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Did you know you have “zombie” cells inside you? Senescent cells were given the nickname “zombie” cells because they’re not quite dead, but they also don’t act like living cells — and they can wreak havoc on your tissues. Scientists think that these cells may be behind the damage our lungs, bones and even brains incur as we age. That has made some wonder: Could getting rid of these zombie cells help us stay healthier for longer?
In a new study published in the journal Nature Medicine, a treatment aimed at killing off these zombie cells showed promise for helping older women’s bodies create new bone, potentially staving off bone loss, a common issue in post-menopausal aging.
Here’s what to know about the latest frontier in the fight against aging.
What are ‘zombie cells’?
More formally called “senescent” by scientists, these are cells that are dying, but are not quite dead. They accumulate more and more as we age, triggering inflammation and damage to otherwise healthy cells.
The same team of Mayo Clinic researchers behind the latest paper “were the leaders in the field [who] demonstrated that senescent cells aren’t just a consequence of aging, but can be considered as driving aging,” Paul Robbins, director of the University of Minnesota’s Institute of Biology of Aging and Metabolism, tells Yahoo Life.
Zombie cells are thought to build up in all manner of tissues, but they don’t seem to necessarily behave the same way in one part of the body that they do in another. But research — primarily done in mice — suggests that clearing the zombies out could extend health span by slowing damage that leads to age-related health problems, including bone density loss, lung scarring and Alzheimer’s disease, Robbins says.
What did the new study find?
Based on previous research in mice and petri dishes, scientists hypothesized that senescent cells contribute to osteoporosis or low bone mass — forms of age-related bone loss that affect about 13% of Americans over 50, including nearly 20% of women, according to the latest national estimates from Centers for Disease Control and Prevention.
The Mayo Clinic team tested a combination of a commonly used cancer drug, dasatinib, and a compound found in some foods and sold as a supplement, quercetin — which had shown promise in killing off senescent cells — in half of a group of 60 otherwise healthy postmenopausal women (the other half did not get the treatment, and served as the control group). Biomarker testing suggested that the treatment — known as D+Q — helped women grow 16% more new bone than those in the control group. But there were caveats.
The benefit was only present two weeks and four weeks after the trial started; the groups evened out by the trial’s end. And the zombie cell-killing drugs didn’t seem to slow bone loss; it just improved bone creation rates.
Perhaps most important, the treatment worked best on women who had high volumes of senescent cells. The research suggests that “only about 30% of all women over age 60 might have a high enough burden of senescent cells to respond to this particular drug combination,” study co-author and Mayo Clinic bone loss researcher Dr. Sundeep Khosla tells Yahoo Life. He adds that that burden, or density of zombie cells, tends to go up noticeably after age 70, so treatments might be most beneficial starting then.
What does it mean for anti-aging and longevity?
It’s a good first step, Khosla and Robbins say. This research was the clinical trial to test a zombie cell-killer treatment in humans. And the fact that it worked at all is promising, Robbins says.
The science of how and why we age is (pardon the expression) still young, and our attempts to slow or stop it are even newer. Scientists have discovered a number of biomarkers, or signals, for biological age — namely, DNA changes — but the challenge is figuring out what might be “a druggable target,” Robbins says. And that’s why he and Khosla have focused on zombie cells.
Based on research in animals, they are among the scientists who believe that “reducing the number of senescent cells will contribute to extending health spans,” he says, but adds that “there are other targets, too.”
D+Q is one possible “geroprotector” — a treatment that may be protective against the harmful processes of aging — but there’s still a lot to learn about how best to use it. The new study, for example, shows that this particular treatment isn’t likely to work very well unless someone already has a lot of zombie cells, which isn’t easy to measure, at least for slowing bone loss, says Khosla. But figuring that out helps scientists know when the treatment could be useful, and working out the correct timing and dosing could make it more effective. And D+Q isn’t the only drug that could potentially fight cellular senescence.
If quercetin helps fight aging, should I take it?
You might be tempted to take quercetin, since it’s being studied for anti-aging properties and can be found on health food and supplement store shelves. But many experts advise holding off, since quercetin is a flavonoid, an antioxidant compound that gives some fruits and vegetables — including citrus fruits, blueberries, apples, onions and parsley — their color, according to Mount Sinai. Robbins warns that “I’m not sure if the doses people take daily is sufficient to kill senescent cells.” But the study suggests that quercetin or another flavonoid, fisetin, in combination with other drugs, might be. However, Robbins and his partner did start taking fisetin once every two weeks after he published a paper showing that quercetin might reduce the risk of severe COVID.
The biggest risk with these supplements is that you simply don’t know what you’re getting because they’re not regulated, and companies often make exaggerated or false health claims. “So if you buy something at [a vitamin shop], you can’t tell if it’s pure,” Robbins says.
But even if you bought the purest form of quercetin, “on its own, it’s not a very effective senolytic,” or zombie-cell killer, Robbins says. And even if it were, the latest research underscores a very important point, he says: “Taking drugs to slow aging at age 20 may have no benefit, and may in fact be harmful.”
