Rosa Rubicondior: Creationism Refuted - How New Genetic Information Causes Diseases

Study shows your genes determine how fast your DNA mutates with age | UCLA Health

Creationist dogma insists that new genetic information can only be created by their putative intelligent designer, so it should be deeply embarrassing for them to learn that certain stretches of our DNA lengthen as we age, that the rate at which this happens is influenced by genes, and that excessive expansion of these sequences can lead to serious liver or kidney diseases.

This was discovered by researchers from the University of California, Los Angeles (UCLA), the Broad Institute, and Harvard Medical School, who analysed whole-genome sequencing data from 490,416 UK Biobank participants and 414,830 participants in the All of Us Research Program. Their findings were published recently, open access, in Nature.

This research is particularly awkward for creationists because of their insistence on the supposedly ‘sacred’ principle that only their intelligent designer can add new information to a genome. If we concede that claim for the sake of argument, then this newly generated genetic information must have been created deliberately and designed to produce a specific outcome — unless creationism’s designer was simply fiddling about aimlessly. Having a specific outcome (as all genes do) is precisely what William A. Dembski of the Discovery Institute insists is evidence for intelligent design, by a neat process of circular reasoning that only creationists find persuasive.

We then have the additional fact that a high rate of expansion of these DNA sequences is controlled by genetic modifiers and does not occur if any of those genes is not functioning properly. In other words, the resulting liver and kidney diseases are due to what Michael J. Behe famously describes as proof of a designer god: ‘irreducible complexity’.

Still conceding creationist claims, then, Dembski’s and Behe’s own logic demonstrates that their intelligent designer deliberately causes these diseases of old age.

Creationists are further hoist by their own petard in that they traditionally blame disease on ‘The Fall’, thereby conceding that intelligent design creationism is a form of fundamentalist religion rather than science. At the same time, however, they insist that only their intelligent designer can produce the new genetic information responsible for the expansion of these DNA sequences, which neatly rules out the involvement of the vague, non-physical agency they refer to as ‘sin’.

This leaves creationists with an uncomfortable dilemma: either their designer god actively causes liver and kidney disease, or new genetic information can indeed be produced by natural processes in which their designer plays no part — in which case a major plank of creationism collapses. The alternative is to concede that their allegedly omnibenevolent god is directly responsible for serious diseases in elderly people.

It is scarcely worth pointing out the glaringly obvious fact that these outcomes are easily explained as the predictable result of an undirected evolutionary process that has no concept of perfection, inevitably settling for compromise and prioritising reproductive success early in life at the expense of longer-term health and wellbeing.

Background information: diseases caused by DNA repeat expansion

Expansion repeats in the HTT gene (unaffected vs Huntington disease)
Source

Source

Expansion of short, repetitive DNA sequences — often called repeat expansion mutations — is a well-established cause of human disease. These expansions typically increase in length over time or across cell divisions, disrupt gene function, and are especially damaging in long-lived tissues such as the brain, liver, and kidneys. Well-documented examples include:

Neurodegenerative and neuromuscular disorders

Huntington’s disease
Caused by expansion of a CAG repeat in the HTT gene. Disease severity and age of onset correlate directly with repeat length.
Myotonic dystrophy (types 1 and 2)
Results from CTG or CCTG repeat expansions that interfere with RNA processing, affecting muscle, heart, and endocrine systems.
Spinocerebellar ataxias (multiple types)
A group of disorders caused by repeat expansions in different genes, leading to progressive loss of coordination and balance.
Fragile X syndrome
Caused by CGG repeat expansion that silences the FMR1 gene; the most common inherited cause of intellectual disability.

Liver, kidney, and metabolic disease

Polyglutamine expansion–associated liver disease
Certain repeat expansions disrupt protein folding and clearance in hepatocytes, leading to progressive liver damage.
Repeat-associated nephropathies
Expanded repeats can impair renal cell function, contributing to chronic kidney disease through toxic RNA or protein accumulation.
Age-related somatic repeat expansion syndromes
Recently identified expansions accumulate in specific tissues with age, increasing disease risk even when inherited repeat length is below the classical disease threshold.

Mechanisms of harm

Repeat expansions cause disease through several non-exclusive mechanisms:

Toxic proteins with abnormally long amino-acid tracts
Toxic RNA molecules that sequester essential cellular factors
Gene silencing through altered chromatin structure
Progressive somatic expansion during ageing, worsening disease over time

Why this matters for creationist claims

Crucially, these expansions:

Create new genetic information in the most literal, measurable sense
Increase in length over time, often predictably
Are regulated by other genes, forming complex molecular systems
Cause disease when functioning “correctly”, not when broken

They are therefore incompatible with claims that new genetic information cannot arise naturally — and deeply problematic for any notion that such outcomes reflect deliberate, benevolent design.

The work of the UCLA-led team is further explained in a UCLA Health news item.

Study shows your genes determine how fast your DNA mutates with age
Researchers identify dozens of genes that speed or slow genetic instability, offering targets for future therapies
An analysis of genetic data from over 900,000 people shows that certain stretches of DNA, made up of short sequences repeated over and over, become longer and more unstable as we age. The study found that common genetic variants can speed up or slow down this process by up to fourfold, and that certain expanded sequences are linked to serious diseases including kidney failure and liver disease.

Why it matters

More than 60 inherited disorders are caused by expanded DNA repeats: repetitive genetic sequences that grow longer over time. These include devastating conditions like Huntington's disease, myotonic dystrophy, and certain forms of ALS. Most people carry DNA repeats that gradually expand throughout their lives, but this instability and what genetic factors control it hadn’t been fully analyzed within large biobanks. This study demonstrates that DNA repeat expansion is far more widespread than previously recognized and identifies dozens of genes that regulate this process, opening new avenues for developing treatments that could slow disease progression.

