Researchers believe they have identified a fundamental cause of aging, according to a study published this week in the journal Cell. The mechanism was previously found in fungus and has now been discovered in mice. It’s likely that the same process applies to humans, said the authors of the research, from Harvard.
The study found that DNA damage, which accrues as we age, decreases a cell’s ability to regulate which genes are turned on and off in particular settings. Though DNA damage speeds up aging, the actual cause is not the DNA damage but the lack of gene regulation. However, this lack of gene regulation, called epigenetics, may be reversible.
For a long time most experts assumed that a sort of unbreakable yin-yang relationship links aging and cancer. Researchers looking for a way to make cells live longer constantly ran into the problem that cancer happens when cells live too long. The perception was reinforced when attempts to prolong life by up-regulating a protein called telomerase, which protects cells from dying after they go through a given number of division cycles, repeatedly ran into cancer problems.
Via resveratrol, research into the sirtuin proteins shattered that misperception. They key, as described in the article, is that aging has less to do with cell death than it does with gene regulation. If we fix gene regulation, or reduce the rate that it slides into dysfunction, then at the cellular level we fight aging. It In fact the new research does better than that: cancer is also a disease of gene dysregulation. It turns out that the famous trade-off is one hundred eighty degrees wrong: if you upregulate DNA quality control then you fight aging and cancer at the same time. As it turns out, the list of other stuff that also starts to work better includes infectious diseases (i.e., we get less of them), mental productivity and cardiovascular fitness.
In fact researchers knew about the effect for decades. However, earlier studies accomplished longevity by cutting a rat’s dietary calories to a point that almost no human could bear. The break came when a team at Harvard guessed that the starvation benefit hinged on a DNA silencing protein called SirT1. When they tried a massive screen for SirT1-activating chemicals the #1 hit was resveratrol, a compound previously known only as a phenolic in red wine. Resveratrol made yeast live longer, it made worms live longer and it had the same effect on flies. Mice and rats followed. Then came a research boom that may never slow down.
It may seem silly that our bodies already have the machinery to live into a healthy old age but prioritize something else. Why do we essentially choose not to live as long as we could? The key insight is that resveratrol, like the starvation diet that it mimics, strongly inhibits the sex drive and reduces the lifetime reproductive output. Nature wants us to get busy, fast, which means that if we want our bodies to prioritize quality control over making whoopee we need to trick it into thinking that we are on the brink of death (dead animals don’t make babies, so the body activates survival mode). We can do that by actually almost starving to death, but it is nice to know that medical science could soon offer a plan B.