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Does Human Evolutionary History Hang on a Sugar Tree?

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Abstract

Evolutionary scientists hope to use a sugar-related molecule preserved in fossils to trace human evolutionary history.

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At-a-Glance

  • DNA has been recovered from a limited number of ancient human fossils in Europe and Asia, but none from Africa.
  • Human and chimpanzee cells are labeled with different kinds of sugar polymers, called glycans.
  • Humans do not have the gene to manufacture the Neu5Gc glycan label found on chimpanzee and most other mammalian cells.
  • Evolutionists believe the ape-like ancestor we (supposedly) shared with chimpanzees had the ability to make Neu5Gc, and that a mutation eventually destroyed it.
  • Evolutionists believe they can use a Neu5Gc breakdown product preserved in fossils to determine which hominin fossils are in the human lineage.
  • The glycans on mammalian cell membranes can make them more or less vulnerable to certain pathogens.
  • Evolutionists believe loss of the gene for the chimp-like glycan protected our ancient ancestors from a malaria-like disease, spurring on the evolution of humans.

DNA is quite the thing these days—the clue in the courtroom, the repository of an unimaginable library of information, the heritable blueprint for life. DNA can reveal family relationships, allowing us to track extended families across the vast expanse of geography and time. Such genealogical applications go far beyond finding a family’s roots. DNA recovered from Neanderthal and Denisovan fossils has confirmed that these now-extinct people groups were part of the family of man, that they themselves intermingled, and that they have left their genetic footprints in the modern human genome.

But what if no DNA is available? No DNA has been recovered from African fossils of either ancient humans or our supposed ape-like ancestors. Could some other biomolecule provide clues to trace humanity’s family tree?

Scientists from the University of California San Diego School of Medicine think so. Led by Professor Ajit Varki, they report that the biochemical footprint of a particular type of sugar polymer—a type that modern humans cannot manufacture—has been detected in an ancient African fossil. Varki hopes to eventually test ancient hominin1 fossils for this molecule. (Hominin is an evolutionary term for humans and all their ancestors back to the common ancestor supposedly shared with apes.) The sugars being explored here are not the sweet kind, but rather chains of sugar molecules. These sugar polymers are called glycans.

The molecule Varki’s team detected is called N-glycolylated chondroitin sulfate, or Gc-CS for short. It contains a breakdown product of a glycan called Neu5Gc.2 Neu5Gc is not produced by modern humans, but it is produced by most mammals including bears, cows, and chimpanzees. Evolutionists believe chimpanzees are our closest evolutionary cousins. Evolutionists believe that our ancestors lost the gene to produce Neu5Gc through mutation after diverging from an ancestor shared with chimpanzees. Varki believes that by analyzing bones belonging to various species thought to be human ancestors, he can use the presence or absence of Gc-CS to trace the path of human evolution.

Sugar in the Bones

The signature breakdown product of Neu5Gc (which is abbreviated Gc) is readily incorporated into bone, bound up with chondroitin sulfate, a glycan-rich component of bone and cartilage. Varki’s group demonstrated that Neu5Gc’s bone-bound footprint is thus detectable as Gc-CS, where CS stands for chondroitin sulfate. Even consumption of Neu5Gc-containing food, like red meat, leaves trace amounts of Gc-CS behind.3 Wondering whether Gc-CS is stable enough to last for a long time in a fossil, Varki tested for it in a cave bear fossil believed to be 50,000 years old. He detected it. Then, with the cooperation of paleoanthropologist Meave Leakey of Kenya’s Turkana Basin Institute, Varki successfully used his new methodology to detect Gc-CS in a fossilized bone fragment from a Turkana Basin buffalo-like animal believed to be four million years old.

