While DNA forms the basis of life, it can also go astray, causing problems within the human body. One such variety of troublesome DNA is known as RTEs, for retrotransposable elements. RTEs act in a parasitic fashion if not held in check by genomes-uncontrolled RTEs replicate themselves and disperse themselves throughout the genome. Recent research at Brown University, discussed in the journal Aging, investigated RTEs with respect to aging.
The research team studied mouse genomes and discovered that with age, RTEs were more readily able to break loose and create copies. Genomes attempt to control the proliferation of RTEs by binding them in a tight DNA configuration known as heterochromatin, and as expected, the genomes of certain tissues showed an increase in heterochromatic structure as the mice aged. However, some areas with high concentration of RTEs showed a loosening of the binding structure, allowing RTEs to copy and spread.
There seems to be a critical age for mice (around age 2, a human equivalent age of near 70 years) where the genomes begin to significantly lose their battle with the RTEs, leading to a higher replication and spreading rate. This mechanism could trigger instability within the genome, and as a result could explain the underlying mechanism of chronic age related diseases such as various cancers. Similar but separate research at Brown using fruit flies backs up the hypothesis of age-related RTE increases.
The effect of aging isn't particularly surprising, but what sets this study apart is the aging mechanism. Previous studies have considered the aging of an individual cell, based on the number of divisions. In this case the research team is looking at the aging of the overall organism (mice in this case, but with reasonable implications for humans). By studying tissues throughout the bodies of the mice, the team found the RTE phenomena to be widespread and not localized to any individual area.
Could RTE replication and proliferation be one of the underlying causes of cancers? It's possible-the research team found higher concentrations of RTEs in mice that were suffering from lymphoma and other cancers that occur naturally.
This research doesn't prove any direct causal link between RTEs and cancer in general, or any specific cancers in particular, but it does represent important groundwork for further study. Drugs that inhibit the copying of RTE's already exist, so there should be a straightforward analytical path to test the links between RTE expansion and cancers (and for other chronic conditions as well).
New drugs may end up being important in controlling RTE proliferation, but the research team found something else that may help control RTEs-diet. Mice that consumed 40% less calories than the baseline diet showed less proliferation of RTE's, while maintaining adequate nutrition. This makes sense, given that calorie restriction has been found to be helpful in a variety of animal studies-and human studies as well. That's one more reason to think twice before loading up on that second helping at the holiday table, or super-sizing your fast food meal.