The problems with evolutionary theory, however, do not stop with the origin, age, and evolution of the Universe itself. Biological evolution (or “macroevolution”) is just as much a problem as is cosmic evolution.⁵ At some point(s) in the past, if evolution is true, life must have arisen from lifelessness and somehow changed into all species which have ever roamed planet Earth. Does the evidence support biological evolution?

Problem #1: Life from Non-life

Before life can evolve, life has to exist. If evolution is true, that first life had to come about from non-life, a phenomenon called “abiogenesis” or “spontaneous generation.” Abiogenesis, however, has long been acknowledged to be an unprovable, though necessary, part of evolution. In 1960 G.A. Kerkut published The Implications of Evolution. Therein he listed seven non-provable assumptions upon which evolution is based. “The first assumption is that non-living things gave rise to living material, i.e., spontaneous generation occurred.”⁶ In spite of the admission that evolution is based on non-provable assumptions, many today in the evolutionary community boldly assert that their theory is a scientific fact. However, the unbiased observer must ask: what does the scientific evidence actually have to say about the origin of life?

The work of various scientists over the centuries disproved the superstitious idea that life can come from non-life (e.g., Francesco Redi and Lazzaro Spallanzani). Louis Pasteur is generally acknowledged to be the scientist whose experiments drove nails into the proverbial abiogenesis coffin. Even standard evolution-based high school biology textbooks have historically acknowledged that fact. For example, one such popular textbook stated, “It was not until 1864, and the elegant experiment of French scientist Louis Pasteur, that the hypothesis of spontaneous generation was finally disproved.”⁷ They acknowledged that, “Pasteur, like Redi and Spallanzani before him, had shown that life comes only from life.”⁸ This truth is so absolute that it has been deemed a scientific law: the Law of Biogenesis. Evolutionist George G. Simpson, one of the most influential paleontologists of the 20^th century, articulated well the findings of science: “[T]here is no serious doubt that biogenesis is the rule, that life comes only from other life, that a cell, the unit of life, is always and exclusively the product or offspring of another cell.”⁹ Though many attempts have since been made to initiate life from non-life, none have succeeded. Leading evolutionary biologists have been forced to acknowledge, therefore, that abiogenesis is “impossible,” “absurd,” and an “obsolete concept,”¹⁰ but without it, evolution cannot even get started!

Notice the following acknowledgements by leading evolutionists over the years. Evolutionist and Nobel Laureate, George Wald, of Harvard University wrote: “As for spontaneous generation, it continued to find acceptance until finally disposed of by the work of Louis Pasteur.”¹¹ He further admitted, “One has only to contemplate the magnitude of this task to concede that the spontaneous generation of a living organism is impossible. Yet here we are, as a result, I believe, of spontaneous generation.”¹² Notice that his belief in spontaneous generation is not based on the actual evidence but, instead, on blind faith in evolution in spite of the evidence. In the lecture series, Origins of Life,¹³ evolutionary geologist Robert Hazen made notable admissions: “The origin of life is a subject of immense complexity, and I have to tell you right up front, we don’t know how life began.” “How can I tell you about the origin of life when we are so woefully ignorant of that history?” Evolutionists do not know how life could emerge from non-life within their naturalistic theory, but they believe in it anyway.

Evolutionist Paul Davies, theoretical physicist, cosmologist, astrobiologist, and professor at Arizona State University, writing in New Scientist, said, “One of the great outstanding scientific mysteries is the origin of life. How did it happen?…The truth is, nobody has a clue.”¹⁴ Evolutionist John Horgan did not even try to veil his admission within an article. He titled one of his articles, “Pssst! Don’t Tell the Creationists, but Scientists Don’t Have a Clue How Life Began.”¹⁵ Such admissions are quite telling, albeit incorrect. What Davies and Horgan mean is, no naturalistic evolutionist “has a clue.” Biblical supernaturalists, on the other hand, know exactly how life originated, and the answer harmonizes perfectly with the Law of Biogenesis—unlike evolution’s life-origins fairytale. If one sticks with the evidence, he must conclude that to believe life can come from non-life would be irrational, unscientific, and requires blind faith in evolution.¹⁶

Problem #2: The Nature of the First Life

Life coming from non-life, in actuality, is the “easy” part. The difficulty of getting life from non-life is so overwhelming that we usually fail to realize other daunting aspects of the equation that compound the difficulty of the problem for evolutionists. The distinguished British astronomer, Sir Fred Hoyle, once highlighted the gravity of the abiogenesis problem.

