How Naked Mole-Rats Avoid Mutations
Naked Mole-Rat Research Eloquently Supports the Creationists’ Position that
Mutations Are Dominant in Causing Disease, Aging, and Eventually, Death
These unusual digging mammals give no support for progressive molecules-to-man evolution
by Jerry Bergman, PhD
Naked mole-rats are one of the ugliest animals one will ever encounter in the study of nature; ugly but amazing (Figure 1). Their wrinkly grayish-pink skin makes them appear very old even when young. They can live up to 30 years, a lifespan unprecedented among small rodents. Most rats and mice have a lifespan from 24 months to, in the most ideal conditions, 4 years. If the longevity of a naked mole-rat in comparison to other rodents were applied to humans, an adult man instead of being considered a “senior” at age 80 could live up to 600 years!
Unique Among Rodents
Rodents are among the most successful of all mammals. Slightly less than half of all mammals living today are rodents. Mole-rats live exclusively in underground burrows they dig through hard-packed soil with their powerful muscles and prominent ever-growing incisor teeth. Their diet is high in cellulose, requiring high densities of gut bacteria to aid in digestion. Ironically, they consume all of the nutrients, minerals, and water they require from plant roots. They also practice coprophagy, the reingestion of feces that maximizes their nutrient uptake from the roots.
Like bees, mole-rats have a queen, the largest member of the colony, and workers. Like reptiles, they are cold-blooded. As a result they must huddle together in large masses to stay warm. They also bask as needed in their shallow surface tunnels, which are warmed by the sun. Nothing so far mentioned gives even a hint to explain their longevity.
Explaining Why They Live So Long
Several new studies have investigated reasons for the longevity of naked mole-rats. Aging is caused by a progressive decline in body functions which results in an increased risk of disease leading to death. One of the major causes of aging is the progressive decline of stem cells that lose their ability to maintain tissue health.
Stem cells can differentiate into many cell types, such as heart muscle cells, blood cells, or nerve cells. The two main stem-cell classes are embryonic stem cells and adult stem cells. Embryonic stem cells are totipotent, differentiating into all the tissues and organs of the animal during development. Adult stem cells live throughout the body in various organs. When an adult cell dies or becomes damaged, it can be replaced by new cells of the same type to maintain the organism’s health. Stem cells are able to divide and renew themselves over a long period of time, effectively repairing and replacing damaged or worn-out body cells.
Eventually, though, stem cell exhaustion occurs. When they can no longer replace cells, it leads to diminished organ function, aging, and increased risk of malignancies and an impaired response to infections. Research on naked mole-rats by Mikkola and Orkin focused on the loss of hematopoietic stem cells. These stem cells can develop into different blood cell types, including white blood cells (leukocytes) and red-blood cells (erythrocytes), plus platelets. They are located in circulating blood and bone marrow.
Mutation Rates Vary by Species
Mikkola and Orkin investigated naked mole-rats out of a quest to improve human health and lifespan. By learning how these small mammals age slowly, they hoped to develop interventions to ameliorate the negative effects of human aging. A major finding of their work concerns mutation rates. They found that different species experience mutations at different rates. Furthermore, animals that live longer acquire mutations at a slower rate. This helps explain why cancer risk does not directly correlate with an animal’s lifespan. A summary in Nature explains the relationship:
It is well known that somatic mutations — mutations in our body’s genetic code that accumulate over time — can cause cancer… Now a team of researchers have measured the somatic mutation rates of a range of mammals and discovered a striking correlation between mutation rate and lifespan. Lending [sic] evidence to the theory that somatic mutations are a cause of ageing rather than a result of it.
