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Inflammation, obesity and risk of hypertension: shared pathways or independent risk factors?

Journal of Human Hypertension volume 25, pages 71–72 (2011)Cite this article

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The temporal and causal relationships between hypertension and chronic low-grade inflammation are still unclear, despite extensive research over the last decades. In population-based studies, hypertension is usually associated with raised levels of various markers of inflammation.1 Longitudinal studies over the last years have shown that markers of inflammation, such as white blood cells,2 complement factor C3,3 C-reactive protein (CRP),4 fibrinogen5 and a score of five acute-phase proteins,6 are associated with incidence of hypertension or increasing blood pressure levels. These studies show that inflammation predicts the development of hypertension, and suggest that inflammation could have a function in this process.

However, the interrelations between obesity, inflammation and hypertension are complex and the nature of these results is still controversial. Obesity is a major risk factor for hypertension and also associated with systemic low-grade inflammation. In fact, prospective studies have shown that inflammation is a risk factor for future weight gain, independently of initial weight, smoking habits and other potential confounding factors.7, 8 This suggests that inflammation is related to the development of obesity. On the other hand, it is now widely recognized that the adipose tissue is a producer of various proinflammatory substances, such as interleukin-6.9 Inflammation could therefore be related to the development of obesity and at the same time be an effect of obesity. Furthermore, angiotensinogen, which is involved in the regulation of blood pressure, is expressed in the adipose tissue.10

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  1. Department of Clinical Science CRC 60, 13, Lund University, Malmo, Sweden

    G Engström

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  1. G Engström
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Correspondence to G Engström.

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The author is employed as senior epidemiologist by AstraZeneca.

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Engström, G. Inflammation, obesity and risk of hypertension: shared pathways or independent risk factors?. J Hum Hypertens 25, 71–72 (2011). https://doi.org/10.1038/jhh.2010.92

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