At all events, anyone with even a nodding acquaintance with the Rubik’s cube will concede the near-impossibility of a solution being obtained by a blind person moving the cubic faces at random. Now imagine 10⁵⁰ blind persons each with a scrambled Rubik’s cube, and try to conceive of the chance of them all simultaneously arriving at the solved form. You then have the chance of arriving by random shuffling at just one of the many biopolymers on which life depends. The notion that not only biopolymers but the operating programme of a living cell could be arrived at by chance in a primordial organic soup here on the Earth is evidently nonsense of a high order.¹⁷

The arrival of life on Earth from non-life is problematic enough, but life cannot exist without an actual “operating program” that tells it how to function once it exists.

The problem does not stop there, either. What would happen to the first life if it could not reproduce itself? Famous evolutionary biologist Richard Dawkins stated in an interview with Ben Stein regarding the origin of life, “Nobody knows how it got started. We know the kind of event that it must have been. We know the sort of event that must have happened for the origin of life. It was the origin of the first self-replicating molecule.” Obviously, the first life had to already have the functionality to reproduce: yet another hurdle that would be impossible for evolution to jump. Stein asked Dawkins, “Right. And how did that happen?” Dawkins replied, “I’ve told you. We don’t know.” Stein then said, “So, you have no idea how it started?” Dawkins replied, “No. Nor has anybody.”¹⁸ John Keosian, biology professor at Rutgers University, said, “Even conceptually, it is difficult to see how a system satisfying the minimum criteria for a living thing can arise by chance and, simultaneously, include a mechanism containing the suitable information for its own replication.”¹⁹ We agree.  

Another problem exists when considering what would have to occur for abiogenesis to be possible. The biomolecules of life generally are only found in one (out of two) of the main three-dimensional biomolecule configurations—a scenario called homochirality. However, as biochemist Joe Deweese of Freed-Hardeman University noted, “in a pre-biotic system (one where life does not yet exist) there is no clear mechanism for preferentially causing the formation of one chiral form over another. This means there is no homochirality. Instead, when chemicals react in experimental systems, researchers tend to get mixtures of L- and D- [i.e., “right-handed” and “left-handed”—JM] forms of molecules,”²⁰ a dilemma called the “homochirality problem” by origin-of-life scientists. Experimental evidence does not support the contention that abiogenesis occurred.

No wonder abiogenesis is deemed by many evolutionists to require a “miracle” that requires blind faith on the part of the evolutionist to accept.²¹ But the problem for evolutionists does not stop there, either. Evolutionist John Maddox, writing in Nature, said, “[I]t is disappointing that the origin of the genetic code is still as obscure as the origin of life itself.”²²

Problem #3: The Origin of Genetic Information

Darwin believed that “natural selection” would serve as a mechanism to make evolution happen. However, in the immortal words of Dutch evolutionary botanist Hugo de Vries, “Natural selection may explain the survival of the fittest, but it cannot explain the arrival of the fittest.”²³ Natural selection is simply a “filtering mechanism” that eliminates those species that are not as well suited to an environment as another species. Those species must already exist, however, in order for them to be filtered. What natural mechanism could create the species in the first place?

Mainstream evolutionary thinking today is that genetic mutations coupled with natural selection will create the best fit species, a belief known as “Neo-Darwinism.” Once again, however, genes must already exist in order for them to be mutated. Where did the first, “simple” genome come from? And how could new genetic information (i.e., new “raw material”) be subsequently spontaneously created naturally as the original life forms morphed into other life forms? In the words of the late, famous evolutionary paleontologist of Harvard University, Stephen Jay Gould, “A mutation doesn’t produce major new raw material. You don’t make a new species by mutating the species…. That’s a common idea people have; that evolution is due to random mutations. A mutation is not the cause of evolutionary change.”²⁴ If a living thing does not already have the genetic code to grow new parts, it cannot grow them, because that would require new raw material.

Consider the analogy of making a digital copy of a file from a computer onto a flash drive. When a file is copied, “mutations” can sometimes occur. The file does not always copy properly. The final copy is not always exactly like the original. Codon errors, duplications, translocations, deletions, and other mutations exist in genetics—errors that cause the final copy to be “mutated.” Do such mutations add new raw material? Do they “write a new sentence” in the file? No. A mutation might cause a fly to have extra wings (homeotic mutations) or a person to have an extra toe (polydactyly), but mutations do not create a new feature or a new creature. A mutation would not cause a wing to appear on a creature, for example, unless the creature already had wings in its genome.

