Several interventions may slow down these processes, preventing or delaying the progression of multimorbidity and disability. In the past few years, for example, data has begun to emerge that metformin, a drug prescribed for Type 2 diabetes and other metabolic diseases, had the “side effect” of reducing the incidence of other diseases of age compared to the purportedly healthy, non-diabetic controls against whom they were compared. In observational studies across 78,000 people, metformin was found to decrease all-cause mortality by 17 percent in the active group, which was more diabetic, more obese and less healthy overall than the control group. Now small off-label trials of metformin and rapamycin, another drug that targets the mTOR pathway, seem to indicate that these small molecule drugs can change the biology of ageing in tissues to a younger profile. Big, multicentre trials are underway or will soon start.¹⁴ Another approach is senolytics, a class of drugs that selectively clear senescent cells.¹⁵ At the moment, most of the work is on small molecules, and lifestyle interventions. The first set of drugs that have been identified as interventions have been shown to affect all hallmarks of ageing, rather than one specific pathway: for example, rapamycin affects cell senescence but it also revitalises adult stem cells, affects protein synthesis and mitochondrial function and reduces inflammation. The same is true of metformin and sirtuins. The therapeutic interventions now going into clinical trials seem to affect the systemic process itself, and may elucidate the unitary hypothesis of fundamental ageing processes.