Why do we age?
There is no single answer, and the honest position is that ageing is multi-causal — a set of interacting processes rather than one clock running down. Researchers have converged on a list of contributing mechanisms, commonly called the hallmarks of ageing.
The main mechanisms:
Genomic instability. DNA accumulates damage from radiation, chemicals and ordinary metabolic byproducts. Repair systems are good but imperfect, and errors accumulate.
Telomere attrition. Chromosome ends shorten with each cell division. When they become critically short the cell stops dividing — a limit long observed in cultured cells.
Epigenetic alterations. The pattern of chemical marks controlling which genes are active drifts over time, so cells increasingly express the wrong genes for what they are. These changes are measurable enough to build epigenetic clocks that estimate biological age.
Loss of proteostasis. The machinery that folds, maintains and clears proteins declines, allowing misfolded proteins to accumulate.
Mitochondrial dysfunction, reducing energy production and increasing reactive byproducts.
Cellular senescence. Damaged cells stop dividing but do not die, and secrete inflammatory signals that damage neighbours. Clearing them in animal models has produced striking results, and senolytic drugs are an active research area.
Stem cell exhaustion, reducing tissue regeneration.
Altered intercellular communication, including chronic low-grade inflammation sometimes called inflammageing.
The evolutionary layer, which explains why these are not simply fixed. Natural selection acts weakly on traits expressed after reproduction. Mutation accumulation allows late-acting harmful variants to persist; antagonistic pleiotropy proposes that genes beneficial early can be harmful later and are still selected for; and the disposable soma theory holds that organisms allocate limited resources between repair and reproduction, and repair is under-funded because most animals die of something else first.
No consensus exists on which mechanisms are primary versus downstream — and that question is exactly what the field is arguing about.