The overwhelming balance of scientific evidence shows that damage to nuclear DNA increases with age. This is one of the reasons why cancer is an age-related condition: as time goes by there is an ever greater chance of some cell somewhere in the body suffering just the right combination of mutations to become cancerous. The mainstream position is that this damage also provides a meaningful contribution to the broader aging process by causing disarray in the processes of cells where it occurs, although this point is debated. It may be that beyond cancer incidence the level of nuclear DNA damage suffered over the present human life span is not large enough to provide a significant contribution to age-related disease, frailty, and death.
Here is a review of the literature that confirms the correlation between nuclear DNA damage and age. It is necessary in the scientific process to continually anchor every concept with ever more evidence, especially when the matter at hand is a complex system only partially understood:
Although DNA is not the only target changed with aging, taking account of the major role of this macromolecule in the regulation of all cellular structures and its own cell cycle, DNA damage has been studied with particular attention. The alterations could have several consequences for genome stability with repercussions on cellular component synthesis, cell cycle machinery and signaling pathways that control cell cycle arrest, and programmed cell death or apoptosis. The consequences of DNA damage will depend on the type of damage, genes affected and type of cell and tissue damaged.
The prevailing view is that there is a tendency for an age-related DNA damage accumulation. However, on examination, results of studies show inconsistency; it is possible that confounding factors influence this relation and explain some of the inconsistency. Factors such as diet, lifestyle, exposure to radiation and genotoxic chemicals seem to have a significant influence on the relationship between cumulative DNA damage and age. Methodological factors might have also influenced the observed results. Indeed, different assays may be used to measure DNA damage. Furthermore, the measured DNA damage could reflect changes in the causative factors, and/or changes in DNA protection and/or changes in DNA repair capacity. It must also be noted that the type of cell and tissue used could reflect different aging rates within the organism.
Although there are several excellent narrative reviews on age-related nuclear DNA damage, they usually refer to individual animal and humans studies and, as far as we know, no meta-analytic technique has been used to estimate the extent of effect of potential moderators on age-related DNA damage in humans. Thus, the overall goal of this paper is to address this important gap in the literature.
Electronic databases and bibliographies for studies published since 2004 were searched. A total of 76 correlations from 36 studies with 4676 participants were included. Based on our analysis, a correlation between age and DNA damage was found. The test for heterogeneity of variance indicates that the study's results are significantly high. Moderator variables such as smoking habits, technique used, and the tissue/sample analyzed, are shown to influence age-related DNA damage. Nevertheless, sex did not show any influence on this relation.
In conclusion, this meta-analysis showed an association between age and DNA damage in humans. It was also found that smoking habits, the technique used, and tissue/sample analyzed, are important moderator variables in age-related DNA damage.