Rosa Rubicondior: Unintelligent Design - Men Lose Their Y Chromosome

Men lose their Y chromosome as they age. Scientists thought it didn’t matter – but now we’re learning more

Creationists who point to the supposed 'perfection' of the human body as evidence of intelligent design have yet more evidence to ignore if they are to retain that belief. In my book, The Body of Evidence: How the Human Body Refutes Intelligent Design, I listed many of the conditions and vulnerabilities from which humans suffer precisely because our bodies are the products of evolution, not intelligent design. Viewed objectively, rather than through the rose-tinted lens of creationism, the human body is one of the strongest arguments against intelligent design and in favour of evolution.

We now have additional evidence of this. As men age, increasing numbers of their cells lose the Y chromosome — the chromosome that males normally possess alongside a single X chromosome, while females usually have two X chromosomes. It is becoming increasingly clear that this loss is implicated in several diseases that affect men disproportionately, including cardiovascular disease, Parkinsonism, and some cancers such as ocular melanoma. Together, these help to explain men's lower life expectancy.

According to the ID creationist paradigm, the human body is the supreme achievement of their god's design. So, if we assume, as they do, that this designer is the omniscient and omnibenevolent god of the Bible and Qur'an, then this male-specific vulnerability must either have been intended or be the accidental result of incompetence and lack of foresight. Traditionally, of course, ID creationists try to absolve their designer of responsibility for such flaws by blaming them on some other entity supposedly capable of thwarting the divine plan, with humans bearing the guilt because of the 'sin' of a mythical ancestral couple. This merely exposes Intelligent Design for what it really is: not science, as the Discovery Institute and its allies insist, but biblical literalism in a lab coat, forced to rely on fundamentalist superstition to explain away the failures of its own claims when the facts are examined.

How scientists are discovering this age-related loss of the Y chromosome in men's cells, and the damaging effects it has on male health, is the subject of an article in The Conversation by the distinguished geneticist Jenny Graves, Distinguished Professor of Genetics and Vice-Chancellor's Fellow at La Trobe University, Australia. Her article is reproduced here under a Creative Commons licence, reformatted for stylistic consistency.

First, some background information on the origins and function of the Y chromosome:

Background^ the origin and function of the Y chromosome. In mammals, the X and Y chromosomes did not begin as radically different chromosomes at all. They evolved from an ordinary matching pair of autosomes. The crucial change came when one member of that ancestral pair acquired a sex-determining gene, which in therian mammals became SRY, the switch that normally triggers development of testes in the embryo. Once that happened, recombination between most of the proto-X and proto-Y was progressively suppressed, preserving the male-determining region but also trapping the Y chromosome on an evolutionary path of gradual gene loss. [1]

That is why the modern human Y chromosome is so much smaller than the X chromosome. The X still carries hundreds of genes, whereas the Y retains relatively few functional genes, many of them connected with sex determination, sperm production, and a smaller set of broadly important regulatory functions. Far from being a useless remnant, the Y chromosome still carries genes essential for male fertility and normal development, but it is also unusually vulnerable because most of it no longer has a recombining partner with which to swap DNA and repair mutational damage in the usual way. [1]

Only small regions at the tips of the X and Y chromosomes — the pseudoautosomal regions — still recombine with one another during meiosis. The rest, about 95% of the human Y, is the male-specific region. That lack of recombination helps explain why the Y has shrunk over evolutionary time and why it has accumulated a peculiar structure, including repeated DNA sequences and gene families involved in spermatogenesis. [2]

Functionally, the Y chromosome does more than simply “make males male”. Its best-known role is the action of SRY, which initiates the pathway leading the embryonic gonads to develop into testes. But the Y also contains genes involved in sperm production and others that appear to have broader effects on gene regulation, immunity, and health. This is why losing the Y chromosome in ageing cells is no trivial matter: even a chromosome with comparatively few genes can still have important physiological consequences. [3]

Published: February 13, 2026 12.52am GMT

Men lose their Y chromosome as they age. Scientists thought it didn’t matter – but now we’re learning more

Nathan Devery / Getty Images

Jenny Graves, La Trobe University

Men tend to lose the Y chromosome from their cells as they age. But because the Y bears few genes other than for male determination, it was thought this loss would not affect health.

But evidence has mounted over the past few years that when people who have a Y chromosome lose it, the loss is associated with serious diseases throughout the body, contributing to a shorter lifespan.

Loss of the Y in older men

New techniques to detect Y chromosome genes show frequent loss of the Y in tissues of older men. The increase with age is clear: 40% of 60-year-old men show loss of Y, but 57% of 90-year-olds. Environmental factors such as smoking and exposure to carcinogens also play a role.

Loss of Y occurs only in some cells, and their descendants never get it back. This creates a mosaic of cells with and without a Y in the body. Y-less cells grow faster than normal cells in culture, suggesting they may have an advantage in the body – and in tumours.

The Y chromosome is particularly prone to mistakes during cell division – it can be left behind in a little bag of membrane that gets lost. So we would expect that tissues with rapidly dividing cells would suffer more from loss of Y.

Why should loss of the gene-poor Y matter?

The human Y is an odd little chromosome, bearing only 51 protein-coding genes (not counting multiple copies), compared with the thousands on other chromosomes. It plays crucial roles in sex determination and sperm function, but was not thought to do much else.

