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The relationship between metabolic syndrome and cancer is also one of growing concerns in the last few decades. Cardiometabolic syndrome and cancer are the major contributors to the burden of chronic disease and mortality worldwide (Koene et al. 2016). There is emerging evidence for possible interaction between the two with shared risk factors suggesting a similar underlying mechanism of the pathologies (Table 2.1) (O'Neill and O'Driscoll 2015). Additionally, each individual risk factor for metabolic syndrome has also an association with cancer. While inflammation is attributed to be the one of the major amalgamating factors in the onset and progression of the diseases, additional mechanisms or factors have also been identified, which mainly includes diabetes, insulin sensitivity, and obesity (Figure 2.8). It has been reported along with other factors sharing biological roles, phosphatase and tensin homolog (PTEN) is a crucial gene involved in regulating the Akt pathway (Arora et al. 2018) and PTEN mutations are linked to regulating insulin sensitivity and obesity (Mitchell 2012). Thereby, tracking back one of the major causes of cardiometabolic syndrome is obesity. Therefore, it becomes important to understand if cancer, CVD, and obesity have a shared biology. Studies in the United States in the later nineteenth century on cancer reported the association of BMI index and cancer deaths. It was observed that men with a BMI ≥ 40 had a 52% higher death rate from all cancer, while women with a BMI ≥ 40 had a 62% higher death rate from all cancers than men and women of normal weight, respectively. Thereby, if obesity is prevented in individuals, around 10–20% of cancer deaths in the United States could be prevented.

Scientific evidence shows that metabolic syndrome and obesity are contributors to an estimated 6% of all cancers (4% in men, 7% in women) diagnosed in 2007. Beyond being a major risk factor for diabetes, which itself is a risk factor for most cancers, obesity has long been understood to be associated with increased risk of oesophageal, colon, pancreatic, postmenopausal breast, endometrial, and renal cancers. More recently, evidence has accumulated that overweight and/or obesity raise the risk of cancers of the gallbladder, liver, ovaries (epithelial), and advanced prostate cancer, as well as leukaemia (Esposito et al. 2012). The complex relation between all three can be mediated by several factors including diet, physical activity and hormonal signalling (insulin‐like growth factor signalling), oxidative stress (Dara Hope and Derek 2012). Pro‐inflammatory cytokines predominantly secreted by immune cells and also other cell types like endothelial and adipocytes affect all tissues and organ systems including the vasculature system (Dinarello and Pomerantz 2001). The aetiology of cardiometabolic syndrome involves accumulation of visceral fat. This promotes the synthesis and release of pro‐inflammatory cytokines leading to enhanced oxidative stress. Infiltration of immune cells particularly inflammatory macrophages in the adipose tissues further enhance the cytokine burden causing chronic inflammation (DeMarco et al. 2010). Pro‐inflammatory cytokines produced within adipose tissues are also found to be elevated in the serum of obese people. Inflammatory cytokines such as IL‐6, TNF‐α, leptin have been extensively associated with obesity, CVD (upto 20%), and cancer (Grivennikov and Karin 2011; Bielecka‐Dabrowa et al. 2007). Therefore, IL‐6 and TNF‐α and other potential pro‐inflammatory cytokines are probably the factors linking cardiometabolic syndrome, obesity, and cancer together, and pose as potential targets for the treatment of these associated pathologies (Figure 2.8). Therefore, it has been established that a major cause of cancer is metabolic imbalance conditions including hypercholesterolemia, diabetes, hypertension, specific drug use. Effective interventions to reduce their prevalence could potentially reduce cancer risk