The Role of Sarcopenic Obesity in Cancer and Cardiovascular Disease: A Synthesis of the Evidence on Pathophysiological Aspects and Clinical Implications

Abstract

Obesity is globally a serious public health concern and is associated with a high risk of cardiovascular disease (CVD) and various types of cancers. It is important to evaluate various types of obesity, such as visceral and sarcopenic obesity. The evidence on the associated risk of CVD, cancer and sarcopenic obesity, including pathophysiological aspects, occurrence, clinical implications and survival, needs further investigation. Sarcopenic obesity is a relatively new term. It is a clinical condition that primarily affects older adults. There are several endocrine-hormonal, metabolic and lifestyle aspects involved in the occurrence of sarcopenic obesity that affect pathophysiological aspects that, in turn, contribute to CVD and neoplasms. However, there is no available evidence on the role of sarcopenic obesity in the occurrence of CVD and cancer and its pathophysiological interplay. Therefore, this review aims to describe the pathophysiological aspects and the clinical and epidemiological evidence on the role of sarcopenic obesity related to the occurrence and mortality risk of various types of cancer and cardiovascular disease. This literature review highlights the need for further research on sarcopenic obesity to demonstrate the interrelation of these various associations.

Keywords: cancer; cardiovascular disease; mortality; muscle mass; obesity; pathophysiological aspects; sarcopenic obesity.

Figure 1

Main pathophysiological mechanisms shared in developing CVD and cancer in individuals with sarcopenic obesity. AGEs = advanced glycation end products; CLS = crown-like structures; CVD = cardio-vascular disease; GLUT4 = glucose transporter type 4; IGF-1 = insulin-like growth factor 1; IL = interleukin; MAPK = mitogen-activated protein kinase; MCP-1 = monocyte chemoattractant protein 1; p53 = tumor protein P53; RAGE = receptor of advanced glycation end products; ROS = reactive oxygen species; TNF-α = tumor necrosis factor α.