“Because DNA rapidly degrades in the tropics, genetic studies are not possible in fossils of human ancestors older than only a few thousand years, Leakey says. “Therefore such ancient glycan studies have the potential to provide a new and important method for the investigation of human origins.”4

The Golden Role of Glycans

There are a lot of glycans—chains of sugar molecules—in living things. Glycans include structural molecules like cellulose and chitin—the fibrous stiffeners of plants and arthropod exoskeletons. Fuel storage molecules like starch and glycogen are also glycans. Inside cells, glycans are tools the endoplasmic reticulum uses to fold protein molecules, which is essential for them to function properly. The outer surfaces of cells are adorned with glycan chains attached to membrane proteins. Many of the glycans found on the surfaces of cells are categorized as sialic acids. The Neu5Gc glycan Varki’s group has investigated is one of these.

Glycans attached to the surface of cells serve as signals to other cells. They are essential to embryonic development. Glycans are critical components of the immune system, helping cells to distinguish “self” from “non-self.” Variations in the sialic acid glycans tagging the surface of red blood cells, for instance, are responsible for the familiar ABO blood types. Adverse transfusion reactions result if a person’s immune system detects the presence of red blood cells bearing “non-self” glycans.

Glycans and Disease

The presence of particular glycans could prove to be a survival disadvantage or advantage, depending on the glycan-preference of dangerous pathogens.

Glycans on a cell’s surface are also the recognition and docking sites for some disease-causing microbes and viruses. Pathogens that bear glycans resembling those of host cells can masquerade to fool host immune systems. Several pathogens that plague humans but not animals—such as Influenza A virus, malaria-causing Plasmodium falciparum, and Salmonella typhi—target the human-specific glycans labeling our cells. Typhoid toxin selectively binds to the sialic acid glycan (Neu5Ac) found on human cells but not to the Neu5Gc found on chimpanzee cells. Different species of malaria infect humans and chimpanzees for the same reason. Thus the presence of particular glycans could prove to be a survival disadvantage or advantage, depending on the glycan-preference of dangerous pathogens.

Glycans and Evolution

Sialic acid glycans adorn the surface of all vertebrate cells. While humans do not make Neu5Gc, we do manufacture a very similar glycan called Neu5Ac. These differ by only one atom. Neu5Gc is produced by most mammals, but along with its notable absence in humans, it is also absent from ferrets, platypuses, some dogs, and New World monkeys. Neu5Gc is found in trace amounts in humans, but scientists think these trace amounts come from the beef and other animal products we consume. If Neu5Gc or its derivatives were to be found in small amounts in ancient human fossils—and they have not been—it likewise could be an indicator of a meaty diet. But Varki believes a search for Neu5Gc-related substances could tell us a lot about our evolutionary history, both the path it (supposedly) took and the survival-related driving force behind it.

Because glycans are attached to the surface of all eukaryotic cells,5 Varki writes that evolution through “natural selection repeatedly recruited glycans as being the best molecules for decorating the cell surface.”6 And because some pathogens are attracted to specific glycans, Varki believes sialic acid glycans “are at the nexus of an evolutionary arms race between vertebrate hosts and their pathogens.”7 He writes that under such survival pressure these glycans “have been ‘re-invented’ repeatedly via convergent evolution by microbes that interact with vertebrates.”8

Glycan Genetics—Evolution or Design?

The gene CMAH9 is responsible for producing Neu5Gc. It does so in most mammals, including chimpanzees. Humans do not have this gene. The region corresponding to the CMAH gene in human DNA, when compared to chimpanzee DNA, lacks the 92-base pair section required to add the oxygen atom that distinguishes Neu5Gc from Neu5Ac.10 Hence, human cells are labeled with Neu5Ac, not Neu5Gc. In fact, the human immune system is not Neu5Gc friendly. Humans have innate antibodies in place, ready to attack Neu5Gc. The human immune system reacts violently with a vigorous antibody response (serum sickness) when exposed to animal serum containing Neu5Gc.11

Evolutionists think our ape-like ancestors were able to make this enzyme (CMAH) and therefore the Neu5Gc it produces. They believe that a mutation destroyed the CMAH gene in these human ancestors about 3 million years ago, before Homo-species evolved. Fossil analysis shows that, like modern humans, Neanderthals did not produce Neu5GC.12 But chimpanzees do. Therefore, Varki’s team believes that the CMAH gene mutated into nonfunctional oblivion before human evolution got very far from ape-like ancestors. Varki wants to search for Neu5Gc or its stable, long-lasting derivative Gc-CS in hominin fossils to determine the path of human evolution and even to explain why whatever branch of the evolutionary tree we humans sprang from succeeded when others (presumably) failed.