The Y chromosome is frequently lost when cells are cultured in the lab. It is the only chromosome that can be lost without killing the cell. This suggests no specific functions encoded by Y genes are necessary for cellular growth and function.

Indeed, males of some marsupial species jettison the Y chromosome early in their development, and evolution seems to be rapidly dispensing with it. In mammals, the Y has been degrading for 150 million years and has already been lost and replaced in some rodents.

So the loss of Y in body tissue late in life should surely not be a drama.

Association of loss of Y with health problems

Despite its apparent uselessness to most cells in the body, evidence is accumulating that loss of Y is associated with severe health conditions, including cardiovascular and neurodegenerative diseases and cancer.

Loss of Y frequency in kidney cells is associated with kidney disease.

Several studies now show a relationship between loss of Y and cardiac disease. For instance, a very large German study found men over 60 with high frequencies of loss of Y had an increased risk of heart attacks.

Loss of Y has also been linked to death from COVID, which might explain the sex difference in mortality. A tenfold higher frequency of loss of Y has been found in Alzheimer’s disease patients.

Several studies have documented associations of loss of Y with various cancers in men. It is also associated with a poorer outcome for those who do have cancer. Loss of Y is common in cancer cells themselves, among other chromosome anomalies.

Does loss of Y cause disease and mortality in older men?

Figuring out what causes the links between loss of Y and health problems is difficult. They might occur because health problems cause loss of Y, or perhaps a third factor might cause both.

Even strong associations can’t prove causation. The association with kidney or heart disease could result from rapid cell division during organ repair, for instance.

Cancer associations might reflect a genetic predisposition for genome instability. Indeed, whole genome association studies show loss of Y frequency is about one-third genetic, involving 150 identified genes largely involved in cell cycle regulation and cancer susceptibility.

However, one mouse study points to a direct effect. Researchers transplanted Y-deficient blood cells into irradiated mice, which then displayed increased frequencies of age-related pathologies including poorer cardiac function and subsequent heart failure.

Similarly, loss of Y from cancer cells seems to affect cell growth and malignancy directly, possibly driving eye melanoma, which is more frequent in men.

Role of the Y in body cells

The clinical effects of loss of Y suggest the Y chromosome has important functions in body cells. But given how few genes it hosts, how?

The male-determining SRY gene found on the Y is expressed widely in the body. But the only effect ascribed to its activity in the brain is complicity in causing Parkinson’s disease. And four genes essential for making sperm are active only in the testis.

But among the other 46 genes on the Y, several are widely expressed and have essential functions in gene activity and regulation. Several are known cancer suppressors.

These genes all have copies on the X chromosome, so both males and females have two copies. It may be that the absence of a second copy in Y-less cells causes some kind of dysregulation.

As well as these protein-coding genes, the Y contains many non-coding genes. These are transcribed into RNA molecules, but never translated into proteins. At least some of these non-coding genes seem to control the function of other genes.

This might explain why the Y chromosome can affect the activity of genes on many other chromosomes. Loss of Y affects expression of some genes in the cells that make blood cells, as well as others that regulate immune function. It may also indirectly affect differentiation of blood cell types and heart function.

The DNA of the human Y was only fully sequenced a couple of years ago – so in time we may track down how particular genes cause these negative health effects.

Jenny Graves, Distinguished Professor of Genetics and Vice Chancellor's Fellow, La Trobe University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Published by The Conversation.
Open access. (CC BY 4.0)

What this research adds to the growing catalogue of evidence is yet another reminder that the human body is not the work of a competent, foresighted engineer producing flawless machinery from first principles. It is exactly what evolutionary theory says it should be: a cobbled-together, makeshift product of descent with modification, shaped by whatever happened to work well enough in the short term, not by any long-term plan for perfection. The age-related loss of the Y chromosome in men's cells, and the diseases associated with it, are precisely the sort of vulnerability we would expect in an evolved system burdened with historical constraints and compromises.

For Intelligent Design creationists, this presents the usual dilemma. If the human body really is the deliberate masterpiece of an omniscient designer, why build into it a chromosome that can be lost from cells with harmful consequences later in life? Why create a sex-determining system that leaves one half of the species with this particular built-in fragility? And if this is dismissed as the result of some cosmic sabotage following the mythical 'Fall', then ID creationism has once again abandoned science entirely and retreated into theology and superstition, where any defect can be excused by inventing invisible agents and untestable events.

By contrast, evolution has no such difficulty. The Y chromosome has a well-understood evolutionary history, a reduced gene set, and a peculiar structural vulnerability resulting from the fact that most of it no longer recombines with a matching partner. That makes it exactly the sort of chromosome that can accumulate problems and produce downstream health consequences. In other words, this is not evidence of elegant, optimal design; it is evidence of evolutionary tinkering, with all the inelegance, wastefulness and susceptibility to failure that such tinkering inevitably produces.

So, once again, the facts fit evolution far better than they fit any notion of intelligent design. What creationists need to explain away as either mysterious purpose or accidental corruption is readily understood as the predictable outcome of a long, blind evolutionary history. Far from revealing the hand of a designer, the ageing male Y chromosome is one more sign that the human body bears all the marks, not of perfection, but of descent from imperfect ancestors.

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