Rosa Rubicondior: Malevolent Design - What A Benevolent Designer Could Have Given Us, But Chose Not To, Apparently.

Ring-tailed Lemur, Lemur catta.

Study Suggests Lemurs Age Differently Than Humans | Duke Today

According to creationist superstition, humans were specially created by a perfect, anthropophilic, omnibenevolent creator god. If that were true, it would be reasonable to expect humans to be perfectly designed—free from defects or anything likely to cause long-term suffering.

However, the facts do not support this view. For example, as humans age, they increasingly suffer from a condition known as inflammaging — low-grade, chronic inflammation that contributes to a range of health problems, including heart disease, strokes, diabetes, cancer, and osteoarthritis.

Properly understood, this should give creationists cause for concern. The same designer god apparently gave some other primates—most notably, certain species of lemur—the ability to avoid this consequence of ageing. In fact, these lemurs even show a reduced tendency toward inflammatory conditions as they grow older.

This raises a serious question for Intelligent Design creationists: if the same designer god was capable of creating such a mechanism for lemurs, why did it not see fit to bestow the same gift upon its supposed favourite creation—humans? Or are these inflammatory conditions intended to cause suffering and disease as we age?

The discovery that some lemurs appear to have been specially favoured by a creator god—if we accept the ID creationist premise for the sake of argument—was made by a team of researchers led by Elaine Elizabeth Gomez Guevara, a biological anthropologist in the Department of Evolutionary Anthropology at Duke University, Durham, USA. As a scientist and biologist, however, she attributes the differences between lemurs and humans to evolution — not to indifference or malevolence on the part of a designer god.

The team has just published their findings in the Journal of Comparative Physiology B.

What is the aetiology of 'inflammaging'? Inflammaging (a portmanteau of inflammation and ageing) is a chronic, low-grade inflammation that develops with age, even in the absence of overt infection. It plays a key role in the development of age-related diseases such as cardiovascular disease, type 2 diabetes, Alzheimer's disease, cancer, and osteoarthritis. The aetiology of inflammaging is multifactorial and involves several overlapping biological processes:

Cellular Senescence

As cells age, they enter a state called senescence — a permanent halt in cell division. These senescent cells secrete inflammatory factors (cytokines, chemokines, proteases), known as the senescence-associated secretory phenotype (SASP).
SASP contributes to tissue dysfunction and chronic inflammation.

Mitochondrial Dysfunction

Ageing cells often have impaired mitochondria, leading to increased production of reactive oxygen species (ROS).
ROS damage DNA, proteins, and lipids, triggering inflammation.

Immunosenescence

The immune system ages, becoming less efficient at clearing damaged cells and pathogens (reduced adaptive immunity) but more prone to pro-inflammatory activity (innate immunity dominance).
This imbalance contributes to a background state of inflammation.

Gut Microbiota Changes

Ageing is associated with dysbiosis, or imbalance, in the gut microbiome.
This can increase gut permeability, allowing microbial products like lipopolysaccharides (LPS) to enter the bloodstream and trigger systemic inflammation.

Accumulation of Cellular Debris and Damage

With age, there’s a build-up of damage-associated molecular patterns (DAMPs) such as extracellular DNA, oxidised lipids, and misfolded proteins.
These are recognised by the innate immune system as danger signals, maintaining a state of chronic inflammation.

Decline in Autophagy

Autophagy—the process by which cells remove damaged components—declines with age.
Reduced autophagy leads to accumulation of cellular damage and pro-inflammatory signalling.

Chronic Infections

Persistent, latent infections (e.g. CMV, herpesviruses) may continuously stimulate the immune system, contributing to the inflammaging phenotype.

Summary

Inflammaging is the result of a complex interplay between ageing cells, the immune system, environmental exposures, and lifestyle factors. While it is a normal part of ageing, it is also a risk factor for multiple chronic diseases. Interventions like exercise, caloric restriction, anti-inflammatory diets, and senolytics (drugs that clear senescent cells) are being studied for their potential to mitigate inflammaging.

Have these evolved because they convey an advantage to our genes or are they the result of evolutionary compromises?

That’s an excellent and nuanced question. The answer is that the mechanisms underlying inflammaging are primarily the result of evolutionary compromises—by-products of systems that were selected for their early-life benefits, even though they may have detrimental effects in later life.

Here’s a breakdown of the evolutionary logic:

Antagonistic Pleiotropy

This is a key evolutionary theory proposed by George C. Williams in 1957. It posits that:

Some genes or traits are beneficial early in life (especially for growth, reproduction, or immune defence), but harmful in old age.
These genes are selected because of their early-life advantages, even if they cause ageing-related decline later—after reproduction has typically occurred.