Though he has not yet been able to examine any hominin fossils, Varki believes this discovery will be the tool that allows human evolution in Africa to be unraveled. “In recent decades, many new hominin fossils were discovered and considered to be the ancestors of humans,” Varki says. “But it’s not possible that all gave rise to modern humans—it’s more likely that there were many human-like species over time, only one from which we descended. This new type of glycan we found may give us a better way to investigate which lineage is ours, as well as answer many other questions about our evolution, and our propensity to consume red meat.”13 Envisioning the story he hopes Gc-CS analysis will tell, he adds, “It's possible we'll one day find three groups of hominin fossils—those with Gc-CS before the human lineage branched off, those without Gc-CS in our direct lineage, and then more recent fossils in which trace amounts of Gc-CS began to reappear when our ancestors began eating red meat.”14

Does the absence of that 92-base pair CMAH region in human DNA prove humans used to have it and lost it?

But does the absence of that 92-base pair CMAH region in human DNA prove humans used to have it and lost it? No. Observations can only show that an active CMAH gene is not there now. And if humans used to have an active CMAH gene and lost it, would that mean that humans and chimpanzees shared a common ancestor? Again, no. Humans and animals, observation shows, only reproduce and vary within their created kinds, as we would expect from the opening chapters of God’s Word where we learn that God designed the biological world to function that way. If we were able to confirm through observational science that ancient human DNA had this gene and that such a deletion is now evident in all humans, we would know something about information loss within the human genome, but nothing about its supposed evolution from nonhuman antecedents.

That being clear, let’s take a closer look at the interaction of glycans and disease-causing organisms. Glycans do affect susceptibility to some diseases. Evolutionist Varki believes this may be key to understanding human evolution from ape-like ancestors.

Glycans, Malaria, and Survival

Varki is hopeful that the biochemical footprints of Neu-5Gc will reveal the survival advantage that enabled early prehuman creatures to succeed after diverging from their ape-like forebears. The key, he thinks, lies with the varying attraction of malarial parasites for the glycan markers on red blood cells.

Malaria is a deadly disease in which a parasite invades and ultimately destroys its host’s red blood cells. The deadliest of the malaria-causing protozoan, Plasmodium falciparum, is attracted to human red blood cells, which are all tagged with Neu5Ac. This human-loving malarial parasite also attacks New World monkeys, whose red blood cells—like those of humans—are tagged with Neu5Ac, not Neu5Gc. Plasmodium falciparum does not cause severe infection in chimpanzees, not being particularly attracted to the Neu5Gc covering their red blood cells. Chimpanzees are however quite susceptible to malaria caused by a different malarial parasite, Plasmodium reichenowi. That parasite is attracted to the Neu5Gc covering chimpanzee red blood cells, but it does not infect humans.

Evolutionists like Varki believe that millions of years ago a malarial-like pathogen was highly attracted to blood cells tagged with Neu5Gc in our ape-like ancestors and decimated their population. The surviving population was dominated by those prehumans that had a CMAH-destroying mutation and hence could not produce Neu5Gc. Eventually, the story goes, these survivors evolved into the first humans. During human history, then, a malaria-causing variety attracted to Neu-5Ac emerged through the observable processes of variation and selection, giving rise to the deadliest pathogen afflicting modern humans.15

Glycans—Markers of Design or Evolution?

Varki, as an evolutionist, believes that genetic differences between the genomes of creatures he already believes to be evolutionarily related indicate genetic changes that happened during the evolutionary process.

Differences, however, are simply differences. Chimpanzees and countless other mammals have a CMAH gene. New World monkeys, ferrets, and modern humans do not. We share with all these animals a common Creator Designer, not a common ancestor. We therefore share many genetic similarities in addition to our uniqueness. Genetic similarities and differences are the hallmarks of our Common Designer. Nothing about them demonstrates these similarities and differences are evolutionary footprints.

