Why does a long life lead to more health problems?

The main idea is known as the ‘shadow of selection’. Put simply, natural selection is better at ‘spotting’ factors that influence youthfulness and the production of offspring. Harmful effects that manifest themselves later in life, however, often go almost entirely unnoticed by evolution.

This does not mean that ageing can be explained by a single cause, or that scientists have found a way to stop it. This is a major review: the authors have compiled data from evolutionary theory, genetics, comparative biology and research into the mechanisms of ageing.

Details

Natural selection works most strongly where a trait affects survival and reproduction. If a particular trait helps a young organism to survive, grow faster or produce offspring, it can become established across generations.

But if that same trait later increases the risk of disease, it has a weaker influence on evolution. In the past, many organisms simply did not live long enough to reach the age when such consequences became apparent.

This gives rise to two important mechanisms.

The first is the accumulation of late-onset mutations. If a harmful genetic variant only manifests in old age, natural selection is less effective at eliminating it.

The second is the side effect of genes that are beneficial in youth. The same biological mechanism may be helpful in early life but harmful later on. For example, pathways associated with growth, nutrition, reproduction and tissue repair are beneficial in youth, but in old age their function may be linked to age-related disorders.

Put simply, the body was not ‘designed’ for an infinitely long, healthy life. It evolved as a system that needs to function well during growth, survival and reproduction. Today, however, people are living to an age where the long-term costs of this system become apparent.

The authors of the review note that modern conditions have exacerbated this effect. We live longer, have fewer children, receive medical care, and recover better from infections and injuries. Consequently, age-related diseases have become a significant part of society’s life.

Why this matters

This perspective helps us understand why diseases of old age are often interlinked. Cardiovascular diseases, neurodegenerative processes, metabolic disorders and other age-related conditions may share common biological roots.

The review discusses the so-called hallmarks of ageing: DNA damage, impaired mitochondrial function, disrupted nutrient metabolism, and the accumulation of damaged proteins and ageing cells. Many of these processes are regulated by ancient signalling pathways found in various animal species.

This is important for medicine, but it is not sensational. Scientists are not claiming to have found a ‘cure for old age’. Rather, they are demonstrating why the same ancient biological systems may be linked to several age-related diseases at once.

If we learn to gently influence such common mechanisms, in the future we will be able not simply to prolong life, but to increase the number of years a person spends in good health.

Background

The idea of the ‘shadow of selection’ is not new. Classic evolutionary theories of ageing have long explained that the force of natural selection typically diminishes with age. But scientists now have more data: human and animal genomes, large medical databases, biomarkers of ageing, and studies of molecular mechanisms.

A new review brings these areas together. It shows that ageing cannot be explained by a single cause. It is influenced by genes, the environment, lifestyle, species history, population size, the age at which children are born, and how long people now live.

The main idea is simple: age-related diseases have become particularly noticeable not because ‘something suddenly went wrong’ with humans, but because modern life has taken us far beyond the age at which evolution selected protective mechanisms particularly rigorously.

Source

Study: Handan Melike Dönertaş, Linda Partridge, Evolutionary genetics of ageing, Nature Reviews Genetics, 2026.