Linking obesity to colorectal cancer: recent insights into plausible biological mechanisms

Curr Opin Clin Nutr Metab Care. 2013 Sep;16(5):595-600. doi: 10.1097/MCO.0b013e328362d10b.


Purpose of review: This review will examine the recent scientific literature on the mechanisms that are thought to link obesity to colorectal cancer (CRC) risk.

Recent findings: Obesity has emerged as a leading environmental risk factor for the development of CRC. However, the mechanisms underlying this relationship have not yet been fully elucidated. Recent literature has focused on inflammatory processes, adipokines, and estrogen. Obesity-enhanced inflammation is largely orchestrated by increases in adipose tissue macrophages leading to the secretion of inflammatory cytokines including tumor necrosis factor-α, monocyte chemoattractant protein-1, and interleukin-6, all of which are linked to CRC. Adiponectin is decreased with obesity and has been reported to be negatively associated with CRC, whereas leptin, which is increased, is positively associated with the disease. Estrogen has been shown to influence CRC, although its role remains controversial; some studies have implicated estrogen as being protective, whereas others have suggested it to be a risk factor. We highlight the most important recent advances that have been made on the aforementioned mechanisms that are thought to link obesity to CRC.

Summary: A better understanding of the mechanisms linking obesity to CRC risk is necessary for the design of effective treatment approaches in future clinical trials.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adiponectin / blood
  • Adipose Tissue / metabolism
  • Adipose Tissue / pathology
  • Chemokine CCL2 / metabolism
  • Colorectal Neoplasms / etiology
  • Colorectal Neoplasms / pathology*
  • Estrogens / blood
  • Humans
  • Inflammation / etiology
  • Inflammation / pathology
  • Interleukin-6 / metabolism
  • Leptin / blood
  • Macrophages / metabolism
  • Macrophages / pathology
  • Obesity / complications
  • Obesity / pathology*
  • Tumor Necrosis Factor-alpha / metabolism


  • Adiponectin
  • Chemokine CCL2
  • Estrogens
  • Interleukin-6
  • Leptin
  • Tumor Necrosis Factor-alpha