Many components of inflammaging fit this model:

Inflammation is essential for fighting infection and healing injury—key to survival in youth.
But persistent low-level inflammation in later life (when there's less evolutionary pressure) can damage tissues and promote age-related diseases.

Evolutionary Trade-offs and Imperfections

Evolution is a tinkerer, not an engineer. Many ageing-related changes are the result of compromises:

Senescence evolved as a tumour-suppressing mechanism to prevent damaged cells from proliferating. But those senescent cells linger and contribute to inflammaging.
Innate immune hyperactivity in old age may be a response to increased pathogen exposure or internal damage, but at the cost of chronic inflammation.

In short, evolution optimises for reproductive success, not long-term health. Traits that help organisms reach reproductive age and raise offspring will be favoured—even if they carry baggage that leads to decline post-reproduction.

Declining Selective Pressure with Age

After reproductive age, the force of natural selection weakens. There is less evolutionary incentive to “fix” late-acting harms like inflammaging, because they don’t typically affect reproductive output.

Genes that cause age-related diseases often persist simply because they don't affect reproduction.

Summary

Inflammaging is not an adaptation per se. It is a non-adaptive consequence of evolved systems—especially inflammation, immunity, and cellular senescence—that serve important functions earlier in life. These systems were selected because they enhanced fitness in youth, but they become maladaptive with age, leading to inflammaging and other degenerative processes.

In evolutionary terms, it’s the price we pay for having survived long enough to reproduce—and for not being “designed” for indefinite longevity.

Their work is also explained in lay terms in Duke Today, Duke University's online news magazine.

Study Suggests Lemurs Age Differently Than Humans
Research can offer clues into why we suffer from age-related conditions
What can lemurs tell us about inflammation and aging, aka “inflammaging” in humans? That’s the question Elaine Guevara, a biological anthropologist who studies the evolution of life history and aging in primates, set out to understand.

Elaine Elizabeth Gomez Guevara, Evolutionary Anthropologist.

In newly published research on age-related inflammation in ring-tailed and sifaka lemurs, Guevara discovered that perhaps we should rethink the inevitability of inflammaging in humans.

Although similar in many ways, ring-tailed and sifaka lemurs show differences in life pacing and lifespan, making useful comparisons. Because lemurs and humans are primates and share a common ancestor that lived millions of years ago, they offer valuable insights into human evolution.

Her findings, she said, were “surprising.”

Contrary to our predictions, neither species showed age-related change in either marker of oxidative stress. Neither lemur species exhibited age-related change in inflammation; if anything, contrary to our prediction, ring-tailed lemurs showed marginal declines in inflammation with age.

Elaine E. Guevara, lead author.
Department of Evolutionary Anthropology
Duke University, Durham, USA.

This finding, consistent with a few recent studies of other non-human primates, suggests that lemurs avoid the phenomenon of “inflammaging” widely observed in humans.

The study shows inflammaging is not a universal feature of primates, pointing to some differences that might suggest it turns out it's not even a universal feature of humans, according to Christine Drea, a professor of evolutionary anthropology who was one of the researchers working with Guevara.

What is Inflammaging?

As we grow older, low-grade chronic inflammation sets in, which in turn can cause health problems such as heart disease, strokes, diabetes, cancer and osteoarthritis.

Why inflammaging increases with age in humans, what causes it and how it can be prevented are answers to questions that can unlock critical information to help humans live longer and healthier lives.

Collecting Data from Lemurs

Drea said the team first had to find a way to measure oxidative stress, which can be found in blood, urine and saliva. They settled on urine.

Our role at the beginning was planning, designing, brainstorming, comparing and getting these samples.

Christine M. Drea, co-author
Department of Evolutionary Anthropology
Duke University, Durham, USA.

The Lemur Center does not allow research that will harm the animals.

Ring-tailed lemur, Lemur catta.

The next step says Guevara is to conduct similar research with lemurs in the wild.

There are a lot of good reasons to think that aging can be quite different in captivity and in the wild, and that in itself, is informative to evaluating the degree to which human inflammation is intrinsic versus environmental.

Elaine E. Guevara.

In the meantime, Guevara says this study serves as the first step in unraveling the question of why humans are suffering from inflammatory-related and age-related conditions and finding ways to treat them.

Neither lemur species exhibited age-related change in inflammation; if anything, contrary to our prediction, ring-tailed lemurs showed marginal declines in inflammation with age. [With a rapidly aging global population], these insights are essential for mitigating disability and improving quality of life in later years.

Elaine E. Guevara.

