Distinguishing these concepts can help guide how to live longer and for more years in good health.
Living longer and living more years looking and feeling youthful and disease-free are not one and the same. Although our life expectancies are getting longer, people are also spending more years with age-related chronic diseases. That is to say, we are not necessarily getting more years of vitality and good health but instead are getting to experience more years of illness.
With major advances in sequencing technologies and analytical algorithms, the ability to define aging and longevity separately has become possible only in recent years. These definitions are essential for improving aging and longevity and living longer lives filled with lots of energy and good health.
Know thy enemy, and know thyself
One way to think about aging and longevity is in terms of healthspan and lifespan, respectively:
- Healthspan: the part of a person’s life during which they are generally in good health.
- Lifespan: the time a person or animal lives.
With these concepts in mind, the scientific community has come up with some general definitions for aging and longevity, which can be roughly stated as the following:
- Aging: the progressive, event-dependent decline in the ability to maintain biochemical and physiological function.
- Longevity: the length of the lifespan.
Now, just because these two concepts are different doesn’t mean they are not intertwined. Distinguishing human biological aging from longevity can be difficult because the rate of aging may affect the length of the lifespan. With that being said, some researchers argue that lifespan and longevity are independent of healthspan and aging. That is to say, there are different forces at play.
The forces driving aging and longevity
Researchers have demonstrated with complex mathematics that longevity is determined from evolutionarily selected genes for reproductive advantage (i.e., survival of the fittest). Human longevity should best be thought of as an accidental byproduct of fixed genetic programs that optimize growth, development, reproduction, and ensure offspring’s reproductive success, such as grandparenthood.
On the other hand, aging is driven by a balance of damage and repair processes, influenced by environmental exposures and genetic variation. There is genetic evidence for the importance of several damage pathways in humans. Damage can be intrinsic, for example, through non-reproductive cell mutations arising during cell division. Also important are health behavioral risk factors such as smoking and obesity, which are also influenced by gene-environment interactions. The net impact of damage depends on the activity of repair and response mechanisms. At the cellular level, complete repair can yield undamaged cells.
By contrast, unrepaired damage can lead to cell death (apoptosis), preventing cancers but leading to the depletion of stem cells and loss of regenerative capacity. Cells with somatic oncogene mutations can survive and replicate, sometimes leading to tumor development. Alternatively, damaged cells can enter senescent states and produce a secretory senescence phenotype (SASP), resulting in inflammation and reduced repair that contributes to degenerative diseases. These mechanisms can result in reduced repair and increasing incidence of chronic diseases of aging but with decreased cancer risks, or vice versa.
Limits to aging and longevity
The rise in human longevity is one of humanity’s crowning achievements. Although advances in public health beginning in the 19th century initiated the rise in life expectancy, recent gains have been achieved by reducing death rates at middle and older ages. A debate about the future course of life expectancy has been ongoing for the last quarter-century.