Scientists have determined that nobody, not even a centenarian, dies of old age.
The traditional view is that ‘old age’ is a cause of death; that as a person gets older, their systems gradually decline and they die.
But new research from the German Center for Neurodegenerative Diseases posits that old age isn’t actually a true cause of death; it is just a time on a biological clock when specific diseases overwhelm the system and a person dies.
Researchers propose that the famous ‘Hallmarks of Aging,’ like lingering dead cells, damaged DNA and worn out chromosome caps might not be the direct killers, but rather the symptoms of the deeper aging process and a state of increased vulnerability to deadly diseases like heart failure.
An analysis of 2,410 human autopsy reports identified the circulatory system as the body’s primary point of failure. The overwhelming cause of death was cardiovascular disease, heart attacks specifically, often undiagnosed until autopsy, accounting for 39 percent of all cases.
Even among centenarians, people 100 years and older, seen overall as healthy, autopsies revealed that they didn’t die of ‘old age.’ Nearly 70 percent died from cardiovascular causes, a quarter from respiratory failure, and smaller percentages from other specific organ failures.
This theory deals a major blow to the longevity industry, arguing that increasingly popular ‘anti-aging’ drugs do not slow aging; rather, they merely delay one particular disease.
While heart attacks caused 39 percent of deaths, general heart or lung failure was behind 38 percent of deaths, stroke nearly 18 percent and blood clots in the lungs caused 10 percent. A major artery rupture accounted for just under 10 percent of deaths.
These percentages add up to more than 100 percent because many people had a combination of these issues; a heart attack led to heart failure, for instance.
For humans, the Achilles’ heel isn’t aging, it’s the failure of the circulatory system.
The hallmarks are not the direct cause of death on a death certificate.
Instead, they are indicators of a body in a weakened state, which is then more likely to succumb to a diagnosable fatal disease like a heart attack, stroke or organ failure.
The researchers said: ‘Aging research has long been shaped by assumptions that may not fully account for the complexity… of the aging process. One of the most persistent assumptions is that extending lifespan equates to slowing aging.
‘However… age-related mortality is often determined by a narrow set of life-limiting pathologies rather than by a generalized, systemic aging process.
‘As a result, lifespan extension frequently reflects the delayed onset of specific diseases rather than a slowing of aging per se.’
The researchers argued that the foundation of anti-aging science is built on flawed logic.
When they reviewed the key studies used to validate the ‘Hallmarks of Aging,’ they found that 57 percent to 100 percent of the experiments had only been tested in already-old animals, leaving a major gap in proof about whether targeting these hallmarks can actually slow aging from the start.
Scientists, they argued, cannot tell if something slows aging or just treats symptoms in the already-old. Most studies only treat old animals, conflating disease treatment with aging modification.
In the few studies that included young animals, the treatment helped both young and old animals equally 72 percent of the time. This means it was just a general health boost, not something that changed the rate of aging.
For instance, one major hallmark is ‘zombie cells,’ which refer to damaged cells that stop dividing but do not die and instead linger in the body and release inflammatory chemicals, contributing to aging and diseases like Alzheimer’s, arthritis, cancer, and diabetes.
The claim is that these cells are a primary driver of aging itself. If true, removing them should not just make old bodies less sick, it should fundamentally slow down the rate at which multiple organs deteriorate over time.
To effectively study these interventions’ ability to slow the systemic deterioration that leads to disease-related deaths, the researchers argue that scientists should give experimental treatments to animals in middle age so that they can track decline as they age, not just when they’re already old and frail.
‘Biological clocks’ have emerged from this space, promising to predict people’s biological age and mortality risk based on data patterns, like DNA changes that turn certain genes on and off, that correlate with age.
But the researchers say that these clocks track biomarkers that change alongside aging, not necessarily ones that drive it. Changing one’s clock score might mean they have altered a sign of aging, but not necessarily the underlying process.
