Our study indicated that smoking, age, BMI, and education level were common risk factors for SPs and common adenomas. Smokers were 41% more likely to develop adenomas (OR: 1.41, 95%CI: 1.29–1.54) and 62% to develop SPs (OR: 1.62, 95%CI: 1.46–1.81), respectively. SPs and adenomas located in the distal colon were more strongly associated with smoking than the proximal colon (P < 0.05). The risk of adenomas and SPs in middle-aged adults was 1.92 fold (OR: 1.92, 95%CI: 1.55–2.37) and 1.36 fold (OR: 1.36, [95%CI: 1.07–1.73]) compared with young adults, respectively. SPs were more strongly correlated with BMI than adenomas (P < 0.05). SPs located in the distal colon (OR: 1.09, 95% CI: 1.05–1.13) had a stronger association than the proximal colon (OR, 1.08; 95% CI: 1.03 ~ 1.14, P < 0.05). This suggests that although SPs and adenomas share many CRC risk factors, some factors are more associated with one lesion than other lesions. Overall, this is the first study of the association of lifestyle with adenomas and SPs in a physical examination population in northern China. Our results support the aetiological heterogeneity of colorectal lesions, with potential clinical implications for CRC prevention.
Previous studies have consistently implicated smoking as increasing the risk of colorectal polyps [21]. In particular, smoking has been significantly associated with a higher risk of SSA/P, a subtype of the SP family and a precursor lesion to CRC[22]. In our study, we also found that smoking is closely related to adenomas and SPs and that it is more strongly correlated with SPs than with adenomas. On the other hand, we found that smoking is more strongly associated with SPs in the distal colon than in the proximal colon, which is consistent with He X et al[23]. Other studies have not observed a consistent association between smoking and proximal SPs[24], although SSA/Ps tend to arise from the proximal colon[25]. We assume that smoking, as well as other factors associated with the proximal colon, such as certain bacteria, are involved in the initiation of SPs[26]. Indeed, the underlying mechanism of the close association between smoking and increased risk of serrated tumours is not clear. Smoking may promote aberrant DNA promoter methylation leading to tumours with high MSI and positive CIMP. In addition, cigarettes contain a variety of carcinogens, such as polycyclic aromatic hydrocarbons, which can be ingested directly into the colorectal mucosa or circulatory system, thereby increasing the risk of colon polyps.
Age is one of the non-negligible pathogenic factors of CRC[27]. In this study, the prevalence of adenomas in middle-aged men was higher. Men have a higher prevalence of risk factors, especially abdominal obesity in middle-aged men. The higher prevalence may be related to hormone levels, social pressure, dietary habits and lifestyle habits. Therefore, for high-risk age groups, it is crucial to pay attention to relevant early warnings and timely endoscopic screening to improve the detection rate of endoscopy.
BMI has been positively associated with the risk of APs in some studies. Although the association between BMI and APs varies in the literature, our results are consistent with meta-analysis results[28]. In our study, we observed a strong association between high BMI and an increased risk of adenomas and SPs. The ORs comparing the overweight population to the normal weight population were increased of 38% for adenomas and 93% for SPs. In contrast to most previous studies, BMI was found to be more strongly associated with SPs than for colonic adenomas. Obesity may promote CRC through the associated chronic subclinical inflammatory state[29]. It is worth noting that inflammation plays a more important role in SP tumour progression than adenomas. Compared with the traditional pathway, the association between obesity and the serrated pathway is stronger, suggesting that obesity may alter the local inflammatory state to promote the development of SPs[30]. In addition, gut microbes, such as Fusobacterium nucleatum, have been shown to be more abundant in obese people and to be more strongly associated with the serrated pathway than with the conventional pathway[31, 32], suggesting that obesity may alter regional inflammatory status and abundance of specific microbes to promote the development of SPs.
This study found that education level was associated with colon polyps. In particular, highly educated people are more prone to developing colon adenomas. Considered to be associated with relatively less physical activity, moderate physical activity may reduce the incidence of colon polyps.
The positive association between elevated blood glucose and APs has been noted previously in adenomas[33], and diabetes may be a relevant risk factor for CRC[34]. Our study supports hyperglycaemia as a risk factor, and the possible mechanism mainly focuses on insulin resistance. Elevated insulin levels, commonly resulting from obesity or other similar morbidities, and the insulin to insulin-like growth factor axis may create a favourable environment for formation of CRC tumours. Furthermore, the inflammatory state associated with obesity may contribute by increasing tumorigenic cytokines [35]. Additionally, elevated high-density lipoprotein cholesterol has been found to be a protective factor for SP formation. Patients with uric acid > 360 mg/dL (women) and > 420 mg/dL (men) were more likely to develop intestinal polyps, which was consistent with previous studies[36].
This study has several limitations. First, this was a single-centre cross-sectional
study; therefore, information on temporality could not be ascertained. Second, since our subjects were an average-risk population in northern China, we were unable to compare risk factors for SPs and adenomas according to ethnicity, which needs to be analysed in further studies. Although a strength of our study was a larger population sample size of individuals with APs and SPs, the sample size of these populations with SSPs remained small.