We are living longer than our predecessors. Much of that is due to improvements in prevention of early life mortality relating to diet, control of infectious disease, sanitation, and similar items. A person who suffers many more infections and other health challenges in younger life, while eating a poor diet, will be more frail in later life. Thus methods of reducing early life mortality have the additional effect of extending life expectancy at older ages as well.
This first phase of technological improvement in overall wealth, medicine, and sanitation is largely done, the big initial gains secured. The present trend of interest is a slow upward movement in adult life expectancy driven by (a) continued smaller gains in control of disease and other forms of medicine for young adults, and (b) improvements in the treatment and control of age-related disease. The pace is slow in the latter case because age-related diseases are late stage manifestations of spiraling damage and dysfunction in the body, well past the point at which the web of biological consequences and relationships are easy to understand or treat.
Aging is an accumulation of damage: broken DNA, damaged molecular machinery, malprogrammed cells, metabolic waste products gumming up necessary functions, and more. Our biology can and does repair some of these issues on an ongoing basis, but as the damage accumulates even normally very efficient damage repair systems start to fail, driving a downward spiral of ever-faster dysfunction. Nonetheless, we are living longer and so we must expect that at any given age we are, on balance, less damaged than our ancestors. Since we are living measurably longer than people did even half a century ago (by something like ten years of life expectancy at birth, and more like five for adult life expectancy), this decline in damage must be visible over even such a short time frame.
Below you'll fine an example of such a measure. Amyloid is a precipitation of misfolded proteins that forms in old tissues in fibrils and other structures. There are numerous different types of amyloid, not all definitively tied to specific forms of age-related degeneration at this time, but if you have heard of amyloid then it is probably in connection with Alzheimer's disease (AD), in which amyloid buildup is thought to play an important role. The presence of amyloid is a noteworthy difference between young and old tissue, and levels of amyloid tend to correlate with levels of dysfunction and disease.
We compared amyloid deposition in autopsied cases aged 65 years and older who died between 1972 and 2006. We included consecutive cases for 1972-1975, 1980, 1985, 1990, 1995, and 2000-2006. We used linear regression models to assess period effects after adjustment for age, cognitive status, and neurofibrillary tangle (NFT) staging. We calculated amyloid/NFT stage ratios to account for possible changes in AD prevalence/severity over time.
Mean amyloid stage was significantly related to year of death in the total population (1,599 cases, mean age 82 ± 8 years) and decreased 24% in 1,265 individuals without dementia. This decrease was particularly marked in the oldest age groups; people 85 years and older in 2006 had less amyloid deposition compared with those aged 75 to 84 years in 1972. Recent cohorts had lower amyloid deposition. The amyloid/NFT stage ratio [decreased], confirming that more recent cases had less amyloid despite higher NFT densities.
The strong cohort effect we describe [provides] preclinical evidence supporting recently described decreases in AD incidence.