Thursday, 15 January 2026

Unintelligent Design - A Brain 'Designed' for Memory Loss in Old Age

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New Mega-Analysis Reveals Why Memory Declines With Age | Hebrew SeniorLife

A paper published last November in Nature Communications by an international team lead by scientists from the University of Oslo, is just the sort of evidence against intelligent design and for evolution that creationists normally misrepresent, lie about or ignore, because it illustrates the stark difference between what ID creationism predicts and what we see, and of course, what we see is exactly what the Theory of Evolution predicts. And it's another superb example of how the human body refutes the childish notion of intelligent design by a magic invisible designer, many more of which I have included in my book, The Body of Evidence: How the Human Body Refutes Intelligent Design.

There is a persistent tendency among creationists and Intelligent Design advocates to imagine biology as if it were the product of a competent, benevolent engineer, optimised for lifelong performance and reliability. Real organisms, however, stubbornly refuse to behave like that. Evolution does not design for comfort, longevity, or even cognitive elegance; it shapes traits that maximise reproductive success in the environments in which our ancestors actually lived. Once reproduction has occurred and offspring are independent, the force of natural selection weakens dramatically. From that point on, biological systems are increasingly free to accumulate compromises, trade-offs, and outright failures — not because they are useful, but because there is little evolutionary incentive to eliminate them.

Nowhere is this more obvious than in the ageing human brain. Memory, learning, and cognitive flexibility are exquisitely tuned for early and mid-life, precisely when they matter most for survival, social navigation, and reproduction. Later in life, however, those same systems reveal a striking lack of long-term maintenance. This is not a mystery, nor is it a design flaw crying out for a supernatural explanation. It is exactly what evolutionary theory predicts under mechanisms such as antagonistic pleiotropy, mutation accumulation, and the diversion of finite biological resources away from indefinite repair and towards reproduction. In short, evolution produces brains that are *good enough* for long enough — not brains that are guaranteed to remain intact into old age.

That expectation is strongly reinforced by the paper in Nature Communications, which combines large-scale neuroimaging and cognitive data to examine why memory reliably declines with age even in otherwise healthy adults. Rather than pointing to a single failing component or a neatly isolated genetic “defect”, the study reveals a diffuse pattern of structural brain change, with memory loss emerging from the cumulative erosion of multiple interconnected regions. This kind of widespread, variable vulnerability is exactly what an evolutionary framework anticipates — and exactly the opposite of what Intelligent Design would lead us to expect. What follows is not evidence of poor design, but evidence of no design at all: only the predictable consequences of evolution’s ruthless focus on reproductive success early in life, and its indifference to what happens long after that job is done.

Why Natural Selection Allows Memory to Decline with Age.
  1. The Declining Force of Natural Selection
    Natural selection acts most strongly on traits that influence survival and reproduction early in life. As individuals age beyond their peak reproductive years, the evolutionary “penalty” for late-acting biological problems diminishes. Traits that impair health or cognition in old age therefore experience much weaker selection pressure and can persist across generations.

  2. Antagonistic Pleiotropy: Early Gains, Late Costs
    Some genes improve early-life survival, fertility, or brain performance but carry harmful effects later in life. Because early benefits increase reproductive success, such genes are favoured by selection despite their late-life consequences. Memory decline is consistent with this model: neural systems optimised for rapid learning and flexibility earlier in life may trade long-term stability for short-term performance.

  3. Mutation Accumulation in Late Life
    Harmful mutations whose effects are expressed only in later life are less efficiently removed by natural selection, simply because many individuals in ancestral populations never lived long enough for those effects to matter. Over evolutionary time, this leads to a gradual build-up of late-acting vulnerabilities affecting maintenance, repair, and cognitive resilience.

  4. The Disposable Soma Principle
    Organisms operate under finite energy budgets. Evolution favours allocating resources to growth, reproduction, and early survival rather than to indefinite cellular and neural repair. Long-term maintenance of complex systems such as the brain is therefore necessarily incomplete, making gradual cognitive decline an expected outcome rather than a pathological anomaly.

  5. Why Humans Didn’t Evolve “Lifelong Memory”
    In prehistoric environments, few individuals lived into advanced old age, and those who did rarely depended on peak cognitive performance for reproductive success. While some late-life cognitive function may have been favoured through social and kin-based advantages, there was no evolutionary incentive to engineer a brain immune to decades of cumulative wear, metabolic stress, and structural degradation.

