Human Sweat Glands Show Design
Yet Another Difference Found Between Humans and Apes:
Study Attempts to Document Evolution, Ends Up Supporting Intelligent Design
by Jerry Bergman, PhD
Another of the thousands of differences between humans and our claimed ape relatives has been found. Humans have more sweat glands, called eccrine glands, than any of the great apes. This is a reason why a Scientific American cover story was titled, “Humans: Why we’re unlike any other species on the planet.”
Furthermore, eccrine glands are indispensable for human thermoregulation. Without them, unless another method could be improvised, humans could not maintain the close to 98.6 degrees Fahrenheit required body temperature, which would be lethal. Another difference between humans and apes is
humans are unique in having nearly naked skin. Every other member of our extended family has a dense covering of fur—from the short, black pelage of the howler monkey to the flowing copper coat of the orangutan—as do most other mammals. Yes, we humans have hair on our heads and elsewhere, but compared with our relatives, even the hairiest person is basically bare.
The press release reviewed here, titled “The Chillest Ape: How Humans Evolved A Super-High Cooling Capacity,” claimed to explain how this difference evolved, but was unable to do so. Specifically, the difference is humans have ten times the density of sweat glands in their skin than our closest relatives, the chimpanzees. Humans have between two million and four million eccrine sweat glands in total. They are on both glabrous (palms, soles) and non-glabrous (hairy) skin. Combined, they produce up to 12 liters of thin, watery sweat every day. The human “cooling system is so superior that in a marathon on a hot day, a human could outcompete a horse.” The reason for the difference between humans and apes is genetic. The enhancer region that regulates the expression of the sweat gland-building gene is turned up in humans. This is often the reason for higher expressions of some trait in living organisms. A past study published in PNAS added among the many
unique features of humans, one of the most salient is the ability to effectively cool the body during extreme prolonged activity through the evapotranspiration of water on the skin’s surface. The evolution of this novel physiological ability required a dramatic increase in the density and distribution of eccrine sweat glands relative to other mammals and a concomitant reduction of body hair cover. As a result, human skin is dramatically different in comparison with that of other primates and facilitates efficient evaporative eccrine cooling.
Another difference between humans and all other mammals is, “in most other mammals, eccrine glands are not thermoregulatory, but instead serve a role in traction during locomotion and are restricted to the volar surfaces of the fore- and hind feet.” In other words, the sweat reduces the level of the animal’s slipping and falling when walking or running.
In attempting to produce a hierarchy that documents evolution, what was found were discrete differences between humans and apes. Generally, loss of body hair is correlated with an increase of eccrine glands. Humans have very little body hair and produce large amounts of sweat. In contrast, apes are covered with thick amount of body hair and produce only small amounts of sweat. One “rare exception among mammals, the mouse has both hair and eccrine glands interspersed in a distinct domain of the hindfoot where the density of the two appendage types can be easily scored” for comparison. It was this area of mice that the researchers studied.
The Study Results
The finding was an example of good science. In short, Kamberov et al., using mice, found the expression level of the Engrailed-1 gene (EN1) is important in determining eccrine gland density in mice. The EN1 gene codes for a transcription factor protein that induces immature skin cells to form eccrine glands. The activity of most genes is regulated by DNA regions that up-regulate the gene’s expression. In this study, an enhancer region called hECE18 boosts EN1 production causing the development of more eccrine glands. Because the EN1 gene is also found in humans, the researchers concluded the gene has the same effect in humans. The researchers also found the human hECE18 gene is more active than the ape versions. They also found both systems were very well-designed for each organism, both humans and apes. Nevertheless, an evolutionary speculation to explain the chance origin of the difference was attempted by the authors.
One notices at the onset their dogmatic assertion that evolution explains the origin of this trait in humans. Evolutionists talk like they “know” the eccrine glands evolved from an organism with few eccrine glands which, in turn, evolved from an organism lacking eccrine glands. We just have to figure out, they suppose, how and when this happened. They also “know” that the increase in human eccrine gland number compared to our primate ancestors evolved. And the
evolution of this novel physiological ability required a dramatic increase in the density and distribution of eccrine sweat glands relative to other mammals and a concomitant reduction of body hair cover…. the gene “En1 in later patterning of the distal limb in mice and [ellipsis omission makes quote flow awkward here] may provide clues as to the molecular pathways that were modified during human evolution to drive changes in eccrine gland density.”
