C-reactive protein (CRP) is an acute phase protein that is synthesised in the liver in response to cytokines released during infection, inflammation and from adipose tissue1. The plasma levels of CRP can rise 1000-fold during times of acute injury or infection and its production is regulated by the release of interleukin-6 (L-6), interleukin-1 (IL-1) and tumour necrosis factor alpha (TNF-α). As white adipose tissue accumulates inflammation increases due to an influx of macrophages to fat cell. These macrophages release cytokines which stimulate the release of CRP from hepatocytes, and evidence is accumulating that obesity is a chronic disease characterised by metabolic dysfunction and systemic inflammation. The main action of CRP is to bind to receptors on cells in order to activate the compliment system or stimulate tissue factor production and a subsequent production of thrombin and the coagulation cascade.
C-reactive protein is known to bind to both low density lipoprotein (LDL) and very low density lipoprotein (VLDL). This leads to the activation of compliment system and the coagulation cascade which may increase the risk of cardiovascular disease. Plasma levels of CRP fall with weight loss due to the release of adiponectin, an adipokine that is inversely associated with white adipose tissue levels. Fibre and flavonoid (quercetin, kaempferol, malvidin, peonidin, daidzein and genistein) levels in the diet have both been identified as being inversely associated with CRP plasma levels in research. Soy protein has been shown to lower levels of CRP, possibly because it is a rich source of the flavonoids daidzein and genistein. Studies involving the addition of n-3 fatty acids and eggs to the diet have both shown that they are able to lower levels of CRP in the plasma and so decrease the risk of cardiovascular disease.
Researchers1 have investigated the association between inflammatory markers and obesity in 472 Spanish adolescents aged between the ages of 13 and 18.5 years. The subjects had their serum analysed for levels of various inflammatory markers and cytokines, and anthropometric measurements were taken to assess body fat. The results showed that CRP was associated with central obesity as measured by waist circumference. The authors concluded that total body fat was associated with a systemic low grade inflammation in apparently healthy individuals. This supports the growing body of research that identifies obesity as a cause of systemic inflammation. The fact that these subjects were otherwise healthy would suggest that any disease associated with this chronic inflammation may take a long time to manifest. Weight loss appears to be the most beneficial treatment to lower plasma levels of CRP because it increases adiponectin levels.
RdB
