It is a scientific fact that the morphology of the human skull and brain size differs from that of chimps and apes. The question that has continuously eluded evolutionists is what caused this change? For decades, theories have been paraded before us as scientists try to strengthen the connection between what we see today, and the theory they believe is responsible for it all. The most recent addition can be summed up by this simple equation: weaker jaws = bigger brains.
Hansell Stedman and his colleagues have suggested that a gene mutation may have played a key role in the evolution of modern humans. The gene mutation is alleged to have created smaller muscles and weaker jaws in humans, thus reportedly allowing the skull to expand, making more room for the brain. The gene in question is myosin heavy chain 16 (MYH16). In their comprehensive review of mammalian myosin, Allison Weiss and Leslie Leinwand defined myosin as a “highly conserved, ubiquitous protein found in all eukaryotic cells, where it provides the motor function for diverse movements such as cytokinesis, phagocytosis, and muscle contraction” (1996, 12:417). Stedman and his colleagues found that in chimpanzees and gorillas, this particular gene was larger than the one found in humans. Stedman and his colleagues believe the difference can be blamed on a mutation they speculate occurred 2.4 million years ago, leaving humans with a reduction in the number of muscle fibers that work our jaws. They speculate that this reduction in masticatory muscles made possible an expansion in brain size. As Stedman and his colleagues suggested: “Our findings on the age of the inactivating mutation in the MYH 16 gene raise the intriguing possibility that the decrement in masticatory muscle size removed an evolutionary constraint on encephalization, as suggested by the anatomy of the muscle attachments relative to the sutures” (2004:418).
While many evolutionists have already rallied around the weak-jaw theory to explain the larger brains seen in humans, some realize that this is not exactly a “cure-all” in explaining human evolution. “Such a claim is counter to the fundamentals of evolution,” said C. Owen Lovejoy of Kent State University (see Verrengia, 2004). He went on to note: “These kinds of mutations probably are of little consequence.” In reporting on this new theory, Associated Press science writer Joseph B. Verrengia observed: “Jaws have been a focus of evolutionary research since Darwin, and the mutation offers a tantalizing theory. But it is unlikely that one mutation—even at a crucial evolutionary juncture—would make a person…” (2004). Ralph Holloway, a physical anthropologist at Columbia University correctly asserted: “To suggest that the brain is constrained by chewing muscles is just rubbish” (Pennisi, 2004, 303:1957).
Rubbish indeed! Are scientists really ready to believe that a loss of jaw muscles caused: (1) the brain to enlarge; (2) venous sinuses of the cranium to change their drainage patterns; (3) cranial nerves to shift in order to accommodate a growing skull; (4) new blood vessels formed to compensate for the growing brain case; and (5) this phenomenon to occur in the brain, but not other places in the body (why haven’t other organs caused a vast change in anatomy if everything hinges on musculature)? Yes, we know that muscle can affect the structure of bone—but what data do we have which show that a loss in muscle tissue can activate brain growth? Richard Potts, director of the Human Origins Program at the Smithsonian Institution, observed: “…their suggestion connecting it to the brain is way too speculative” (as quoted in Verrengia, 2004). Also, what effect would this sudden loss have on animals that were accustomed to having the muscles, when suddenly their offspring found themselves without it? Additionally, one must ask why our brains are not still enlarging today? And if they have stopped, could we cut the jaw bones of our infants to allow for bigger brains?
In order to determine the point at which this alleged mutation occurred, Stedman and his colleagues employed a molecular clock (for problems with the molecular clock see “The Demise of Mitochondrial Eve” by Harrub and Thompson, http://www.apologeticspress.org/articles/2095), and estimated that the mutation took place 2.4 million years ago. It would have been at this point—with this alleged loss of jaw strength—that researchers assume brain size began to accelerate. Peter Currie noted: “Remarkably, the timing of the appearance of this genetic alteration, or mutation, roughly coincides with the appearance of ‘human-like’ characteristics in the hominid fossil record” (2004, 428:373). However, a quick check of the Smithsonian Human Evolution Web site shows several problems with this theory. For instance, evolutionists claim that Australopithecus afarensis was around 3-4 million years ago (see chart below)—more than a million years prior to this alleged mutation. Yet a quick look at the fossils representing Australopithecus afarensis reveals no major crest on top of the head for muscle attachment. If we then proceed to Homo habilis (who supposedly existed 2-2.5 million years ago), we have a creature with a cranial capacity between 600cc and 700cc (modern humans have a range from less than 1,000 to more than 2,000 cubic centimeters in volume) with a perfectly smooth skull—again no crest on the cranium. We then move forward to Paranthropus robustus, which allegedly was walking around 2 million to 1.2 million years ago. Fossils of this creature have a prominent sagittal crest—a bony ridge that runs the length of the skull. In regards to P. robustus, the Smithsonian Web page notes: “Adaptations of the cranium were associated with a ‘heavy-chewing complex.’ This complex is thought to have made it possible for these early humans to eat large amounts of tough fibrous foods.” Yet, this creature supposedly came along after Homo habilis, Australopithecus afarensis, and after the alleged gene mutation!? The Web site also lists Paranthropus boisei, which is dated from 2.3–1.2 million years ago. Again, this skull has the crest, and was allegedly “highly specialized for heavy chewing.”
