In this author’s last post, polycysctic ovarian syndrome (PCOS) was explored and its relationship to metabolic syndrome. The following will continue to explore PCOS and its relationship to low-grade chronic inflammation (LGCI) and obesity.
Sirmans and Pate (2014) indicated that weight loss could help control PCOS (control inflammation). Of particular interest is the biochemical relationship between LGCI and obesity; individuals who are overweight/obese have significantly higher levels of inflammatory markers: tumor necrosis factor alpha, and interleukin-6, C-reactive protein, adiponectin, as well as leptin (Ilich, Kelly, Kim, & Spicer, 2014).
Ilich et al. (2014) continued to state that overexpressed cytokines (signaling molecules that help mount an inflammatory response) are produced in the adipose tissue of obese individuals; thus, more body fat produces more cytokines. Additionally, there exists a perpetual interaction between adiponectin (anti-inflammatory) and leptin (pro-inflammatory) molecules.
The coexistence/imbalance of the cytokines (adipolectin and leptin) propagates LGCI; a feedback loop exists whereby obesity perpetuates inflammation, and inflammation perpetuates obesity (Ilich et al., 2014). Thus, a potential method of breaking the inflammatory cycle might be fat loss, thereby reducing the levels of cytokines in adipose tissue.
References
Ilich, J. Z., Kelly, O. J., Kim, Y., & Spicer, M. T. (2014). Low-grade chronic inflammation perpetuated by modern diet as a promoter of obesity and osteoporosis. Archives of Industrial Hygiene and Toxicology, 65(2), 139-148.
Sirmans, S. M., & Pate, K. A. (2014). Epidemiology, diagnosis, and management of polycystic ovary syndrome. Clinical Epidemiology, 6, 1-13.
-Michael McIsaac