Why? Because when the structure of the DNA molecule was discovered in the twentieth century, James Watson and Francis Crick “discovered that DNA stores information using a four-character chemical alphabet. Strings of precisely sequenced chemicals called nucleotide bases store and transmit the assembly instructions—the information—for building the crucial protein molecules and machines the cell needs to survive.”²⁵ Information is packed into our genes, and yet, in the words of information scientist Werner Gitt of the Federal Institute of Physics and Technology, “There is no known law of nature, no known process, and no known sequence of events which can cause information to originate by itself in matter.”²⁶ Bottom line: evolution has no way of getting life from non-life, and no way to evolve it into something different when it arrives. Once again, the evolutionist must rely on blind faith to hold his position.²⁷

Problem #4: Insufficient Evidence for Evolution

In order for a belief to be “rational,” it must have sufficient supporting evidence. After all, the Law of Rationality states that one should only draw those conclusions that are warranted by the evidence.²⁸ Biblical creation is rational, since it is based on evidence that the Bible is of divine origin.²⁹ Is belief in evolution a rational belief or a blind faith? Where is the evidence for evolution?

When a student takes “Biology” class in public high school or college, he will most likely find a section in his textbook listing alleged evidences for evolution. Upon closer examination, without exception, these evidences can be categorized as being one of three possibilities: erroneous, irrelevant, or inadequate. Consider the following commonly listed evidences for macroevolution:

Category 1: Erroneous Evidences

• Embryonic recapitulation: Ernst Haeckel, living at the turn of the 19^th century, asserted that embryos in their development in the womb repeat the evolutionary history of their species. Though his idea quickly became embedded in evolution-friendly textbooks, his claims were not only found to be inaccurate,³⁰ but eventually found to be a hoax.³¹ Upon confrontation, Haeckel eventually acknowledged that several of the charts he used to promote his theory were fabricated to support his theory. He said, “I should feel utterly condemned and annihilated by the admission, were it not that hundreds of the best observers and biologists lie under the same charge. The great majority of all morphological, anatomical, histological, and embryological diagrams are not true to nature, but are more or less doctored, schematized and reconstructed.”³²

• Horse evolution charts: Textbooks often have charts allegedly documenting the evolution of horses from the small, fox-like creature known as eohippus or hyracotherium. Several decades ago, however, leading paleontologists acknowledged that the “uniform, continuous transformation of hyracotherium into equus [modern horses—JM], so dear to the hearts of generations of textbook writers, never happened in nature.”³³ Perhaps the leading paleontologist of the twentieth century, Harvard professor Stephen Jay Gould, subtly chided those who spread misinformation by using horse evolution as proof of evolution:
  
  Once ensconced in textbooks, misinformation becomes cocooned and effectively permanent, because, as stated above, textbooks copy from previous texts. (I have written two essays on this lamentable practice: one on the amusingly perennial description of the eohippus, or “dawn horse,” as the size of a fox terrier, even though most authors, including yours truly, have no idea of the dimensions or appearance of this breed…).³⁴
  
  Keep in mind that even if some or all of the animals on the typical horse charts were, in fact, part of the ancestry of modern horses, hyracotherium (the first animal on the horse evolution chart) is still acknowledged by evolutionists to be a “horse” and, therefore, is argued by some creationists to be part of the “horse kind” which left the Ark. If so, horse evolution charts would be evidence of microevolution (not macroevolution) and would, therefore, constitute inadequate evidence of macroevolution (category three below). Bottom line: evidence for macroevolution cannot be found among the horses.³⁵

• Whale evolution charts: Whale evolution has been called “one of the best documented examples of mammal evolution,”³⁶ and yet the entire timeline of whale evolution is now being revamped (again). Whales were historically argued by many to be descended from hippos, until 1979 when pakicetus became the believed ancestor of the whales. Discovery of more bones over the years caused scientists to completely change their portraits of pakicetus to look something like a land-dwelling, wolf-like mammal, with only a slight resemblance to the whale in its teeth. As would be expected, after further discoveries, pakicetus is now being abandoned and scientists are changing the evolutionary story of whales again. They now suggest that carnivorous whales may have descended from a tiny, deer-like, herbivorous, aquatic creature known as indohyus—a big shift, to say the least, in spite of the supposed documentation of whale evolution. What will be the new supposed evolutionary ancestor of whales in the coming years?

