One recent breakthrough in the understanding of aging, aging-related diseases and cancer has to do with the detailed mechanics of how our human cells divide. It’s really a pretty nifty discussion – and I promise not to get too technical. But it has major implications for research and development of new medical therapies, as well as anti-aging implications, so it’s worth hearing about.
We remember, from high school biology, that our cells DNA is duplicated as cell division takes place, right? Well, it turns out that there is an important detail missing from that explanation, and that our little human DNA photocopier doesn’t make perfect copies.
At the end of a strand of DNA, there is a “cap” called a telomere. Dr. Elizabeth Blackburn, who was later awarded the 2009 Nobel prize in medicine for her work in this area, famously compared telomeres to the little plastic tips on the ends of shoelaces that keep them from fraying. (For those of you in the crowd who like cell biology, a telomere is a long repeating section of DNA, with the base pair pattern TTAAGGG repeating many times.)
As our cells undergo division, our personal little DNA photocopier, called “DNA polymerase”, can’t properly copy this section properly, and so the newly minted telomere gets progressively shorter with each round of cell division. That’s the problem.
This limits cells to a fixed number of divisions, and sets a limit on the cell’s lifespan. Except for cancer cells – which have figured out how to beat this problem with a telomere repair enzyme, called telomerase, giving them the potential for an unlimited number of replications, or a sort of immortality.
Studies have found shortened telomeres in many cancers, including pancreatic, bone, prostate, bladder, lung, kidney, and head and neck. Short telomeres have also been linked to an aging effect on the cells (“senescence”) and are found in multiple non-cancer disease states, like Alzheimer’s dementia, ALS and coronary heart disease.
So, significant research is going into ways to keep telomeres from shortening, or perhaps how to reverse the telomeric shortening process. Not only would this help to fight multiple cancers and Alzheimer’s, but there could be significant anti-aging effects as well. Ideally, we could find a way to keep telomeres nice and long in healthy cells, but not in cancerous cells.
In this week’s issue of JAMA, researchers looked at the effect of a fish oil, omega-3 fatty acid, and its effect on telomere shortening over a 5 year period. It turns out that omega-3 fatty acid is good for your telomeres. People with the lowest levels of omega-3 fatty acids in their blood stream showed the most aging changes in their telomeres, and vice versa. You might want to consider getting some omega-3 supplements!
A double-blind, randomized trial on whether omega-3 fatty acid actually reduces cellular aging is now planned.
Here in Orlando, UCF has a national reputation in this area: much research is done here on the effect of telomere shortening and neuro-degenerative diseases. Go team!