Many believe in evolution because of their exposure to ‘ape-men’. These interpretations of fossils have been presented as ‘proof’ of evolution—that we evolved from apes, which came from a long line of ancestors back to microbial life that arose spontaneously.
The evidence does not speak for itself; it is interpreted within a historical and philosophical framework. We start with Genesis as God’s inspired Word, totally reliable in all that it says, including about history. We believe that this framework makes much better sense of the evidence and provides a more fruitful platform for doing good science, as the following examples show.
A recent focus on human evolution in New Scientist (August 2017) was headlined: ‘Who are you? How the story of human origins is being rewritten’. They had an image of a blackboard with the iconic ape-to-human sequence largely rubbed out. The subheading said, ‘The past 15 years have called into question every assumption about who we are and where we came from. Turns out our evolution is more baffling than we thought.’
Indeed so. Almost every aspect of the account of human evolution previously accepted by mainstream science has been overturned this century. Neither the fossil nor DNA evidence support any clear evolutionary scenario.
Similarly, the recent book, Contested Bones, reviews the opinions of evolutionary paleoanthropologists and shows that there is no consensus on a sequence from ape to human—in summary, there are fossils of varieties of apes and humans, but no ‘ape-men’.
Theistic evolutionists, such as Dr Francis Collins, have asserted that there is no DNA evidence consistent with the Bible’s human origins account. We can only conclude that they have not looked at the evidence from that perspective, because the case is strong indeed. For example:
Mitochondrial DNA is inherited from our mother, so studying the patterns can indicate our maternal ancestry. To the initial surprise of the evolutionary researchers, the evidence showed that there was but one mother of all mankind. Seeking an interpretation compatible with their evolutionary framework, they claimed that this woman lived within a larger population and it just happened that all the other maternal lines died off. However, the data are consistent with there being one woman from whom we all descended, which is what one would expect given the biblical text.
Estimations that this ‘mother of all’ lived about 200,000 years ago added weight to the ‘this is not the biblical Eve’ conclusion. However, other scientists realized that the mutation rate used was far too high. It assumed evolution from a common ancestor with chimpanzees (circular reasoning), whereas the laboratory-measured mutation rates for mitochondrial DNA were much higher, and thus the recalculated age for mitochondrial Eve was now about 6,000–6,500 years.
The Y-chromosome is only inherited from the father. Researchers have found very little variation in the Y-chromosome. The data are consistent with a single father for all mankind. Furthermore, the ‘shocking’ finding that the chimp Y-chromosome was only ~70% like the human forced ‘Y-chromosome Adam’ into a very recent timeframe. Again, the data are consistent with the Bible’s history.
The genetic data consistently give results that surprise, given the deep time assumption that dominates thinking. Indeed, when we analyse the Y chromosomes of modern men, we see that they carry only about 300 mutations, on average, from the consensus sequence of a Y chromosome Adam. Sanford and Carter state, ‘Even if we assume a normal mutation rate for the Y chromosome (about 1 mutation per chromosome per generation), we would only need 300 generations (about six thousand years), to get 300 mutations.’
Global DNA genetic diversity patterns are also consistent with the biblical history of Genesis 1-11, including creation, the Flood, and the dispersion of people by paternal lines after the Tower of Babel. The patterns are also consistent with all modern humans descending from just a handful of females, like the four women who were on the Ark.
J.B.S Haldane was a high-profile population geneticist. He looked at mutation rates and natural selection mathematically to work out how much genetic change could occur in the supposed time since a common ancestor with apes (he generously assumed 10 million years). He concluded that there is not enough time. For creatures like chimps and humans, even with all parameters optimized for evolutionary success, mutations and natural selection could not account for even one average-sized gene. That is, evolution is mathematically impossible. This has been independently confirmed by numerical simulation.
Further work has shown that the calculations are even worse for evolution, because of the ‘waiting time’ needed for specific mutations. In a large population with human-like reproduction, to get a specific string of just 8 bases (genetic ‘letters’) to appear and then to spread to all individuals within the population would take a time that exceeds the ‘deep time’ age of the universe (~13.8 billion years).
For decades it was claimed that human and chimp DNA differ by ‘only’ ~1%. This does not seem like much of a difference, so it was asserted that evolution must be true. However, this is actually a huge difference: about 30 million bases. This alone is enough to sink the notion of human evolution from apes in ~6 million years. With more data, the difference between human and chimp DNA is now recognised to be at least 5% and possibly as high as 30% (it is difficult to compare two large genomes). Consistent with this, a major statistical comparison of all the protein-coding genes of humans with 18 primate species showed that humans are distinctly separate from all other primates.
All of this is bad news for evolutionary notions of human origins, but it is consistent with mankind’s separate, recent origin on Day 6 of Creation Week.
Geneticists have known for decades that the human mutation rate is of the order of 100 new mutations per person per generation. They also recognise that most mutations are slightly harmful, so this would lead inevitably to loss of fitness and extinction, not an upward evolutionary trajectory. In the late 1960s and early 1970s it was decided that 98% of the human DNA was ‘junk’. If this were so, most mutations would occur in the ‘junk’ and would not matter. Thus, the notion of millions of years of human evolution could potentially be retained. However, the ENCODE project demonstrated that at least 80% of the ‘junk’ DNA was functional, and possibly 100%. Because natural selection cannot remove ~80 slightly deleterious mutations per individual per generation, human evolution is impossible, and extinction assured. Indeed, numerical simulation (modelling) of the degradation of the human genome explains the exponential decline in lifespans following Noah’s Flood.
