A number of relatively recent review articles have discussed the connections between inflammation and aging, as well as between aging and cancer. The connections between all three of these scourges have now been reviewed by Vasto et al., who pay special attention to the neglected arm of the triangle — the relationship between inflammation and tumorigenesis.

Inflammation, ageing and cancer

Cancer is generally recognized as an age-related disease. In fact, incidence and mortality rates of most human cancers increase consistently with age up to 90 years, but they plateau and decline thereafter. A low-grade systemic inflammation characterizes ageing and this pro-inflammatory status underlies biological mechanisms responsible for age-related inflammatory diseases. On the other hand, clinical and epidemiological studies show a strong association between chronic infection, inflammation and cancer and indicate that even in tumours not directly linked to pathogens, the microenvironment is characterized by the presence of a smouldering inflammation, fuelled primarily by stromal leukocytes. In this review, we have briefly mentioned inflammatory mediators involved in cancer although we decided to choose the ones which show a strict association with ageing and longevity. Inflammation is necessary to manage with damaging agents and is crucial for survival. But, in our opinion, the pro-inflammatory status of ageing might be one of the mechanisms which relate cancer to ageing. The most appropriate inflammatory genes have been selected to survive and to reproduce. Paradoxically, inflammatory age-related diseases (including cancer) are the marks of the same evolutionistic trait. Centenarians are characterized by a higher frequency of genetic markers associated with better control of inflammation. The reduced capacity of centenarians to mount inflammatory responses appears to exert a protective effect towards the development of those age-related pathologies having a strong inflammatory pathogenetic component, including cancer. All in all, centenarians seem to carry a genetic background with a peculiar resistance to cancer which is also an anti-inflammatory profile.

Note that bit about centenarians at the end of the abstract. The reduction in inflammatory capacity they’re talking about isn’t large (not even two-fold at the level of primary cytokine output, though quantifying the difference depends ultimately on which endpoint one is measuring), so the observation gives credence to the idea that tailored anti-inflammatory drugs — perhaps targeted to individual tissues, or to specific types of cytokine responses — might help slow aging in tissues throughout the body.

In the meantime, keep popping those baby aspirins.