Publication:
Elaine E. Guevara, Nicholas M. Grebe, Richard R. Lawler, Anne Crowley, Savannah Lo, Elise N. Paietta, Janet L. Huebner, Virginia B. Kraus & Christine M. Drea
Comparison of age-related inflammation and oxidative stress in two lemur species
Journal of Comparative Physiology B, 2 Jul 2025 DOI: 10.1007/s00360-025-01619-y

Abstract
Oxidative damage and inflammation are mechanisms proposed to contribute to physiological senescence. Variation in oxidative damage and inflammation may reflect differential allocation of resources to reproduction and survival, contributing to differences in species-typical longevity and resulting from distinct, evolved life-history strategies. To investigate the link between molecular processes and physiological senescence, we compared urinary biomarkers of oxidative stress (8-isoprostane and 8-OHdG) and inflammation (neopterin) in a cross-sectional sample of two species that differ in life-history schedules: the relatively fast-paced ring-tailed lemur (Lemur catta; n = 41; ages = 1–32 years) and slow-paced Coquerel’s sifaka (Propithecus coquereli; n = 49; ages = 1–27 years). Consistent with a faster life-history pace, ring-tailed lemurs showed significantly higher average levels of DNA damage than did sifakas (8-OHdG: ring-tailed lemur mean: 18.6 ± 10.3 ng/mg Cr, sifaka mean 8.0 ± 9.0 ng/mg Cr, p = 0.001). Species differences in lipid damage and inflammatory biomarkers were not significant (8-isoprostane: ring-tailed lemur mean: 0.5 ± 0.3 ng/mg Cr, sifaka mean: 0.3 ± 0.2 ng/mg Cr, p = 0.11), although sifakas tended to show greater inflammation (neopterin: ring-tailed lemur mean: 0.01 ± 0.02 ng/mg Cr, sifaka mean: 0.02 ± 0.02 ng/mg Cr; p = 0.14), which may reflect health challenges faced by this species in captivity. Contrary to our predictions, neither species showed age-related change in either marker of oxidative stress. Thus, although lemurs appear not to experience an increase in the rate of oxidative damage incurred with age, we cannot exclude the possibility that accumulated damage contributes to aging. Neither lemur species exhibited age-related change in inflammation; if anything, contrary to our prediction, ring-tailed lemurs showed marginal declines in inflammation with age. This finding, consistent with a few recent studies of other non-human primates, suggests that lemurs avoid the phenomenon of “inflammaging” widely observed in humans.

Elaine E. Guevara, Nicholas M. Grebe, Richard R. Lawler, Anne Crowley, Savannah Lo, Elise N. Paietta, Janet L. Huebner, Virginia B. Kraus & Christine M. Drea
Comparison of age-related inflammation and oxidative stress in two lemur species
Journal of Comparative Physiology B, 2 Jul 2025 DOI: 10.1007/s00360-025-01619-y

© 2025 Springer Nature Ltd.
Reprinted under the terms of s60 of the Copyright, Designs and Patents Act 1988.

The discovery that some lemur species appear to age without developing the chronic low-grade inflammation seen in humans—*inflammaging*—presents a significant challenge for Intelligent Design creationists. According to ID doctrine, humans were created as a special, favoured species by an intelligent, purposeful designer—often implicitly understood to be a benevolent deity. In that context, one might reasonably expect that humans would be endowed with optimal physiological features, or at the very least, not burdened by damaging traits that undermine health and longevity.

Yet the evidence suggests otherwise. Humans are prone to a host of age-related inflammatory conditions—heart disease, type 2 diabetes, stroke, osteoarthritis, and more—driven in part by inflammaging. Lemurs, by contrast, seem to avoid this fate, maintaining a healthier inflammatory profile as they age. If an intelligent designer was both able and willing to confer such protection on lemurs, the question naturally arises: why withhold it from humans? Why would the “pinnacle of creation” be saddled with a chronic process that degrades the body over time, while distant primate relatives benefit from a seemingly more elegant solution?

For evolutionary biology, such discrepancies are not puzzling. Evolution by natural selection produces solutions that are local, contingent, and imperfect. Traits that improve reproductive success—even at the cost of long-term health—are favoured, and different lineages adapt in different ways. There is no expectation of universal optimisation. But for ID creationism, which posits deliberate, purposeful design with some degree of favouritism toward humans, such findings are hard to reconcile without invoking special pleading or ad hoc rationalisations. If the designer had both the power and intention to craft efficient biological systems, why do some species appear better designed to cope with ageing than humans?

This is not a trivial anomaly. It strikes at the heart of the ID claim that complex biological traits are best explained by design rather than by natural processes. If some mammals exhibit superior age-related adaptations than humans, despite supposedly lacking our privileged status, it raises the uncomfortable possibility that natural selection, not divine design, is the real architect of life’s diversity.

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