This paper notes that long-lived humans show lower levels of nuclear DNA damage and better preservation of mechanisms that repair and prevent that damage - which is as one would expect given that interventions that slow aging in laboratory species tend to produce much the same comparative outcomes in DNA integrity over a life span. Damage to nuclear DNA occurs constantly, but is repaired very efficiently. Nonetheless, mutational damage accumulates randomly in an individual's cells, a change here, a change there. The level of this damage correlates with age, and is lowered in individuals of the same chronological age as a result of interventions that slow aging, such as calorie restriction. Rising levels of nuclear DNA damage are definitely a cause of the increased cancer risk in aging, but it is the general consensus in the research community that, going beyond cancer, this damage also contributes to degenerative aging in other ways, such as by producing increasing disarray in cellular activities. This consensus doesn't have the robust demonstrations in animal studies needed to back it up at the present time, however, and has been challenged. It is difficult to split apart this aspect of aging from all others in a living organism so as to produce a study in which just the effects of DNA damage can be isolated.
Reductions in DNA integrity, genome stability, and telomere length are strongly associated with the aging process, age-related diseases, and the age-related loss of muscle mass. However, in people reaching an age far beyond their statistical life expectancy the prevalence of diseases, such as cancer, cardiovascular disease, diabetes or dementia, is much lower compared to "averagely" aged humans. These inverse observations in nonagenarians (90-99 years), centenarians (100-109 years) and super-centenarians (110 years and older) require a closer look into dynamics underlying DNA damage within the oldest old of our society.
Available data indicate improved DNA repair and antioxidant defense mechanisms in "super old" humans, which are comparable with much younger cohorts. Partly as a result of these enhanced endogenous repair and protective mechanisms, the oldest old humans appear to cope better with risk factors for DNA damage over their lifetime compared to subjects whose lifespan coincides with the statistical life expectancy. This model is supported by study results demonstrating superior chromosomal stability, telomere dynamics and DNA integrity in "successful agers". There is also compelling evidence suggesting that life-style related factors including regular physical activity, a well-balanced diet and minimized psycho-social stress can reduce DNA damage and improve chromosomal stability. The most conclusive picture that emerges from reviewing the literature is that reaching "super old" age appears to be primarily determined by hereditary/genetic factors, while a healthy lifestyle additionally contributes to achieving the individual maximum lifespan in humans.
More research is required in this rapidly growing population of super old people. In particular, there is need for more comprehensive investigations including short- and long-term lifestyle interventions as well as investigations focusing on the mechanisms causing DNA damage, mutations, and telomere shortening.