 1.35, 95% CI 1.21-1.51), AA (pooled OR 1.66, 95% CI 1.46-1.88), and AN (pooled OR 1.58, 95% CI 1.44-1.73). The positive associations persisted in all examined subgroups. The risk of adenoma (pooled OR 4.18, 95% CI 1.76-9.91), AA (pooled OR 2.42, 95% CI 1.72-3.40), and AN (pooled OR 2.00, 95% CI 1.68-2.38) was more evident among individuals with 2 or more affected FDRs. DISCUSSION:Family history of CRC is associated with increased risk of adenoma, NAA, AA, and AN totally, and in all available subgroups. The findings further strengthen the necessity and importance of an intensified screening strategy for individuals with a positive family history of CRC, which is very useful for related health resource allocation and policymaking.

Evidence regarding associations of general and abdominal obesity with the risk of conventional adenomas (ADs) and serrated polyps (SPs) from Asian population is scarce. Our study aimed to investigate the independent and joint associations of general obesity assessed by body mass index (BMI) and abdominal obesity assessed by waist circumference (WC) or waist‐to‐hip ratio (WHR) with the risk of ADs and SPs among 25 222 participants recruited by a population‐based screening program. Compared to participants with normal BMI, those with a BMI ≥28 kg/m2 had increased risk of ADs (odds ratio [OR] 1.52, 95% confidence interval [CI]: 1.36‐1.70) and SPs (OR 1.69, 95% CI: 1.38‐2.07). For participants with a WC ≥102 cm (≥88 cm for females), the risk of ADs (OR 1.37, 95% CI: 1.25‐1.51) and SPs (OR 1.81, 95% CI: 1.52‐2.16) was higher than that of the reference group. For participants with a WHR ≥0.95 (≥0.90 for females), the risk of ADs (OR 1.26, 95% CI: 1.16‐1.36) and SPs (OR 1.46, 95% CI: 1.26‐1.69) was higher than that of the reference group. Moreover, participants with both BMI ≥28 kg/m2 and WC ≥102 cm (≥88 cm for females) had 61% and 119% higher risk of ADs (OR 1.61, 95% CI: 1.39‐1.85) and SPs (OR 2.19, 95% CI: 1.70‐2.82) compared to those with both normal BMI and WC. These findings indicate that both general and abdominal obesity are associated with SPs and ADs, presenting stronger association with SPs than ADs. Moreover, the association is more evident when both obesities exist.

Objective To explore the association between whole blood lead concentration and advanced colorectal neoplasia (CRN) and to provide evidence for colorectal cancer (CRC) prevention and control. Methods The cases of the study were 272 advanced CRN identified from April 2014 to December 2016 in the participants of a CRC early diagnosis and treatment program including face-to-face questionnaire interview, physical examination and laboratory test conducted among the residents of Jiashan county, Zhejiang province; the 605 controls were gender- and age (± 5 years)-frequency matched healthy participants of the program. Results The geometric mean (geometric standard error) of whole blood lead concentration (μg/L) were 28.11(1.64) and 26.87 (0.93) for the cases and controls, without statistically significant difference (P > 0.05). After adjusting for gender, age, education, smoking, alcohol consumption, physical exercise, family history of CRC and body mass index (BMI), unconditional multivariate logistic regression analysis demonstrated that the participants with the highest quintile (Q5) of whole blood lead concentration were at an increased risk of advanced CRN (odds ratio [OR] = 1.87, 95% confidence interval [95%CI] : 1.15 – 3.04) compared to those with the lowest quintile (Q1) and the increased risk was much higher for the male participants (Q5 vs. Q1: OR = 2.12, 95%CI : 1.05 – 4.30). Furthermore after base 10 logarithm conversion, each unit increment in blood lead concentration was associated with a 1.86 (OR = 2.86, 95%CI : 1.28 – 6.35) and 3.98 (OR = 4.98, 95%CI : 1.62 – 15.35) times higher risk of advanced CRN for the all and the male participants, respectively. Restricted cubic spline analysis revealed a significant linear correlation between the increment of whole blood concentration and the increased risk of advanced CRN after adjusting for potential confounders mentioned above (χ2 total = 8.79, Ptotal = 0.012; χ2 non-linearity = 2.17, Pnon-linearity = 0.141). ConclusionBlood lead concentration may be associated with an increased risk of advanced colorectal neoplasia, suggesting a potential role of lead exposure in the etiology of colorectal carcinogenesis.

