New study argues aging isn't the cause of death; autopsy findings point to heart and lung failure as leading killers

A German-led study challenges the long-held view that old age itself is a cause of death. Researchers at the German Center for Neurodegenerative Diseases reviewed autopsy records from 2,410 adults and found that the circulatory system is the body’s primary point of failure. Cardiovascular disease, particularly heart attacks, accounted for the largest share of deaths, with 39% attributed to heart attack, about 38% to heart or lung failure, roughly 18% to stroke, and 10% to blood clots in the lungs. The researchers note that many of those deaths were due to recognizable diseases that were undiagnosed in life, and the pattern held across age groups, including people 100 years and older who are often thought to be exceptionally healthy. The findings imply that aging may represent a state of heightened vulnerability to specific diseases rather than a direct, generalized aging process that alone causes death.

Among centenarians, the study found that nearly 70% died from cardiovascular causes, about a quarter from respiratory failure, with the remainder from other organ failures. Notably, not a single autopsy cited death as the result of “old age.” The authors acknowledge that the percentages add up to more than 100 because many patients suffered multiple, interacting health events—such as a heart attack leading to heart failure or a stroke contributing to multiple organ complications. Even in the oldest survivors, heart problems remained the dominant thread in mortality.

The researchers emphasize that the so‑called hallmarks of aging—features such as lingering damaged cells, degraded DNA, and worn chromosomes—are not in themselves direct causes of death on death certificates. Instead, they argue these hallmarks signal a body in a weakened state that is more likely to succumb to a diagnosable, fatal disease such as heart attack, stroke, or organ failure. In other words, the hallmarks may reflect the vulnerability created by aging rather than being the actual drivers of mortality.

The team contends that aging research has long operated under two assumptions that their analysis challenges. First, they say, extending lifespan has often been equated with slowing aging itself. Second, they argue that many key studies validating the hallmarks of aging rely on experiments conducted in old animals, a setting that may not reveal whether targeting these hallmarks truly slows the aging process from its onset. When middle-aged animals are included, many interventions yield different results than they do in older subjects, sometimes showing little effect on the rate of aging and instead providing general health boosts.

One of the hallmarks frequently cited is the presence of “zombie cells”—senescent cells that stop dividing but do not die, releasing inflammatory signals that may contribute to aging and diseases such as Alzheimer's disease, arthritis, cancer, and diabetes. The researchers argue that if zombie cells were a true driver of aging, removing them should slow systemic deterioration across organs, not merely improve symptoms in old age. They propose a shift in how interventions are tested: administering treatments to middle-aged animals to track decline over time, rather than waiting until animals are already old and frail. This approach would help determine whether a given intervention truly slows the aging process or merely postpones specific diseases.

Biological clocks—patterns of DNA changes and other biomarkers used to estimate a person’s biological age—have emerged as tools to predict mortality risk. The study, however, cautions that these clocks track biomarkers that change with age without necessarily identifying the underlying processes that drive aging. Altering a clock score might reflect a change in a biomarker rather than a fundamental modification of the aging process itself. The researchers say that relying on clock metrics to claim true aging modification could be misleading if the core biology remains unaffected.

The authors’ conclusions carry potential implications for how aging research is framed and funded, as well as how products marketed as anti-aging therapies are evaluated. They caution that extending lifespan in some models may reflect delayed onset of specific diseases rather than a slowed rate of aging across the body. If confirmed, the findings would emphasize prevention and management of cardiovascular and pulmonary diseases as central to improving longevity, regardless of people’s chronological age. While the work does not deny that aging occurs, it reframes the narrative around what ultimately causes death and how scientists should test interventions intended to alter the aging process.

For policymakers, clinicians, and the public, the study underscores the importance of robust cardiovascular and respiratory health across the lifespan. It also highlights the need for rigorous, age-spanning testing of anti-aging interventions to determine whether they alter the rate of aging or simply delay particular diseases. In an era when longevity research and the market for anti-aging products are expanding rapidly, the researchers call for a careful, evidence-based approach to claims about slowing aging rather than prolonging life by postponing the onset of specific ailments.

Ultimately, the study suggests that humans’ Achilles’ heel may be the circulatory system rather than aging itself as a universal, inexorable process. By focusing on preventing and treating cardiovascular and respiratory conditions, clinicians may improve survival and quality of life in ways that were previously attributed primarily to delaying an abstract notion of aging. The researchers acknowledge that aging is a complex, multifaceted phenomenon, but they argue that a clearer accounting of its relationship to concrete diseases could reshape both scientific inquiry and public expectations about what it means to grow old.