Obesity, (particularly central obesity), has been associated with an increased risk of colorectal adenoma development [17] . Domestic studies by Liu Yang et al. have reported that obese individuals are more likely to develop colon polyps and face a higher risk of cancer [18] . In a study conducted by Comstock et al., colonoscopies performed on 128 asymptomatic men revealed that those with a BMI of 25 kg/m² were 6.5 times more likely to detect three or more polyps compared to men with a BMI of less than 25 kg/m². Additionally, obese individuals were found to have a higher prevalence of polyp-type adenomas [19] . Several mechanisms have been proposed to explain the increased risk of colorectal adenoma among obese individuals. Firstly, obesity is often accompanied by insulin resistance, manifesting as hyperinsulinemia. When insulin and its analogues bind to their corresponding receptors, they can promote colorectal epithelial proliferation and differentiation while inhibiting apoptosis. This process can induce the formation of adenomatous polyps, which may further progress to carcinogenesis [20] . Secondly, obesity is associated with a chronic inflammatory response. Long-term stimulation from this chronic inflammation can elevate the risk of developing colorectal adenomas [21] . Thirdly, increased adipose tissue in obese individuals has endocrine functions, secreting inflammatory factors and protein hormones, including tumor necrosis factor and leptin. These secretions create a favorable environment for precancerous lesions [22] . Research has specifically highlighted the role of leptin in promoting intestinal mucosal hyperplasia, which over time can contribute to the transformation of colorectal polyps into adenomas [23] .

Type 2 diabetes, a prevalent chronic metabolic disease, not only affects large blood vessels, microvascular, and nervous system lesions but also significantly increases the risk of tumors [24] . Meta-analytic studies indicate a consensus that diabetes serves as an independent risk factor for the progression of colorectal polyps to colorectal cancer, increasing the risk of intestinal polyps by approximately 30% [25] . The development of colorectal adenomas in the context of high blood sugar levels is primarily associated with insulin resistance and hyperinsulinemia, which are critical elements in both type 2 diabetes and colorectal cancer pathogenesis. Elevated insulin levels promote intestinal cell proliferation, differentiation, and migration through several signaling pathways, following the “hyperplasia-adenoma-cancer” sequence, thereby facilitating carcinogenesis [26] . During insulin resistance, there is a compensatory increase in the body’s insulin level, leading to an enhanced synthesis of insulin-like growth factor binding protein (IGFBP) in vivo. Consequently, the content of insulin-like growth factor (IGF-1) increases. Upon the binding of IGF-1 to IGFBP, tyrosine kinase receptors are activated, ultimately participating in cell proliferation and differentiation through two signaling pathways: the PI3K/Akt pathway and MAPK/Ras pathway. Notably, heightened insulin levels not only impact metabolic pathways but also lead to the overstimulation of the pro-mitotic pathway, thereby promoting the excessive proliferation of tumor cells within the digestive system. The proliferative effect on epithelial cells is a critical factor in the development of colorectal malignancy [27] . Additionally, high insulin and IGF-1 levels activate the Ras system, which subsequently stimulates the mTOR and Wnt signaling pathways. This activation heightens the sensitivity of colorectal cells to growth factors, accelerating the transition from adenoma to carcinoma [28] . Furthermore, type 2 diabetes can induce gastrointestinal dysfunction, resulting in symptoms such as delayed gastric emptying, diarrhea, and constipation, which can prolong the exposure of colonic mucosa to potential carcinogens [29] . The compromised immune surveillance in patients with type 2 diabetes further elevates their susceptibility to developing colorectal adenomas [30] . Collectively, these factors underscore the heightened risk of colorectal cancer development in individuals with type 2 diabetes.

Many studies have shown that the sympathetic nervous system is a crucial factor in promoting the occurrence of hypertension. Activation of the β-adrenergic receptor (β-AR) signaling pathway leads to increased adrenaline levels and cellular sensitivity, which are believed to contribute to the progression and infiltration of various malignant tumors. Research indicates that the activation of the β-AR pathway is significant in the onset and advancement of colon cancer and breast cancer malignancy [31] . According to an animal experiment, catecholamine release can enhance tumor propensity in mice. This effect may be linked to catecholamines’ ability to induce an oxidative stress response [32] [33] . Studies have also revealed that hypertension triggers a chronic inflammatory process by activating the renin-angiotensin system. In recent years, inflammation has been recognized as a key player in the development of colorectal adenomas and tumors [34] . Chronic inflammatory cells and factors are not only critical for the prognosis of colorectal malignant tumors but also closely associated with tumor cell proliferation, apoptosis, and metastasis in colorectal cancers [35] . Aspirin is commonly used as a prophylactic drug for precancerous lesions, with its anti-inflammatory properties believed to be pivotal in its pharmacological action against tumors [36] .

The association mechanism between dyslipidemia and colorectal adenoma indicates that hyperlipidemia can increase the risk of colorectal adenoma. One potential factor is the elevation of blood lipid levels, which can raise bile acid levels in the body. These primary bile acids are converted to secondary bile acids by intestinal bacteria, and these secondary bile acids can activate proteins such as α-protein kinase C. The activation of α-protein kinase C may lead to the hyperplasia of intestinal mucosal cells, potentially progressing to polyp formation [37] . Additionally, hyperlipidemia, particularly elevated triglyceride levels, can enhance inflammation and increase peroxidation levels within the body [38] . This inflammation activates oxidative stress and reactive oxygen species, which may cause DNA structural damage, gene mutations, and chromosomal abnormalities, thereby impacting the growth, proliferation, and apoptosis of colorectal epithelial cells, potentially resulting in polyp formation. Rajnadas et al. have also suggested that abnormalities in apolipoprotein metabolism and the function of lipid metabolism enzymes such as COX and PLA2 can disrupt the differentiation balance of intestinal epithelial cells, leading to excessive hyperplasia and an increased incidence of polyps [39] . Furthermore, some scholars posit that insulin-like growth factor-1 (IGF-1), a cytokine that inhibits cell apoptosis and promotes cell proliferation, can stimulate the transition from adenoma to adenocarcinoma by upregulating the activity of the K-ras protein. Elevated triglycerides can promote the secretion of IGF-1, thereby contributing to this process [40] .