Inflamm-Aging: How To Stop The Aging Accelerator

Aging, although inevitable, is a highly variable process. A crucial component of how well we age is related to the levels of inflammation in the body. Although inflammation is a natural and healthy response, prolonged elevated levels become disastrous for the body, linked to chronic diseases, and accelerated aging. This interconnected link has given rise to a new term, ‘inflamm-aging’. 

Although research is still elucidating the exact causes of “inflamm-aging”, a common finding involves the dysregulation of the cytokine network[1]. Cytokines, from the Greek cyto meaning “cell” and kinos meaning “movement”, are tiny protein molecules secreted by cells that communicate with other cells. Cytokines may be classified as peptides, proteins, exosomes, secretomes or glycoproteins. Sophisticated and profound complexes of cytokines found in our bodies are involved in cellular communications. It might help to think of cytokines as the body’s mobile phone system. 

As a main component of cell-to-cell communication, it makes sense that cytokines can be the difference between accelerated or graceful aging. Research has shown that as we age, cytokine dysregulation gets worse, leading to a progressive tendency to a pro-inflammatory state[1]. Key pro-inflammatory cytokines, including IL-6, TNF- α, and IL-1α, contribute to inflamm-aging seen in both healthy elderly people2 and elderly with age-related diseases[3,4].  

In a 2018 review paper, the authors concluded that “The key to healthy aging must lie in the ability to maintain a balanced response to these immune messengers [i.e. cytokines] and a prompt and integrated return to inflammation resolution and immune homeostasis.”[1]

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  1. Rea IM, Gibson DS, McGilligan V, et al. Age and Age-Related Diseases: Role of Inflammation Triggers and Cytokines. Front Immunol (2018) 9;9:586. doi: 10.3389/fimmu.2018.00586. 
  2. Franceschi C, Bonafè M, Valensin S, Olivieri F, De Luca M, Ottaviani E, et al. Inflamm-aging. An evolutionary perspective on immunosenescence. Ann N Y Acad Sci (2000) 908:244–54. doi:10.1111/j.1749-6632.2000.tb06651.x 
  3. Franceschi C, Campisi J. Chronic inflammation (inflammaging) and its potential contribution to age-associated diseases. J Gerontol A Biol Sci Med Sci (2014) 69(Suppl 1):S4–9. doi:10.1093/gerona/glu057
  4. Harris TB, Ferrucci L, Tracy RP, Corti MR, Wacholder S, Ettinger WH Jr, et al. Associations of elevated interleukin-6 and C-reactive protein levels with mortality in the elderly. Am J Med (1999) 106(5):506–12. doi:10.1016/ S0002-9343(99)00066-2
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