Risk Factors and Prevention of Cancer and CVDs: A Chicken and Egg Situation

Abstract

Cardiovascular diseases and cancer are the two primary causes of mortality worldwide. Although traditionally regarded as distinct pathologies, they share numerous pathophysiological mechanisms and risk factors, including chronic inflammation, insulin resistance, obesity, and metabolic dysregulation. Notably, several cancers have been identified as closely linked to cardiovascular diseases, including lung, breast, prostate, and colorectal cancers, as well as hematological malignancies, such as leukemia and lymphoma. Additionally, renal and pancreatic cancers exhibit a significant association with cardiovascular complications, partly due to shared risk factors and the cardiotoxic effects of cancer therapies. Addressing the overlapping risk factors through lifestyle modifications-such as regular physical activity, a balanced diet, and cessation of smoking and alcohol-has proven effective in reducing both CV and oncological morbidity and mortality. Furthermore, even in patients with established cancer, structured interventions targeting physical activity, nutritional optimization, and smoking cessation have been associated with improved outcomes. Beyond lifestyle modifications, pharmacological strategies play a crucial role in the prevention of both diseases. Several cardiovascular medications, including statins, aspirin, beta-blockers, and metformin, exhibit pleiotropic effects that extend beyond their primary indications, demonstrating potential anti-neoplastic properties in preclinical and observational studies. Recently, novel therapeutic agents have garnered attention for their possible cardioprotective and metabolic benefits. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and sodium-glucose cotransporter-2 inhibitors (SGLT2is), initially developed for managing type 2 diabetes, have shown CV and renal protective effects, alongside emerging evidence of their role in modulating cancer-related metabolic pathways. Inclisiran, a small interfering RNA targeting PCSK9, effectively lowers LDL cholesterol and may contribute to reducing CV risk, with potential implications for tumor biology. Additionally, sacubitril/valsartan, an angiotensin receptor-neprilysin inhibitor, has revolutionized heart failure management by improving hemodynamic parameters and exerting anti-inflammatory effects that may have broader implications for chronic disease prevention. Given the intricate interplay between CVD and cancer, further research is essential to clarify the exact mechanisms linking these conditions and assessing the potential of CV therapies in cancer prevention. This review aims to examine shared risk factors, consider the role of pharmacological and lifestyle interventions, and emphasize crucial epidemiological and mechanistic insights into the intersection of CV and oncological health.

Keywords: cancer; cardiovascular disease (CVD); prevention; risk factors.

Figure 1

Adverse health impacts of certain foods. Legend: CVD: cardiovascular diseases. ↓: REDUCTION; ↑: INCREASE.

Figure 2

Pathophysiological mechanisms correlating inflammation, metabolic syndrome, and neoplasms. Legend: IGF1: Insulin-like growth factor, IL6: interleukin-6, SHBG: sex hormone-binding globulin, TNFα: tumor necrosis factor-α. The enlargement of adipose tissue triggers the infiltration of macrophages and T cells into adipocytes, releasing proinflammatory cytokines and alterations in circulating adipokine levels. This process fosters insulin resistance, primarily affecting metabolic tissues, resulting in hyperinsulinemia and increased insulin-like growth factor 1 (IGF-1) synthesis. These metabolic disruptions not only underlie the development of metabolic syndrome but also play a significant role in promoting tumor initiation and progression. Additionally, bioactive molecules secreted by macrophages and adipocytes exert autocrine and paracrine effects, further exacerbating the inflammatory response.

Figure 3

Cancers most commonly associated with diabetes.