
Judith Campisi began her career studying cancer, but now investigates the molecular causes of aging
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Scientists have long thought that aging could be caused by molecular damage that accumulates in our bodies over the course of time. The damage is an unavoidable by-product of breathing oxygen and other metabolic processes that are necessary to life. Eventually, damaged cells stop working, or worse, adopt new functions that trigger cancerous growth or degrade important tissues in the brain, skin and other organs.
But as Melinda Wenner Moyer reports in the February issue of Scientific American, investigators have conducted several experiments over the past few years that challenge this so-called oxidative stress theory of aging. For example, a tiny mouselike creature known as the naked mole rat manages to live up to 30 years (about 10 times longer than a similarly sized mouse) despite accumulating a much greater level of oxidative damage in its tissues than other rodents.
These and other often surprising results have led to a boom in research on aging in the past few years, as investigators learn more about the inner workings of the cells at the molecular and genetic levels.
Scientific American spoke to Judith Campisi, a professor at the Buck Institute for Research on Aging and senior scientist at the Lawrence Berkeley National Laboratory, for a quick overview of the field. You can read more about Campisi’s research on cell senescence as one possible cause of aging in the August 2012 issue of Scientific American.
[An edited transcript of the interview follows.]
Why is it so hard to figure out what causes aging?
In many ways we already know what causes aging. We just don't know what causes aging in the kind of molecular detail that would allow us to intervene in large meaningful ways. It's not even clear that once we solve those mysteries we will be able to intervene in aging or dramatically extend longevity.
I started my career studying cancer. Look at all the things we have learned since the 1970s about how cancers form in the body. And yet, still the best cures we have for most cancers are sledgehammers. Biology is complex—and this is a reality that the public has to come to grips with and our legislators have to come to grips with.
I predict aging will follow the same trajectory as cancer research. Why is aging so difficult to figure out? It's because it's a really tough problem. I think it's tougher than cancer. The time has come to really wallow in the complexities.
How many different causes of aging do you think there will turn out to be?
I don't think there will be hundreds of causes of aging. But I don't think there will be just one, either, or we would have gotten a handle on it by now. It's sort of like asking me what the stock market would be tomorrow. I could give you an answer but you'd be crazy to believe me!
How about just a couple causes of aging?
Well, we know that there is molecular damage and what I will refer to as genetic damage—although that doesn't necessarily mean a mutation. By genetic damage, I am referring to both changes in the genes themselves as well as in the epigenetic switches that regulate how the genes are expressed.
Why does this damage occur? Basically, there are two main reasons: One, breathing oxygen is dangerous to your health. Your body makes certain harmful compounds just as a result of breathing oxygen. Two, the cells inside your body make mistakes when they divide. Most of the cells in your body are not dividing at any given time. Many have the ability to divide but don't. But when a cell does divide, it has to copy three billion base pairs of DNA exactly right. Inevitably mistakes happen and cells become damaged.




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4 Comments
Add CommentOxidative damage, an idea once central to the mechanism of aging, seems unlikely now.
Reply | Report Abuse | Link to thisI think it's be interesting to go back and interview the aging 'experts' of 10 & 20 years ago to see what they'd have said. I bet it'd be pretty entertaining, as this will likely be 10 or 20 years from now...
Reply | Report Abuse | Link to thisThe answer is, Yes!
Reply | Report Abuse | Link to thisThe length of our telomers get shorter as we age...Telomers are the strands of DNA at the ends of our chromosomes. So, when the length of our telomers get shorter our DNA gets damaged more often as our cells continue to divide. I believe that a good diet, along with healthy lifestyle, sufficient sleep, telmoer lengthening (or prevention from telomer shrinkage), stem cells, and gene therapy will all take part in increasing human lifespan.
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