2016 March 15; 133(11): 1104–1114. doi:10.1161/CIRCULATIONAHA.115.020406. | Ryan J. Koene, MD1, Anna E. Prizment, PhD2,4, Anne Blaes, MD, MS3, and Suma H. Konety, MD, MS1
Cardiovascular disease (CVD) and cancer are the leading causes of death globally, and while traditionally viewed as separate entities, they share common risk factors and biological mechanisms. This review explores the shared risk factors, such as obesity, diabetes, hypertension, and inflammation, and their roles in both diseases. Chronic inflammation is a key unifying factor, influencing the progression of both CVD and cancer. Oxidative stress and reactive oxygen species also contribute to the pathogenesis of both conditions. Shared biological mechanisms include hormonal and metabolic pathways, such as those involving leptin, insulin, and growth factors.
The review highlights the impact of modifiable risk factors like obesity, diabetes, and hypertension on both CVD and cancer. For instance, obesity is associated with increased cancer risk through mechanisms such as chronic inflammation and hormonal changes. Diabetes is linked to both CVD and cancer, with hyperinsulinemia and insulin-like growth factors playing significant roles. Hypertension, while primarily a CVD risk factor, is also associated with certain cancers, possibly through mechanisms involving angiogenic factors and oxidative stress.
The article also discusses the role of lifestyle factors, such as diet, physical activity, and tobacco use, in influencing the risk of both diseases. Anti-inflammatory agents, including statins and non-steroidal anti-inflammatory drugs (NSAIDs), may have protective effects against both CVD and cancer. Additionally, the review addresses the impact of CVD treatments on cancer risk and vice versa, emphasizing the need for integrated approaches in prevention and treatment.
In conclusion, the shared risk factors and biological mechanisms between CVD and cancer suggest the potential for combined prevention strategies. Understanding these interactions may lead to improved prevention, early detection, and safer treatment approaches for both diseases.Cardiovascular disease (CVD) and cancer are the leading causes of death globally, and while traditionally viewed as separate entities, they share common risk factors and biological mechanisms. This review explores the shared risk factors, such as obesity, diabetes, hypertension, and inflammation, and their roles in both diseases. Chronic inflammation is a key unifying factor, influencing the progression of both CVD and cancer. Oxidative stress and reactive oxygen species also contribute to the pathogenesis of both conditions. Shared biological mechanisms include hormonal and metabolic pathways, such as those involving leptin, insulin, and growth factors.
The review highlights the impact of modifiable risk factors like obesity, diabetes, and hypertension on both CVD and cancer. For instance, obesity is associated with increased cancer risk through mechanisms such as chronic inflammation and hormonal changes. Diabetes is linked to both CVD and cancer, with hyperinsulinemia and insulin-like growth factors playing significant roles. Hypertension, while primarily a CVD risk factor, is also associated with certain cancers, possibly through mechanisms involving angiogenic factors and oxidative stress.
The article also discusses the role of lifestyle factors, such as diet, physical activity, and tobacco use, in influencing the risk of both diseases. Anti-inflammatory agents, including statins and non-steroidal anti-inflammatory drugs (NSAIDs), may have protective effects against both CVD and cancer. Additionally, the review addresses the impact of CVD treatments on cancer risk and vice versa, emphasizing the need for integrated approaches in prevention and treatment.
In conclusion, the shared risk factors and biological mechanisms between CVD and cancer suggest the potential for combined prevention strategies. Understanding these interactions may lead to improved prevention, early detection, and safer treatment approaches for both diseases.