In our sin-cursed, disease-ridden world, the differences in the glycans decorating mammalian red blood cells may well result in differing susceptibility to malaria and other pathogens. These differences may therefore offer a survival advantage for those humans or animals bearing the glycans less desirable to deadly pathogens. But to suppose that those differences or the improved survival of one population subset over another today shows how a human population emerged from ape-like ancestors millions of years ago is completely speculative. This claim is completely dependent on an evolutionary worldview, not observational science.

Observable science is consistent with God’s Word.

In fact, nothing in observational science has ever demonstrated any mechanism by which one kind of creature—like an ape—can acquire the genetic information to evolve into a different kind—like a human. Varki believes that glycan-based differences in malarial susceptibility in the observable present reveal a significant stimulus that helped humans evolve from nonhuman ancestors. But this belief is quite unscientific. It is a marriage of solid observable science to fanciful evolutionary notions. Observable science is consistent with God’s Word, wherein we find the only eyewitness account of where we came from and even where disease came from.

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Answers in Depth

2017 Volume 12

Footnotes

  1. The terms hominin and hominid are both words whose definitions embody the evolutionary assumptions (1) that humans evolved from an ape-like ancestor through a series of prehuman and extinct human species and (2) that humans and modern Great Apes (chimpanzees, gorillas, and orangutans) share a common ancestor. Hominid (as it is currently used by most writers) refers to all these individuals—modern humans, modern Great Apes, and all presumed the ancestors of both, back to the common ape-like ancestor. Hominin refers only to the human side of the evolutionary lineage after it branched off from the common ancestor supposedly shared with apes. When we use the terms hominins, therefore, we are referring to all modern and extinct humans and all their immediate ancestors (both real and imagined), back to the common ape-like ancestor imagined by evolutionists.
  2. N-Glycolylneuraminic acid.
  3. Anne K. Bergfeld et al., “N-glycolyl Groups of Nonhuman Chondroitin Sulfate Survive in Ancient Fossils,” Proceedings of the National Academy of Sciences (2017): doi:10.1073/pnas.1706306114.
  4. University of California–San Diego, “When Ancient Fossil DNA Isn’t Available, Ancient Glycans May Help Trace Human Evolution,” Science Daily, September 11, 2017, https://www.sciencedaily.com/releases/2017/09/170911150946.htm.
  5. Eukaryotic cells are nucleated cells as well as cells like our mature red blood cells, which have nuclei early in their development.
  6. Ajit Varki, “Uniquely Human Evolution of Sialic Acid Genetics and Biology,” Proceedings of the National Academy of Sciences 107 (suppl. 2) (2010): 1, doi:10.1073/pnas.0914634107.
  7. Ibid.
  8. Ibid.
  9. CMP-N-acetylneuraminic acid hydroxylase.
  10. Hye Ji Oh et al., “Loss of Gene Function and Evolution of Human Phenotypes,” The Korean Society of Biochemical and Molecular Biology Reports 48, no. 7 (2015): 373. doi:10.5483/BMBRep.2015.48.7.073.
  11. Ajit Varki, “Uniquely Human Evolution of Sialic Acid Genetics and Biology.”
  12. Toshiyuki Hayakawa et al., “Fixation of the Human-Specific CMP-N-Acetylneuraminic Acid Hydroxylase Pseudogene and Implication of Haplotype Diversity for Human Evolution,” Genetics 172, no. 2 (2016); 1139, doi:10.1534/genetics.105.046995.
  13. University of California–San Diego, “When Ancient Fossil DNA Isn’t Available, Ancient Glycans May Help Trace Human Evolution.”
  14. Ibid.
  15. Indeed, microbes that happen to be more attracted to similar but slightly different glycans—just like antibiotic-resistant bacteria—are more likely to survive and produce highly virulent populations of pathogens, like our modern deadly form of malaria. Yet nothing about this reveals an evolutionary source of genetic information. The malaria-causing protozoans are still malaria-causing protozoans, regardless of their variety.

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