• Transitional fossils: As we have shown elsewhere, the fossil record is, perhaps, one of the strongest evidences in favor of Creation, not evolution.³⁷ Abrupt appearance, stasis, and mass extinction characterize the fossil record from bottom to top, exactly as creationists would predict and exactly the opposite of what evolution would predict. While there should be billions of transitional fossils linking all life forms to previous ancestors if Darwin was correct, in truth, there are no undisputed transitional forms.³⁸ While change should characterize the fossil record, leading paleontologists have long acknowledged instead that stasis is the rule.³⁹ If Darwinian evolution actually happened, transitional forms would be prevalent, especially among the invertebrates which fossilize more easily and make up most of the fossils on the planet by far. However, few if any alleged transitional forms among the invertebrates have even been uncovered by evolutionists. Even among the few alleged vertebrate transitional forms, as time passes, the fossil is ultimately re-considered and marked off the list of supposed evidences for evolution. To illustrate, perhaps the two most oft-cited alleged transitional creatures in the animal kingdom would be tiktaalik and archaeopteryx.
  
  Tiktaalik has been hailed as the transitional creature linking fish and amphibians, a creature whose pelvic fins (its front fins) are thought to have been evolving into legs. However, in 2010 researchers⁴⁰ in Poland discovered four-limbed animal tracks in fossil strata believed to be nine million years older than the tiktaalik strata. How could tiktaalik be the transition from fish to legged amphibians if four-legged creatures were already around and fully-functional “nine million years” before tiktaalik was on the scene?
  
  Archaeopteryx is thought to be the creature that linked dinosaurs to their descendants, the birds. Equipped with teeth and claws, but also sporting feathers, a wishbone, and a beak, archaeopteryx looked to scientists as though it was not quite bird and was not quite dinosaur. Some admittedly modern birds and birds within the fossil record, however, have claws⁴¹ and teeth⁴² as well, proving that having them does not imply they descended from dinosaurs. Further, acknowledged birds have been found in fossil strata thought to be “millions of years” older than the strata in which archaeopteryx was found,⁴³ and the supposed feathered dinosaurs do not arrive in the fossil strata until “millions of years” after the strata in which archaeopteryx is found. In the words of British paleontologist and senior editor of Nature, Henry Gee, concerning the “dethronement of Archaeopteryx,” “Archaeopteryx is just another dinosaur with feathers.”⁴⁴ Bottom line: archaeopteryx is now considered by most to be a true bird. It is not transitional.⁴⁵

Category 2: Irrelevant Evidences

The logical Fallacy of Equivocation occurs when the same word is used in at least two unclear ways in an argument, and the two are treated as though they are one and the same.⁴⁶ “Trees have branches. My bank has branches. Therefore, my bank is a tree.” Richard Dawkins was no doubt referring to this category of evidence when he claimed that evolution is a “fact that is proved utterly beyond reasonable doubt.” He claimed, “It is absolutely safe to say that if you meet somebody who claims not to believe in evolution, that person is ignorant, stupid or insane (or wicked, but I’d rather not consider that).”⁴⁷ If, by “evolution” is meant the concept that change happens over time (e.g., we are not exactly the same as our parents), then perhaps only “ignorant, stupid or insane” people reject evolution. If, however, by “evolution” Dawkins is referring to molecules-to-man evolution, then evolution certainly is not a “fact that is proved utterly beyond reasonable doubt.” However, without clarification, many students fall victim to the Fallacy of Equivocation, assuming that since change happens, (Darwinian) evolution must be true.

With that in mind, the Biology student should be careful not to be swayed by this category of alleged evidences for evolution—a category which is, perhaps, proclaimed the loudest. This category contains, for example, instances of “evolution” which are not disputed by creationists (i.e., microevolution), but which do not provide evidence for the form of evolution accepted by mainstream secular scientists today (i.e., macroevolution)—“molecules-to-man” naturalistic evolution.

