Why does the risk of cancer increase with age?
The older you get, the more damage accumulates in your cells and the worse your body becomes at repairing or detecting that damage. This makes cancer, at its core, a disease of ageing, one in which lifestyle choices can strongly influence the pace.
Age is the single greatest risk factor for cancer in the Western world. This is not due to one cause, but to an interplay of processes that build up over decades.
Throughout a lifetime, cells are repeatedly attacked by carcinogens, radiation and metabolic errors. Each attack can leave a small mistake in the DNA. When we are young, the body is good at detecting and repairing such mistakes. As we age, that repair mechanism works less effectively, allowing errors to accumulate. Enough errors in the right genes can turn a cell malignant.
Senescent cells play a separate, ambiguous role. They stop dividing, which normally puts a brake on cancer propagation. But they do not disappear; they remain in the tissue and disrupt the environment around healthy cells. In doing so, they actually undermine the very system that normally suppresses tumours.
Added to this is a smouldering chronic inflammation, known as 'inflammaging'. As people grow older, the immune system becomes mildly but persistently activated. This low-grade inflammation promotes the development of cancer, but also of cardiovascular disease and diabetes. At the same time, the immune system becomes less sharp at detecting early-stage tumour cells, so a malignant cell is more likely to go unnoticed.
Finally, the systems by which cells 'sense' how many nutrients are available, such as insulin and growth-factor signalling, also change with age. Disruption of these systems accelerates the ageing process and contributes to age-related diseases including cancer. Lifestyle amplifies all of these processes: smoking, physical inactivity and excess weight drive the accumulation of damage even further, as is visible in the rise of colorectal cancer in Western countries.
The claims are based on review articles and an overview study on ageing biology and cancer (PMID 22975005, 38762096, 31806905, 27189416, 38147966). The mechanisms are well supported biologically; precise quantification of each individual mechanism is not available in the sources consulted.