Why Y? It’s More than Just a Guy Thing
Creation and evolution generate
very different perspectives on sex
and on scientific understanding
Evolutionists Make Another Blunder
The Y chromosome does far more than just produce males
by Jerry Bergman, PhD
Introduction
Sperm carrying an X chromosome make girls; those with a Y chromosome make boys. For decades, the Y was dismissed as mostly useless beyond that — it degenerates over evolutionary time, has few genes, and is the only chromosome that can vanish from cells in lab cultures without killing them. This data was interpreted as evidence that the specific functions encoded by the genes on the Y chromosome are not required for cellular growth and function,[1] a perspective criticized in a recent article by Jenny Graves at The Conversation.
Men lose their Y chromosome as they age. Scientists thought it didn’t matter – but now we’re learning more (The Conversation, 12 February 2026).
According to Jenny Graves, a Distinguished Professor of Genetics at La Trobe University, Australia, many biologists believed or assumed that its genes had little role outside male development and reproduction. Consequently, losing the Y in aging men was seen as harmless.[2] Dr Graves shows this is not the case.
Y Facts
The X chromosome has 155 million base pairs and close to 1,400 genes compared to 57 million base pairs and over 70 genes for the Y chromosome. While the X chromosome spans approximately 155 million base pairs and contains nearly 1,400 genes, the Y chromosome is much smaller, at about 57 million base pairs, with just over 51 confirmed protein-coding genes. The human Y chromosome was only fully sequenced a few years ago, and the number of genes is not yet known, partly because the Y chromosome is highly repetitive, making it very difficult to sequence. In particular, it includes large “ampliconic” regions—extensive palindromic sequences that read the same forward and backward (similar to words like “madam” or “racecar”).[3] These complex repeated structures have historically hindered precise mapping and gene identification.
Because men often commonly lose the Y chromosome in a proportion of their cells as they age, it was long assumed that this would have minimal health consequences. The reason was the Y chromosome contains relatively few genes beyond those involved in male development, spermatogenesis, and secondary sexual characteristics, leading many scientists to believe its absence in somatic cells was largely inconsequential.
The Real Y’s Men
However, this conclusion has now been overturned.[4] Rather than being biologically insignificant, the Y chromosome appears to play broader roles in immune function and cellular regulation than previously recognized.
Loss of the Y chromosome (often termed LOY) occurs in more than 40 percent of men over the age of 70 and has been strongly associated with shorter life expectancy, increased cancer risk, and other age-related diseases.
Importantly, this chromosomal loss does not occur in all cells. Instead, it produces a mosaic pattern—some cells retain the Y chromosome, while others lack it—resulting in cellular heterogeneity within the same individual.
Evolution Misleads Scientific Understanding of Y Chromosome Functions
One major reason for this erroneous view about the importance of the Y chromosome was the prevailing evolutionary view that the “Y chromosomes evolved through the degeneration of autosomes.”[5] Another less popular idea is that the Y chromosome is a “mutilated” version of the X chromosome that evolved a specialized gene called SRY (Sex-determining Region Y)—which acts as the master regulatory switch for male development.
Because the evolutionary framework emphasized gene loss and degeneration, the Y chromosome was often characterized as largely genetically depleted and functionally limited. The influence of this perspective on terminology and interpretation is reflected in the name used to describe Y genes, pseudoautosomal regions which make up most of the Y chromosome.
William Rice, biology professor at the University of California, illustrates this view. In 1996, he wrote that the human Y chromosome is nearly devoid of functional genes compared to the X chromosome:
hundreds of [functional] genes have been found on the X chromosome. Some genes found on the tip of the Y chromosome (the pseudoautosomal region) recombine with homologous genes on the X chromosome. The remaining genes are in the nonrecombining portion of the Y (the “differential segment,” which constitutes most of the Y chromosome).[6]
This notion was based on “comparative studies across many taxa [that] indicate the Y has evolved independently from an ordinary autosome.”[7] Furthermore, evolutionary models have traditionally predicted the continual degeneration of the Y chromosome for several reasons, as described by Rice in his paper. He used the word evolution 58 times.[8]
Evidence for Evolution from Other Mammals?
