Although there have been many theories advanced to account for ageing with none gaining wide acceptance, some generalizations are agreed upon by most investigators. The life span is represented by growth and development and then decline or senescence (normal ageing) over time. These are not static stages but represent the continuously changing processes of the life cycle. Senescence results from declines in actual numbers of active metabolic cells and cellular functions because of the accumulation of environmental exposures and behaviours coupled with genetic vulnerabilities over time (Jazwinski, 1996; Kirkwood, 1996).

However, individuals also have an innate and unique genetic or biological plasticity that is coupled with adaptive or coping strategies for the management of ageing-related somatic changes. Thus ageing also produces increasing heterogeneity between individuals as they age. Coupled with this heterogeneity and particular health behaviours can be seen differential rates of decline and change among cells, tissues and organ systems, so that individuals will age at different rates with some biologically ‘old’ at 45, while others can be vigorous and ‘young’ at 75.

General ageing

Generally, with senescence, there is a quantitative loss of tissue mass as well as functional decline. An example of functional changes can be seen in the timing of circadian rhythms that affect temperature control, sleep patterns and the secretion of hormones such as cortisol, as well as growth hormone, the gonadotropins, thyrotrophin and melatonin.