Furthermore, mitochondrial DNA diversity data in a wide range of organisms, not just humans, are consistent with their existence for only thousands of years. A major independent secular study of mitochondrial DNA ‘barcodes’ among five million species also gave results that fit well with the Bible’s history in Genesis, but don’t sit at all comfortably in a deep-time evolutionary framework.
Similarities in DNA do not prove evolution. Why? Because similarities can also be due to common design. However, shared DNA sequences in functionless (‘junk’) DNA might support evolution. The powerful ENCODE conclusions seriously undermine any such argument, because there is not much ‘junk’ DNA to be shared. Claimed ‘shared mistakes’ could be shared functions.
For example, the ‘pseudogene’ HBBP1 was said to be a broken haemoglobin gene. It is shared by apes and humans and claimed to be proof of evolution. However, this gene is now known to be very important; mutations in it cause the disease β-thalassemia. Thus, this is better evidence of shared design, than common ancestry.
The GULO gene codes for the enzyme that makes vitamin C in many creatures. Humans and various apes do not make vitamin C, but we do have a DNA sequence that partly matches the rat GULO gene. Like HBBP1, GULO was declared a broken gene, a ‘pseudogene’ and ‘proof of evolution’. However, the human GULO pseudogene is very similar to the one found in guinea pigs, sharing many ‘mutations’. This cannot be attributed to common ancestry, so ‘mutational hotspots’ were invoked to explain the similarities. But how can anyone then argue that similarities with ape GULO are not also due to mutational hotspots? Furthermore, the human GULO is only 84% similar to chimps, which makes for a very weak argument for evolution. Also, the pattern of occurrence of the pseudogene in diverse, disconnected creatures does not fit any possible evolutionary pattern. According to Tomkins, the data ‘utterly negate the idea of macroevolutionary common ancestry’.
Another argument based on the junk DNA idea is the coincident placement of many short, repetitive sequences of DNA in chimps and humans. These are called short interspersed elements (SINES), of which a subgroup called Alus are the most important. However, the Alu sequence is now known to have multiple functions, especially in gene regulation. They are not junk and so the argument for evolution collapses.
Probably the most famous argument is the claim that human chromosome 2 derived from the fusion of two chimp progenitor chromosomes. Modern DNA sequencing undoes this argument. The supposed fusion site does not show the DNA sequences expected, and it is a part of a functional gene that regulates a family of genes known as DXX11L.
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As Carter, Lee, and Sanford concluded from their detailed analysis of the DNA data, ‘In the end, there is no reason to reject a literal, historical Adam and Eve. The genetic data are pointing strongly in that direction. In fact, the data we see are exactly what we would expect from the biblical account of human origins.’
 L. Loewe and S. Scherer, ‘Mitochondrial Eve: the plot thickens’. Trends in Ecology and Evolution Vol.12(11), 1997, pp422–423. Further discussion and references at creation.com/topics/mitochondrial-eve.
 R.W. Carter, S. Lee, and J.C. Sanford, ‘An overview of the independent histories of the human Y chromosome and the human mitochondrial chromosome’. Proc. Eighth Int. Conf. Creationism, pp133–151 (Creation Science Fellowship, Pittsburg, PA, 2018), https://digitalcommons.cedarville.edu/icc_proceedings/vol8/iss1/7/.
 J. Sanford, and R. Carter, ‘In light of genetics... Adam, Eve, and the Creation/Fall’, Christian Apologetics. J. Vol.12, 2014, pp51–98.
 See Carter, Lee, and Sanford, Op. cit.
 C.L. Rupe and J.C. Sanford, ‘Using numerical simulation to better understand fixation rates, and establish a new principle: Haldane’s Ratchet’. Proc. 7th Int. Conf. Creationism (Creation Science Fellowship, Pittsburg, PA, 2013), creationicc.org/2013_papers/2013_ICC_Rupe.pdf.
 J. Sanford, et al., ‘The waiting time problem in a model hominin population’. Theor. Biol. Med. Model. Vol.12, 2015, p.18.
 J. Tomkins, ‘Comprehensive analysis of chimpanzee and human chromosomes reveals average DNA similarity of 70%’. Answers Research J. Vol.6, 2013, pp63–69.
 J.K. Lightner and M. Cserhati, ‘The Uniqueness of Humans Is Clearly Demonstrated by the Gene-Content Statistical Baraminology Method’. Creation Research Society Quarterly Vol.55, 2019, pp132–141.
 This was necessary in Kimura’s ‘neutral’ theory of evolution: M. Kimura, ‘Evolution rate at the molecular level’. Nature Vol.217, 1968, pp624–626.
 See overview papers in Nature Vol.489, 6 September 2012; commentary at: D. Batten, ‘Dazzling DNA:
Huge study highlights stupendous design in human DNA’. Creation Vol.35(1), 2013, p38, creation.com/dazzling-dna.
 This is explored in detail by geneticist John C. Sanford in Genetic Entropy (FMS Publications, 4th edition 2014).
 J. Sanford, et al., ‘Genetic entropy recorded in the Bible?’ www.kolbecenter.org/wp-content/uploads/2014/07/Genetic-Entropy-Recorded-in-the-Bible.pdf, 2014.
 J.P. Tomkins, ‘The Human GULO Pseudogene—Evidence for Evolutionary Discontinuity and Genetic Entropy’. Answers Research J. Vol.7, 2014, pp91–101.
 Carter, Op. cit., pp322–324.
 Ibid., pp324–328.
 See Carter, Lee, and Sanford, Op. cit., p148.
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