  6. Why This Is a Problem for Intelligent Design
    A system designed for lifelong cognitive excellence would be expected to show robust redundancy, superior long-term repair, and strong protection against cumulative damage. Instead, human memory decline reflects distributed vulnerability, variable outcomes, and gradual failure — hallmarks of evolutionary compromise, not deliberate engineering.
The research and its implications has been written up in a news item from Hebrew Senior Life.
New Mega-Analysis Reveals Why Memory Declines With Age
Genetic risk for Alzheimer’s and widespread brain shrinkage linked to greater memory loss — even in otherwise healthy adults.
A landmark international study that pooled brain scans and memory tests from thousands of adults has shed new light on how structural brain changes are tied to memory decline as people age.

The findings — based on more than 10,000 MRI scans and over 13,000 memory assessments from 3,700 cognitively healthy adults across 13 studies — show that the connection between shrinking brain tissue and declining memory is nonlinear, stronger in older adults, and not solely driven by known Alzheimer’s-associated genes like APOE ε4. This suggests that brain aging is more complex than previously thought, and that memory vulnerability reflects broad structural changes across multiple regions, not just isolated pathology.

Published in Nature Communications, the study, “Vulnerability to memory decline in aging revealed by a mega-analysis of structural brain change,” found that structural brain change associated with memory decline is widespread, rather than confined to a single region. While the hippocampus showed the strongest association between volume loss and declining memory performance, many other cortical and subcortical regions also demonstrated significant relationships. This suggests that cognitive decline in aging reflects a distributed macrostructural brain vulnerability, rather than deterioration in a few specific brain regions. The pattern across regions formed a gradient, with the hippocampus at the high end and progressively smaller but still meaningful effects across large portions of the brain.

Importantly, the relationship between regional brain atrophy and memory decline was not only variable across individuals but also highly nonlinear. Individuals with above-average rates of structural loss experienced disproportionately greater declines in memory, suggesting that once brain shrinkage reaches higher levels, cognitive consequences accelerate rather than progress evenly. This nonlinear pattern was consistent across multiple brain regions, reinforcing the conclusion that memory decline in cognitively healthy aging is linked to global and network-level structural changes, with the hippocampus playing a particularly sensitive role but not acting alone.

By integrating data across dozens of research cohorts, we now have the most detailed picture yet of how structural changes in the brain unfold with age and how they relate to memory. Cognitive decline and memory loss are not simply the consequence of aging, but manifestations of individual predispositions and age-related processes enabling neurodegenerative processes and diseases. These results suggest that memory decline in aging is not just about one region or one gene — it reflects a broad biological vulnerability in brain structure that accumulates over decades. Understanding this can help researchers identify individuals at risk early, and develop more precise and personalized interventions that support cognitive health across the lifespan and prevent cognitive disability.


Publication:


Abstract
Brain atrophy is a key factor behind episodic memory loss in aging, but the nature and ubiquity of this relationship remains poorly understood. This study leverages 13 longitudinal datasets, including 3737 cognitively healthy adults (10,343 MRI scans; 13,460 memory assessments), to determine whether brain change-memory change associations are more pronounced with age and genetic risk for Alzheimer’s Disease. Both factors are associated with accelerated brain decline, yet it remains unclear whether memory loss is exacerbated beyond what atrophy alone would predict. Additionally, we assess whether memory decline aligns with a global pattern of atrophy or stems from distinct regional contributions. Our mega-analysis reveals a nonlinear relationship between memory decline and brain atrophy, primarily affecting individuals with above-average brain structural decline. The associations are stronger in the hippocampus but also spread across diverse cortical and subcortical regions. The associations strengthen with age, reaching moderate associations in participants in their eighties. While APOE ε4 carriers exhibit steeper brain and memory loss, genetic risk has no effect on the change-change associations. These findings support the presence of common biological macrostructural substrates underlying memory function in older age which are vulnerable to multiple age-related factors, even in the absence of overt pathological changes.



The findings reported here leave Intelligent Design with nowhere to hide. The gradual, uneven decline of memory in later life is not a glitch in an otherwise perfect system, nor evidence of a fall from some mythical biological ideal. It is precisely what evolutionary theory predicts when natural selection prioritises early survival and reproductive success over indefinite maintenance. Brains, like bodies, are shaped to do their job long enough to pass genes on — not to remain pristine for eight or nine decades.

What this research underscores is that memory loss does not arise from a single broken component that a competent designer might have “fixed”, but from the slow accumulation of structural and metabolic compromises across interconnected brain networks. The variability between individuals, the non-linear nature of decline, and the absence of a simple genetic smoking gun all point to evolutionary trade-offs operating over a lifetime, not to intentional optimisation for lifelong cognitive performance.

For creationism, this is yet another example of reality stubbornly refusing to conform to theological expectations. A world designed by an all-powerful intelligence has no obvious reason to produce brains that excel early, falter later, and fail in ways that correlate neatly with declining selection pressure. A world shaped by evolution, however, predicts exactly this pattern — and continues, year after year, to have its predictions confirmed by the evidence.




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