To investigate the association of long-term exposure to ambient air pollution with the risk of allergic rhinitis (AR), we performed a longitudinal analysis of 379,488 participants (47.4% women) free of AR at baseline in the UK Biobank. The annual average concentrations of PM2.5, PMcoarse, PM10, NO2, and NOx were estimated by land use regression models. Cox proportional hazard models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). A weighted polygenic risk score was constructed. During a median follow-up period of 12.5 years, 3095 AR cases were identified. We observed significant associations between the risk of AR and PM2.5 (HR: 1.51, 95% CI: 1.27-1.79, per 5 μg/m3), PMcoarse (HR: 1.28, 95% CI: 1.06-1.55, per 5 μg/m3), PM10 (HR: 1.45, 95% CI: 1.20-1.74, per 10 μg/m3), NO2 (HR: 1.14, 95% CI: 1.09-1.19, per 10 μg/m3), and NOx (HR: 1.10, 95% CI: 1.05-1.15, per 20 μg/m3). Moreover, participants with high air pollution combined with high genetic risk showed the highest risk of AR, although no multiplicative or additive interaction was observed. In conclusion, long-term exposure to air pollutants was associated with an elevated risk of AR, particularly in high-genetic-risk populations, emphasizing the urgent need to improve air quality.

Evidence on the link between healthy lifestyle and colorectal cancer (CRC) precursors is limited. Our study aimed to examine and compare the associations of healthy lifestyle with CRC precursors in adenoma (AD)‐carcinoma and serrated pathways. A total of 24 480 participants including 6309 ADs, 1343 serrated polyps (SPs), and 16 828 polyp‐free controls were included. A healthy lifestyle score (HLS) was constructed based on five lifestyle factors including cigarette smoking, alcohol drinking, physical activity, diet and body weight, and categorized into least, slightly, moderately and most healthy. Multivariable logistic regressions were used to estimate odds ratio (OR) and 95% confidence interval (CI). Inverse dose‐response associations between the HLS and risk of ADs were observed (OR per 1 score increment for ADs: 0.82 [95% CI 0.79‐0.84]; for SPs: 0.73 [95% CI 0.69‐0.78]), and the association with SPs was more evident than with ADs (OR 0.90, 95% CI 0.85‐0.96). Compared to participants with the least healthy lifestyle, those with the most healthy lifestyle had 47% lower risk of ADs (OR 0.53, 95% CI 0.47‐0.59) and 70% lower risk of SPs (OR 0.30, 95% CI 0.23‐0.39), respectively. These inverse associations were consistent across lesion stage and anatomic subsite and not modified by any stratification factors. The risk advancement periods for the most vs the least healthy lifestyle were −9.49 years for ADs and −20.69 years for SPs. Our findings help confirm the preventive role of healthy lifestyle in colorectal carcinogenesis.

Objective To explore the correlation between obesity and the risk of colorectal adenoma,so as to provide theoretic evidence for the intervention of the high-risk population for colorectal cancer.Methods Based on the Screen Project of Early Diagnosis and Treatment of Colorectal Cancer in Jiashan County,from August 2012 to March 2018,the results of colonoscopy and body measurement information of the high-risk population for colorectal cancer were collected.According to the results of colonoscopy,3 895 patients with colorectal adenoma and 11 232 healthy controls were enrolled.Multivariate logistic regression was used to analyze the correlation between overweight (body mass index (BMI) 24.0 to 27.9 kg/m2),obesity (BMI≥ 28.0 kg/m2) and the risk of colorectal adenoma.Results After adjusting for gender and age,compared with that of individuals with normal weight (BMI 18.5 to 23.9 kg/m2),the risk of colorectal adenoma of obese patients increased by 36％ (odds ratio (OR) =1.36,95％ confidence interval (CI) 1.18 to 1.56).After stratifing by gender,compared with that of individuals with normal weight,the risk of colorectal adenoma of obese males increased by 30％ (OR =1.30,95％ CI 1.07 to 1.59),the risk of colorectal adenoma of overweight females and obese females increased by 15％ (OR =1.15,95％ CI 1.01 to 1.31) and 40％ (OR =1.40,95％ CI 1.14 to l.71),respectively.After stratifing by age,compared with that of individuals with normal weight,the risk of colorectal adenoma of obese patients aged between 40 and 59 years increased by 31％ (OR =1.31,95％ CI 1.07 to 1.61),and the risk of colorectal adenoma of overweight and obese patients aged between 60 and 74 years increased by 13％ (OR=1.13,95％CI 1.01 to 1.27) and 39％ (OR=1.39,95％ CI 1.15 to 1.70),respectively.The results of subgroup analysis according to pathological types indicated that the risk of non-advanced adenoma and advanced adenoma of obese patients increased by 35％ (OR =1.35,95％CI 1.16 to 1.57) and 39％ (OR=1.39,95％CI 1.06 to 1.83),respectively.Conclusions Obesity is correlated with colorectal adenoma,which is more significant in women,individuals aged between 60 and 74 years and advanced adenoma.The intervention of high-risk population for colorectal cancer should include body mass control.