• Natural selection: When a species is not as well-suited to a particular habitat as another species, if the less “fit” species does not migrate to a different environment for which it is more suited, the more fit species will tend to thrive and the less fit species will tend to die out. That is natural selection, and it is not rejected by creationists. However, natural selection in no way supports the idea that a fish can turn into an amphibian or a dinosaur can turn into a bird. As discussed earlier, natural selection is merely a filtering mechanism which cannot act until a species already exists. Evolution requires the appearance of a new creature before natural selection can do its work. Natural selection, therefore, is an irrelevant evidence in regard to macroevolution—it neither supports it nor refutes it.

• Geographic distribution and finches: Charles Darwin, in his travels, noted that animals that were slightly different from one another, but clearly still related, would often be found in a single local area, but in different habitats (e.g., slightly different climates). He saw this as evidence that those animals descended from a common ancestor in the area and that natural selection caused certain varieties to thrive in different habitats. He observed varieties of finches (as well as tortoises, iguanas, and plants), for example, with different colored feathers and different sized or shaped beaks. These varieties, he postulated, must have descended from a single ancestor in South America.
  
  However, while variety existed among the finches, they all were still acknowledged to be finches. Further, as biologists Peter and Rosemary Grant of Princeton, who spent 35 years studying the Darwin Galapagos finches, acknowledged, “for beak size and shape to evolve, there must be enough heritable variation in those traits to provide raw material for natural selection.”⁴⁸ In other words, the possible variation seen among the finches was all inherited from the original ancestor—it was not spontaneously generated from thin air. The variation was already built into the species. Nothing new came about, but macroevolution requires new material. Again, therefore, geographic distribution is an irrelevant evidence for macroevolution. Heritable variation within animals implies (1) an initial Creator of the genetic information that was inherited by offspring, and (2) variation is limited by the genetic package that the original ancestor is equipped with. Evolution across phylogenic boundaries from one kind of animal to another, therefore, cannot happen if the ancestor was not already equipped with the genetic information to allow such a change. Since the original, simple single-celled organisms thought by evolutionists to have launched life on Earth would not have been equipped with the genetic information to bring about all of the species on the planet, macroevolution is not possible.
  
  Darwin also acknowledged cases where there were animals in similar habitats across the world that were apparently not descended from the same ancestors but that had similarities in structure anyway. He considered these examples to be evidence of natural selection: that the pressures of natural selection cause certain body characteristics to appear and thrive in certain environments, while other characteristics less suited to the environment die out. This, once again, is merely evidence of natural selection, not macroevolution—an irrelevant evidence.

• Evidences of microevolution: Darwin’s finches are a classic example of microevolutionary change—small changes under the umbrella of the general kind of creature that God originally created (Genesis 1:24). Microevolution is not proof of macroevolution, however, since all available evidence supports a hard reproductive boundary, beyond which an animal cannot evolve. Evolutionary paleontologist Steven Stanley explained: “The known fossil record fails to document a single example of phyletic evolution [i.e., evolution of a new phylum—JM] accomplishing a major morphological transition and hence offers no evidence that the gradualistic model can be valid.”⁴⁹ Change between species seems only to be capable at roughly the genus or family level (e.g., speciation from wolves to dogs). The original kinds that God created had the potential for a certain amount of diversity within them, but not enough to change the kinds into a different kind. Other often cited examples of microevolutionary change would include peppered moth varieties, bacteria “evolving” resistance to antibiotics, and fruit fly varieties. Mutated flies are still flies, resistant bacteria are still bacteria, and dark peppered moths are every bit as much moths as are light colored peppered moths. Microevolutionary evidences are irrelevant evidences in trying to prove that single-celled organisms can evolve into humans over millions of years.⁵⁰

Category 3: Inadequate Evidences

Admittedly, one category of alleged evidence for evolution stands as unrefuted potential evidence for evolution. The evidence is not adequate evidence, however, considering that the same evidence can be used with better consistency in support of biblical Creation as well.

• Homologous structures: Evolutionists argue that similarities in different life are every bit as much evidence for our relation to them as is our similarities to our human ancestors. It is true that if we are related to someone, we would predict there to be similarities between us (we share similarities with our parents, for example). However, as Darwin himself observed (see Geographic distribution above), similarities are often seen in species that clearly share no common ancestor. That concession begs the question: how do evolutionists really know which species are actually related and which are not? Similar bone structures between birds and dinosaurs, or chimps and humans, for example, do not necessarily suggest relationship. Could there be a different explanation? Actually, yes: there is a perfect explanation that fits the evidence better.
  