What the study did

Researchers from UCLA, the Broad Institute, and Harvard Medical School analyzed whole-genome sequencing data from 490,416 UK Biobank participants and 414,830 All of Us Research Program participants. They developed new computational methods to detect and measure DNA repeat lengths and instability from standard sequencing data. The team examined 356,131 polymorphic repeat locations across the genome, tracking how repeat lengths changed with age in blood cells and identifying genetic variants that influenced expansion rates. They also searched for links between repeat expansions and thousands of disease outcomes to discover previously unknown disease associations.

What they found

Common DNA repeats in blood cells expand as people age. The researchers identified 29 genetic locations where inherited variants modified DNA repeat expansion rates, with effects varying up to fourfold between individuals with the highest and lowest genetic risk scores. Interestingly, the same DNA repair genes had opposite effects on different repeats: variants that stabilized some repeats destabilized others. The study also discovered that expansions in the GLS gene which have a prevalence around 0.03% were associated with 14-fold higher risk of severe kidney disease and 3-fold higher risk of liver diseases, representing a newly recognized repeat expansion disorder.

What's next

The findings establish blood-based DNA repeat measurements as potential biomarkers for testing future therapies aimed at slowing repeat expansion in diseases like Huntington's. The research team's computational tools can now be applied to other large biobank datasets to discover additional unstable repeats and disease associations. Understanding why the same genetic modifiers have opposite effects on different repeats will require detailed mechanistic studies of how DNA repair processes vary across cell types and genetic contexts. The discovery of GLS repeat-associated kidney and liver disease suggests additional unrecognized repeat expansion disorders may be lurking in biobank data, waiting to be found.

From the experts

We found that most human genomes contain repeat elements that expand as we age. The strong genetic control of this expansion, with some individuals' repeats expanding four times faster than others, points to opportunities for therapeutic intervention. These naturally occurring genetic modifiers show us which molecular pathways could be targeted to slow repeat expansion in disease.

Assistant Professor Margaux L. A. Hujoel, PhD, lead author.
Department of Computational Medicine
David Geffen School of Medicine
University of California, Los Angeles
Los Angeles, CA, USA.

Publication:
Hujoel, M.L.A., Handsaker, R.E., Tang, D. et al.
Insights into DNA repeat expansions among 900,000 biobank participants.
Nature (2026). https://doi.org/10.1038/s41586-025-09886-z

Abstract

Expansions and contractions of tandem DNA repeats generate genetic variation in human populations and in human tissues. Some expanded repeats cause inherited disorders and some are also somatically unstable1,2. Here we analysed DNA sequencing data from over 900,000 participants in the UK Biobank and the All of Us Research Program using computational approaches to recognize, measure and learn from DNA-repeat instability. Repeats at different loci exhibited widely variable tissue-specific propensities to mutate in the germline and blood. Common alleles of repeats in TCF4 and ADGRE2 exhibited high rates of length mosaicism in the blood, demonstrating that most human genomes contain repeat elements that expand as we age. Genome-wide association analyses of the extent of somatic expansion of unstable repeat alleles identified 29 loci at which inherited variants increased expansion of one or more DNA repeats in blood (P = 5 × 10⁻⁸ to 2.5 × 10^−1,438). These genetic modifiers exhibited strong collective effects on repeat instability: at one repeat, somatic expansion rates varied fourfold between individuals with the highest and lowest 5% of polygenic scores. Modifier alleles at several DNA-repair genes exhibited opposite effects on the blood instability of the TCF4 repeat compared with other DNA repeats. Expanded repeats in the 5′ untranslated region of the glutaminase (GLS) gene associated with stage 5 chronic kidney disease (odds ratio (OR) = 14.0 (5.7–34.3, 95% confidence interval (CI))) and liver diseases (OR = 3.0 (1.5–5.9, 95% CI)). These results point to complex dynamics of DNA repeats in human populations and across the human lifespan.

Hujoel, M.L.A., Handsaker, R.E., Tang, D. et al.
Insights into DNA repeat expansions among 900,000 biobank participants.
Nature (2026). https://doi.org/10.1038/s41586-025-09886-z

Copyright: © 2026 The authors.
Published by Springer Nature Ltd. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

Once again, the empirical evidence stubbornly refuses to conform to creationist dogma. DNA repeat expansions are not rare curiosities, nor are they hypothetical constructs dreamed up to rescue evolutionary theory. They are measurable, mechanistic, predictable processes that generate new genetic sequence length over time, are influenced by other genes, and have real-world biological consequences — frequently harmful ones.

For intelligent design creationism, this is a particularly uncomfortable result. Either these expansions arise through ordinary molecular processes, in which case the claim that new genetic information cannot arise naturally is demonstrably false, or they are deliberately produced by the designer creationists insist must be responsible for all such changes. In that case, the designer is actively engineering diseases that predominantly afflict people late in life, long after reproduction has occurred.

Evolutionary biology, by contrast, has no difficulty accounting for these observations. Natural selection does not strive for perfection, benevolence, or long-term wellbeing. It favours traits that enhance reproductive success, even if the molecular machinery that achieves this is prone to instability, error, and cumulative damage over time. DNA repeat expansion is simply one more example of that trade-off made visible at the molecular level.

As so often, creationism is left oscillating between denial of the data and theological special pleading, while evolution does what it has always done: explain the evidence without embarrassment, without contradiction, and without the need to invent excuses for disease, suffering, or biological imperfection.

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