The XY sex-determination system is used in all mammals with very rare exceptions such as moles, voles and spiny rats which use the XO system. In the XO system some of the Y’s functions are located in either the X chromosome or in an autosome. The evolutionary assumption is that the rare XO system evolved by losing the Y chromosome and an entirely new system evolved to replace it. How and why this switch could be achieved by evolution can only be speculated. An XO species could not reproduce until the new system was fully functional and operational. How it functioned until this transfer was completed is unknown.
Rice even claimed that Y chromosome evolution is so important that “Y chromosome evolution is a model system for the adaptive significance of sexual recombination [of the gametes from the male and female] in whole organisms.”[9] The fact that men lose their Y chromosome in some cells as they age also seems to support the Y evolution degeneration theory.
One result of the dominance of the evolution degeneration theory was that specific functions of the Y chromosome were not viewed as important to life and health. Rice even argued that “Y chromosome evolution is a model system for the adaptive significance of sexual recombination in whole organisms,” emphasizing its theoretical importance within evolutionary biology.[10]
The observation that men commonly lose the Y chromosome in a subset of somatic cells with age (mosaic loss of Y, or LOY) has also been interpreted as consistent with a degenerative trajectory in humans. As a result, the Y chromosome was for decades viewed as genetically diminished and functionally limited, with importance largely confined to male sex determination and reproduction.
Evidence now Disputes the Evolutionary Degeneration Theory
Accumulating evidence has challenged this narrow degeneration perspective. It is now recognized that most of the approximately 50–70 protein-coding genes on the human Y chromosome are functional and contribute to normal physiological processes beyond reproduction. In addition, it has now been confirmed that Y-linked noncoding RNAs participate in gene regulation. Damage to, or loss of, the Y chromosome genes has been increasingly associated with several systemic diseases, immune dysfunction, cancer risk, and reduced lifespan. Rather than being biologically expendable, the Y chromosome has broader roles in maintaining health than earlier models anticipated.
We are more than our chromosomes. (Grok/AI)
It is now recognized that most of the human Y chromosomes’ 70 protein-coding genes are functional and important for normal body health. This is also true of the few noncoding RNAs involved in genetic regulation. Evidence has mounted over the past few years that damage to, or the loss of, Y chromosome genes is associated with serious diseases throughout the body, contributing to premature death.[11]
Diseases and medical conditions caused by loss of Y genes
Cancer and cardiovascular and neurodegenerative diseases are some of the serious diseases associated with the loss of Y chromosome genes, proving that they have important functions in body cells.[12] In fact, several Y genes are widely expressed and have been documented to have several essential functions in gene activity and regulation. Many of these genes have copies on the X chromosome, resulting in both males and females having two copies. This means that the absence of a second copy in Y-less cells results in dysregulation.
Several studies have reported associations between loss of Y chromosome genes (mosaic loss of Y, or LOY) and cardiovascular disease, and a significantly increased risk of heart attacks/myocardial infarction. LOY has also been linked to multiple cancers in men. Because some Y-linked genes function in tumor suppression and immune regulation, their loss contributes to increased cancer susceptibility.
The loss of Y genes involved in cell cycle regulation may also account for this increased susceptibility to cancer. Indeed, loss of the Y chromosome is frequently observed in malignant cells, although it remains an area of active investigation whether this loss is a driver of disease or a consequence of genomic instability. Loss of Y genes has also been linked to death from COVID-19, which potentially contributes to the observed higher disease severity in men. Loss of Y genes has further been associated with increased mortality from COVID-19. A markedly higher frequency of Y chromosome loss has also been reported in men with Alzheimer’s disease. In addition, LOY detected in kidney cells has been correlated with renal dysfunction.[13]
Furthermore, loss of Y genes may directly affect cell growth and malignancy rate, possibly driving eye melanoma, which occurs more frequently in men. 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. The male-determining SRY gene, located on the Y chromosome, is expressed in several tissues beyond the testes. So far, the only effect ascribed to its activity in the brain is its complicity in causing Parkinson’s disease, but it may also influence other neurological processes.