  If Creation, rather than evolution, is true, then similarities seen between different kinds would suggest a common Designer, rather than a common ancestor. Car manufacturers often use the same features and car parts on multiple models (e.g., tires, brake systems, windshield wipers, bolts, light bulbs, etc.), rather than “re-inventing the wheel” with each model. If a particular part has proven to be the most effective part and it can be used multiple times in other applications, it would be extremely inefficient of an engineer to use a different part or design a new part in all new designs. Car manufacturers often even design their various car models with a similar “look” that distinguishes their brand from others.
  
  Similarly, one would expect God, if He is an efficient Engineer, to use similar structures in many life forms on Earth, since they were all designed to live on the same planet. Those designed to live in similar environments on Earth and do similar things would be expected to be even more similar than other species. Those creatures who would be breathing air would be expected to have similar lungs. Many of those creatures designed for swimming in water would be expected to have fins, and so on. If the same Designer was behind the different kinds of animals of the Earth, one would expect similarities between them—and, of course, there are.
  
  Which view—common ancestry or common design—fits the evidence better and more consistently? Several evidences could be highlighted which reveal the superiority of the Creation model in explaining the evidence, but let’s look at one. Recall again the above section on “Geographic distribution.” While similarities between those species living in the same relative environment—species that are distinctive from those found elsewhere—is admittedly suggestive of possible common ancestry (though, once again, not macroevolutionary ancestry), the second category of similarity observed by Darwin (i.e., creatures similar though not related) is a problem for macroevolution. In the case of descent from a common ancestor, the genetic potential for similarities between descendants is at least possible (though Someone would have to create the “heritable variation” in the first place), but when common ancestry has been ruled out, there is no means of creating the observed similar features between creatures. A common Designer, therefore, is the reasonable conclusion from the evidence for both of Darwin’s observations.⁵¹

Conclusion

Even if the Big Bang could create the Universe and explain away all of the inconsistencies we see when studying the cosmos, at some point, in order for biological evolution to occur, life had to come from non-life. If that feat was not difficult enough, that life had to be extremely complex—more complex than we might typically even realize. It had to have an operating program that told it how to function. It had to be able to replicate itself and be homochiral. It had to be equipped with the necessary genome to allow life to continue. That pool of genetic information had to be continually increased spontaneously over millions of years in order to allow that single-celled organism to turn into all of the species on the planet, ending with the genetically complex species we call homo sapiens. The pool had to increase in spite of the fact that there is no known way to spontaneously generate such information in a natural way.

With such facts established, it should come as no surprise to find that evolution has never been able to be substantiated by solid evidence. Its alleged evidences are always, without exception, erroneous, irrelevant or, at the very least, inadequate. Belief in evolution, therefore, requires one to hold a blind “faith” in a superstitious fairytale. It’s no wonder that the late Colin Patterson, senior paleontologist at the British Museum of Natural History in London, said about evolution, “One morning I woke up and something had happened in the night, and it struck me that I had been working on this stuff for twenty years and there was not one thing I knew about it. That’s quite a shock to learn that one can be misled so long. Either there was something wrong with me, or there was something wrong with evolutionary theory.”⁵²

Endnotes

¹ See Jeff Miller (2022), “Should Christians Accept Evolution and an Old Earth to Win Converts?” Reason & Revelation, 42[4]:38-44, April.

² See Jeff Miller (2017), Science vs. Evolution (Montgomery, AL: Apologetics Press), 2nd edition, pp. 9-38.

³ See Jeff Miller (2019), “21 Reasons to Believe the Earth is Young,” Reason & Revelation, 39[1]:2-11, January.

⁴ Ibid.

⁵ Biological evolution, macroevolution, and Darwinian evolution all refer to the theory that all species on the planet evolved from previous species, leading back to original common ancestors of all life.

⁶ Gerald A. Kerkut (1960), The Implications of Evolution (London: Pergamon), p. 6.

⁷ Kenneth R. Miller and Joseph Levine (1991), Biology (Englewood Cliffs, NJ: Prentice Hall), p. 341, emp. added.

⁸ Ibid.

⁹ George G. Simpson and William Beck (1965), Life: An Introduction to Biology (New York: Harcourt, Brace, & World), 2nd edition, p. 144, emp. added.

¹⁰ See Jeff Miller (2017), Science vs. Evolution (Montgomery, AL: Apologetics Press), pp. 61-109.