So, for those keeping track, we had a smooth skull prior to 2.5 million years ago, according to the Smithsonian. Then we developed this sagittal crest in Paranthropus species that was “highly specialized for chewing” about 2.0 million years ago. And yet Stedman and his colleagues are suggesting the opposite. They are saying we had this crest and then lost it 2.4 million years ago! Evolutionists can’t have it both ways! Either we had these major muscles, connected to a sagittal crest before the mutation, and then lost them, or their human family tree needs to be rewritten—again! Add to this the following conundrum. According to the fossil record, Neanderthals had the biggest brains of all. So does that mean our jaw muscles weakened, our brain growth accelerated to a massive size, and then decided to shrink back somewhat?
Consider for just a moment the logical conclusion one could draw from this “weaker jaw = bigger brain” theory. The hypothesis holds little sway when we look across the animal kingdom and compare biteforce to intelligence. If weaker jaws really did allow for bigger brains, then other animals should have incredibly large brains. Also, consider that paleontologists consider the bite force of the Allosaurus (dinosaur) to have been weaker than other dinosaurs and modern crocodiles. Did this creature also possess a brain size and intelligence to match? For instance, the following table tells us that according to this theory, rhesus monkeys should have a proportionally larger brain than humans (adapted from Huber and Motta, 2004).
||Clifton and Motta, 1998
||Huber and Motta, 2004
|Canary Island lizard
||Herrel, et al., 1999
||Clifton and Motta, 1998
||Dechow and Carlson, 1983
||Strom and Holm, 1992
||Evans and Gilbert, 1971
||Binder and Van Valkenburg, 2000
If an individual looked at the data without any evolutionary bias, then an obvious question would come to mind. Could humans have been created with a shorter form of the MYH 16 gene? Is it possible that this was not a mutation, but rather the original plan? An honest look at the available information leads one to answer this question with a simple “yes.”
Binder, W.J. and B.V. Van Valkenburgh (2000), “Development of Bite Strength and Feeding Behavior in Juvenile Spotted Hyenas (Crocuta crocuta),” Journal of Zoology, 252:273-283.
Clifton, K.B. and Philip Jay Motta (1998), “Feeding Morphology: Morphology, Diet, and Ecomorphological Relationships Among Five Carribean Labrids,” Copeia, 1998:953-966.
Currie, Pete (2004), “Muscling in on Hominid Evolution,” Nature, 428:373-374, March 25.
Evans, W.R. And P.W. Gilbert (1971), “The Force of Bites by the Silky Shark (Carcharhinus falciformis) Measured Under Field Conditions,” San Diego Naval Undersea Research and Development Center, pp. 1-12.
Herrel, A., et al., (1999), “Sexual Dimorphism of Head Size in Gallotia galloti: Testing the Niche Divergence Hypothesis by Functional Analyses,” Functional Ecology, 13:289-297.
Huber, Daniel Robert and Philip Jay Motta (2004), “Comparative Analysis of Methods for Determining Bite Force in the Spiny Dogfish Squalus acanthias,” Journal of Experimental Zoology, 301A:26-37.
Pennisi, Elizabeth (2004), “The Primate Bite: Brawn Versus Brain?,” Science, 303:1957, March 26.
Ringqvist, M. (1972), “Isometric Bite Force and Its Relation to Dimensions of the Facial Skeleton, Acta Odont. Scand., 31:35-42.
Stedman, Hansell H., Benjamin W. Kozyak, Anthony Nelson, et al., (2004), “Myosin Gene Mutation Correlates with Anatomical Changes in the Human Lineage,” Nature, 428:415-418, March 25.
Verrengia, Joseph B. (2004), “Gene Mutation that Separated Man from Apelike Creatures Found,” The Commercial Dispatch, National Section, p. 12A, Thursday, March 25.
Weiss, Allison and Leslie A. Leinwand (1996), “The Mammalian Myosin Heavy Chain Gene Family,” Annual Review of Cell and Developmental Biology, 12:417-439.
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