OpinionOpinion |
For nearly all of human history, aging has been accepted as something that simply happens. Bodies ware down, organs falter and the only reasonable response is to endure it with as much grace as one could manage. That assumption is now being challenged with new research and technology.
This subject matter is complicated — but very interesting. I hope to convey this well. Bear with me.
Over the past few years, researchers have begun to identify the specific cellular potential causes that drive aging. Not the symptoms of it — the potential causes. This distinction matters enormously, because a symptom can only be managed, while a cause/mechanism can be targeted.
Much of the attention has landed on the immune system. In August, the journal Nature Aging published a fabulous article about what researchers call immune aging. Our immune system does far more than fend off infection; it repairs tissue, clears away damaged cells and helps keep our organs running. As it falters with age, it settles into a state of low, constant irritation that researchers call inflammaging (chronic, low-grade inflammation that accumulates over the years). It has been linked to cardiovascular disease, diabetes, dementia and cancer. Surprisingly, the process begins earlier than most of us may assume. The thymus, the small organ where a key class of immune cells is trained, starts shrinking at puberty.
Two studies published this summer have explained this issue quite well. The first, from Stanford Medicine and published in July in the journal Science, examined two immune cells working in tandem. Neutrophils are the body’s first responders. We produce roughly 100 billion daily, and most survive less than 24 hours. When they die, they can enter a state called senescence and start leaking a substances that causes inflammation to surrounding tissue. Clearing them away falls to macrophages (white blood cells that protect the body), which Dr. Katrin Andreasson, the study’s senior author, describes as the body’s garbage collection crew.
Her team discovered that with age, a hormone called PGE2 accumulates and overstimulates a receptor known as EP2 on those macrophages. The garbage crew stops collecting garbage. Spent cells pile up in the liver, spleen and bone marrow, and inflammation spreads throughout the body.
Then came the part that should give all of us pause. When researchers disabled that single receptor in older mice, the animals stayed leaner and stronger, showed reduced inflammation in the heart, liver, kidney and brain, and navigated memory and balance tests nearly as well as young mice. Of 71 blood proteins that normally shift with age, 59 held at youthful levels. The same pattern was later confirmed in human liver tissue. “We’ve been trying to figure out why we age,” Andreasson said. “Now we know at least one big reason for it.”
The second study, published in June by MD Anderson Cancer Center at the University of Texas, uncovered an entirely separate trigger. Aging cells begin exporting structures called R-loops (temporary tangles of DNA and RNA) out of the cell nucleus, where they do not belong. The immune system mistakes them for an invader and sounds an alarm that never shuts off. When researchers blocked that export using selinexor, a medication already approved for treating multiple myeloma (a rare cancer), laboratory models showed less inflammation, less liver scarring, healthier body composition and significantly longer lifespans.
While this is exciting and promising, this work has been done in mice and human cells, not patients and no approved medication yet targets EP2 selectively. Still, consider what has happened. Two independent teams, working on separate mechanisms, each found a way to slow aging across multiple organs at once. That is true progress and will lead to great change.
In the meantime, the proactive measures available to us remain simple and genuinely effective. Sleep, physical activity, a diet rich in vegetables, legumes and whole grains, managing stress and avoiding tobacco all measurably lower chronic inflammation. Best to be proactive than reactive.
If any of this stirs your curiosity, follow it. The National Institute on Aging, the Stanford Medicine News Center and the MD Anderson newsroom publish their findings in plain language, free to anyone willing to read them. We are living through the period where aging is no long a great mystery and has started to become something which may have solutions. This is worth paying attention to.
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