All we observe is that the gene-set design is different, but this tells us nothing about its evolution.
This blind confidence in evolution as the explanation is also expressed in the article Kamberov published in an evolution journal. However, when speculating about the details of the gene system’s evolution, Kamberov is less secure, as the following example illustrates:
The increase in eccrine gland density and the reduction in body hair size are adaptations that almost certainly evolved in the hominin lineage. These traits are thought to have facilitated long distance trekking in open habitats in the genus Australopithecus, and were likely critical for the evolution of endurance running capabilities in Homo… ubiquitously distributed eccrine glands appear to be a relatively late innovation that first appears in the catarrhines.
The 2021 review of Kamberov’s study is even more tentative in its evolutionary conclusions:
Scientists broadly assume that humans’ high density of sweat glands … reflects an ancient evolutionary adaptation. This adaptation, coupled with the loss of fur in early hominins, which promoted cooling through sweat evaporation, is thought to have made it easier for them to run, hunt, and otherwise survive on the hot and relatively treeless African savannah, a markedly different habitat than the jungles occupied by other ape species.
Kamberov and her colleagues hypothesized that perhaps one way in which humans could have programmed the system to produce more sweat glands in their skin is to evolve genetic changes caused by mutations that increased the production of the EN1 gene in their skin.
Since evolutionists conclude all genetic differences in humans and apes are due to mutations, they looked for gene differences that distinguish human hECE18, which boosts EN1 gene expression—and then roll back those differences to the chimp hECE18 version which lowers the enhancer activity down to chimp levels. These differences were than claimed to be caused by mutations. The Kamberov results “suggest that the human “high-sweat” trait evolved at least in part through repeated mutations to just one regulatory region, hECE18. This means that this single regulatory element could have repeatedly contributed to a gradual evolution of higher eccrine gland density during human evolution.” No evidence was found to support this “could have” postulation.
What was found in the research is part of the complex genetic mechanism that produces a much larger number of sweat glands in humans compared to other mammals. What one would expect to find is that the variation in the number of eccrine glands is due to regulatory differences and, as expected, that a genetic basis was determined to be behind the regulatory differences. However, no evidence of macroevolution was found that documents the difference. What was shown was that one system produced ten times the number of eccrine glands than the other system.
In summary, “the study is mainly a feat of basic biology” that, contrary to the article’s claims, found nothing to document human evolution. It does document intelligent design that produces the genetic differences found, which the authors attribute to mutations – copy mistakes, which in the vast majority of cases damages the gene. Copy mistakes cannot improve a gene.
 Scientific American 319(3), Special Issue, September 2018.
 Jablonski, Nina J. The Naked Truth: Our nearly hairless skin was a key factor in the emergence of other human traits, Scientific American, November 2012. https://www.scientificamerican.com/article/the-naked-truth/.
 Baker, Lindsay. 2019. Physiology of sweat gland function: The roles of sweating and sweat composition in human health. Temperature. 6(30):211–259. P. 212.
 Jablonski, 2012.
 Kamberov, Yana G. et al., A genetic basis of variation in eccrine sweat gland and hair follicle density, PNAS (Proceedings of the National Academy of Sciences of the United States of America) 112(32): 9932–9937, August 2015; emphasis added.
 Kamberov, et al. 2015, p. 9933.
 Kamberov, et al., 2015, pp. 9932- 9933.
 Kamberov, et al., Comparative evidence for the independent evolution of hair and sweat gland traits in primates, Journal of Human Evolution 125: 99-105, December 2018.
 Kamberov, et al., 2015, p. 9932. Emphasis added.
 Penn Medicine News, 2021.
 Penn Medicine News, 2021.
 Penn Medicine News, 2021. Emphasis added.
 Penn Medicine News, 2021.
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.