Researchers have found that even those who reach the age of 100 do not pass away purely due to old age.

Traditionally, it has been believed that aging itself is a direct cause of death, with the gradual decline of bodily systems leading to demise over time.

However, a new study from the German Center for Neurodegenerative Diseases suggests that old age should not be viewed as a standalone cause of death. Instead, it marks a period when certain diseases become too much for the body to handle, resulting in death.

The research team argues that the well-known “Hallmarks of Aging,” such as the accumulation of dead cells, DNA damage, and the deterioration of chromosome ends, may not directly cause death. Instead, they are signs of the aging process, which increases susceptibility to fatal conditions like heart disease.

An examination of 2,410 human autopsy reports highlighted the circulatory system as the primary area of failure in the body. Cardiovascular disease, particularly heart attacks often undiagnosed until post-mortem, emerged as the leading cause of death, responsible for 39 percent of cases.

Even among centenarians, individuals over 100 years old who are generally considered healthy, autopsies indicated that ‘old age’ was not the cause of death. Approximately 70 percent succumbed to cardiovascular issues, about a quarter died from respiratory failure, and smaller percentages were attributed to failures of specific organs.

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. 

Even in people over 100 who seemed healthy, autopsies showed 70 percent died from heart problems, 25 percent from lung failure, and the rest from other specific causes. Not one died from ‘old age’ (stock image)

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.