Some Interpretive Cautions
Determining what causes the links between loss of Y and health problems is difficult because health problems may cause loss of Y, not the other way around, or a third factor might cause both problems. Importantly, genes on the Y chromosome influence the regulation of genes across multiple autosomes, including those involved in hematopoiesis and immune function. Thus, loss of Y-linked genes could have widespread biological effects beyond sex determination. For example, genes on the Y chromosome can affect the expression of genes that make blood cells, as well as other genes that regulate immune function.
Determining whether loss of the Y chromosome (LOY) is a cause of disease or a consequence of underlying pathology remains challenging. Health conditions themselves may promote chromosomal instability, leading to LOY, or a third factor—such as aging or systemic inflammation—may contribute to both LOY and disease.
Learn about other blunders made by evolutionists in this book by Dr Bergman. Click to order.
Summary
The prevailing evolutionary model proposes that the Y chromosome originated from an ancestral autosome that progressively degenerated over time. This view led to the Y chromosome being viewed primarily as a reduced or vestigial structure, slowing full exploration of its broader biological functions. In contrast, a creation-based perspective holds that Y-linked genes were purposefully designed with specific roles in human biology, a view that would naturally encourage investigation into their structure and systemic function.
Most mammals utilize an XY system; however, rare exceptions exist, such as certain moles, voles and spiny rats that exhibit an XO system in which typical Y-linked functions appear to be relocated to the X chromosome or to autosomes. Within evolutionary biology, these systems are generally interpreted as the result of Y chromosome loss followed by compensatory genetic reorganization. The precise mechanisms by which such transitions could occur remain an area of debate.
In short, the evolutionary assumption about the origin of the Y genes from degenerated somatic cell genes has impeded understanding the Y chromosome genes’ functions. A creation based perspective, by contrast, holds that all of the genes on the Y chromosome were specifically designed for a purpose in humans. This view would naturally encourage investigation into their structures and functions.
References
[1] Graves, Jenny, “Men lose their Y chromosome as they age. Scientists thought it didn’t matter – but now we’re learning more,” https://theconversation.com/men-lose-their-y-chromosome-as-they-age-scientists-thought-it-didnt-matter-but-now-were-learning-more-275823, 12 February 2026.
[2] Wachtel, Stephen S. (ed)., Molecular Genetics of Sex Determination, Academic Press, San Diego, CA, 1994.
[3] Brashear, Wesley, et al., “Evolutionary conservation of Y Chromosome ampliconic gene families despite extensive structural variation,” Genome Research 28(12):1841-1851, December 2018.
[4] Fukami, Maki, et al., “Mosaic loss of the Y chromosome and men’s health,” Reproductive Medicine and Biology 21(1), https://onlinelibrary.wiley.com/doi/10.1002/rmb2.12445, 7 February 2022.
[5] Rice, William R., “Evolution of the Y sex chromosome in animals. Y chromosomes evolved through the degeneration of autosomes.” Bioscience 46(5):331-343, May 1996.
[6] Rice, 1996, p. 331.
[7] Rice, 1996, p. 331.
[8] Rice, 1996, p. 331.
[9] Rice, 1996, p. 331.
[10] Rice, 1996, p. 331
[11] Fukami, et al., 2022.
[12] Graves, 2026.
[13] Graves, 2026.
Dr. Jerry Bergman has taught biology, genetics, chemistry, biochemistry, anthropology, geology, and microbiology for over 40 years at several colleges and universities including Bowling Green State University, Medical College of Ohio where he was a research associate in experimental pathology, and The University of Toledo. He is a graduate of the Medical College of Ohio, Wayne State University in Detroit, the University of Toledo, and Bowling Green State University. He has over 1,900 publications in 14 languages and 40 books and monographs. His books and textbooks that include chapters that he authored are in over 1,800 college libraries in 27 countries. So far over 80,000 copies of the 60 books and monographs that he has authored or co-authored are in print. For more articles by Dr Bergman, see his Author Profile.