The research found that somatic mutagenesis was dominated by specific mutational processes in all species they studied including 5-methylcytosine deamination and oxidative damage. With some minor differences, mutational pattern in the other species researched resembled those in humans,. although
the somatic mutation rate per year varied greatly across species and exhibited a strong inverse relationship with species lifespan, with no other life-history trait studied showing a comparable association. Despite widely different life histories among the species we examined—including variation of around 30-fold in lifespan and around 40,000-fold in body mass—the somatic mutation burden at the end of lifespan varied only by a factor of around 3. These data unveil common mutational processes across mammals, and suggest that somatic mutation rates are evolutionarily constrained and may be a contributing factor in ageing.
This research has documented the fact that mutations, rather than providing the main source of variation for innovation as evolutionists teach, cause aging and disease such as cancer. And also—contrary to evolutionary predictions—the higher the rate of mutation, the shorter the lifespan and the higher the disease rate.
I noticed that discussions of the research about naked mole-rats never once mentioned how mutations could produce progressive evolution. Instead, they supported the view that mutations are, as a whole, deleterious to life.
The main finding from the naked mole-rat research is that mutational clocks tick at different rates in different species:
Throughout life, cells accrue mutations. It now emerges that longer-lived animals acquire mutations at a slower rate than do short-lived species, potentially explaining why cancer risk does not increase with lifespan.”
The findings by Mikkola and Orkin support the creation view and reject the Darwinian view. Evolutionary progress cannot proceed from mistakes and damage in the DNA code. Mutations are not benefits that can be filtered by natural selection. Evolutionists continue to teach that all of life is ultimately the result of the accumulation of mistakes in the genetic code.
Naked mole-rats contradict the evolutionary view. From the research completed to date, the comparatively long lifespan if these small mammals is due in part to their efficient maintenance of their stem cells against mutations. This design controls the mutation rate, resulting in efficient repair and replacement of damaged stem cells. It works more effectively in naked mole-rats than in other rodents. We can also infer that this design, which regulates longevity, is innate to the organism. Thus longevity is, in part, genetically regulated—which might explain why most animal types have similar lifespans as shown in the chart below (Figure 2).
 Gorbunova, Vera, et al., Rodents for comparative aging studies: From mice to beavers, Age 30(2-3):111-119, 2008.
 Andersson, Rebecca, and Marie Florian, Living a longer life: Unique lessons from the naked mole-rat blood system. EMBO Journal 41(15):1-4, p. 1, https://www.embopress.org/doi/full/10.15252/embj.2022111759, 2022.
 Mikkola, Hanna K.A., and Stuart H. Orkin, The journey of developing hematopoietic stem cells, Development 133(19):3733-3744. doi:10.1242/dev.02568, 2006.
 Emmrich, Stephen, et al., Characterization of naked mole-rat hematopoiesis reveals unique stem and progenitor cell patterns and neotenic traits, The EMBO Journal 41(15):e109694, https://www.embopress.org/doi/abs/10.15252/embj.2021109694, 2022.
 Howe, Nick Petrić, and Benjamin Thompson, Why do naked mole rats live as long as giraffes? Identifying how animals’ mutation rates line up with their longevity, Nature, https://www.nature.com/articles/d41586-022-01062-x, 13 April 2022.
 Fox, Dan, The lifespan secret: Why giraffes live longer than ferrets. Ageing is linked to accumulated mutations – according to new research, Nature, https://www.nature.com/articles/d41586-022-01042-1, 2022.
 Cagan, Alex, et al., Somatic mutation rates scale with lifespan across mammals, Nature, 604(7906):517–524, https://www.nature.com/articles/s41586-022-04618-z, 2022.
 Gorelick, Alexander, and Kamila Naxerova, Mutational clocks tick differently across species. Nature: News and Views, https://www.nature.com/articles/d41586-022-00976-w, 13 April 2022.
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 1,300 publications in 12 languages and 40 books and monographs. His books and textbooks that include chapters that he authored are in over 1,500 college libraries in 27 countries. So far over 80,000 copies of the 40 books and monographs that he has authored or co-authored are in print. For more articles by Dr Bergman, see his Author Profile.