¹¹ George Wald (1962), “Theories on the Origin of Life” in Frontiers of Modern Biology (Boston, MA: Houghton-Mifflin), p. 187, emp. added.

¹² George Wald (1954), “The Origin of Life,” Scientific American, 191[2]:44-53, August, p. 47, emp. added.

¹³ Robert Hazen (2005), Origins of Life (Chantilly, VA: The Teaching Company).

¹⁴ Paul Davies (2006), New Scientist, 192[2578]:35, November 18, emp. added.

¹⁵ John Horgan (2011), “Pssst! Don’t Tell the Creationists, but Scientists Don’t Have a Clue How Life Began,” Scientific American, http://www.scientificamerican.com/blog/post.cfm?id=pssst-dont-tell-the-creationists-bu-2011-02-28, emp. added.

¹⁶ For an in depth study on the Law of Biogenesis and its implications, see Miller, 2017, pp. 61-109.

¹⁷ Fred Hoyle (1981), “The Big Bang in Astronomy,” New Scientist, 92:527, November 19, first emp. in orig.

¹⁸ Ben Stein and Kevin Miller (2008), Expelled: No Intelligence Allowed (Premise Media), emp. added.

¹⁹ John Keosian (1964), The Origin of Life (New York: Reinhold), pp. 69-70, emp. added.

²⁰ Joe Deweese (2023), “Homochirality and the Origin of Life,” Reason & Revelation, 43[11]:122-124, November, emp. added.

²¹ See Miller (2017), pp. 61-109.

²² John Maddox (1994), “The Genesis Code by Numbers,” Nature, 367:111, January 13, emp. added.

²³ Hugo De Vries (1905), Species and Varieties: Their Origin by Mutation, ed. Daniel Trembly MacDougal (Chicago, IL: Open Court), pp. 825-826, emp. added.

²⁴ Stephen J. Gould (1980), “Is a New and General Theory of Evolution Emerging?,” Hobart College speech, 2-14-80; quoted in Luther Sunderland (1984), Darwin’s Enigma (San Diego, CA: Master Books).

²⁵ Stephen C. Meyer (2009), Signature in the Cell (New York: Harper Collins), Kindle file, Ch. 1, emp. added.

²⁶ Werner Gitt (2007), In the Beginning was Information (Green Forest, AR: Master Books), Kindle file, Ch. 6.

²⁷ For an in depth study of the problem of the origin of genetic information, see Miller (2017), pp. 111-132.

²⁸ Lionel Ruby (1960), Logic: An Introduction (Chicago, IL: J.B. Lippincott), pp. 130-131.

²⁹ See Kyle Butt (2022), Is the Bible God’s Word? (Montgomery, AL: Apologetics Press); Dave Miller (2020), The Bible is from God: A Sampling of Proofs (Montgomery, AL: Apologetics Press).

³⁰ Aaron O. Wasserman (1973), Biology (New York: Appleton-Century-Crofts), p. 497; George G. Simpson and William S. Beck (1965), Life: An Introduction to Biology (New York: Harcourt, Brace, & World), pp. 240-241; Erich Blechschmidt (1977), The Beginnings of Human Life (New York: Sringer-Verlag), p. 32; Sir Arthur Keith (1932), The Human Body (London: Thornton and Butterworth), p. 94.

³¹ W.R. Thompson (1956), “Introduction,” Origin of Species, by Charles Darwin (London: Dent, Everyman’s Library edition),  p. xvi; Jane M. Oppenheimer (1988), “Haeckel’s Variations on Darwin,” Biological Metaphor and Cladistic Classification, ed. H.M. Hoenigswald and L.F. Wiener (Pittsburgh, PA: University of Pennsylvania Press), p. 134; Kenneth R. Miller and Joseph S. Levine (2006), Biology (Upper Saddle River, NJ: Prentice Hall), p. 385.

³² As quoted in Malcolm Bowden (1977), Ape-Men: Fact or Fallacy? (Bromley, England: Sovereign Publications), p. 76.

³³ George Gaylord Simpson (1953), Life of the Past (New Haven, CT: Yale University Press), p. 125, emp. added.

³⁴ Stephen Jay Gould (2000), “Abscheulich! (Atrocious),” Natural History, 109[2]:42-50, March, paren. in orig., p. 45.

³⁵ See also D. Raup (1979), “Conflicts Between Darwin and Paleontology,” Field Museum of Natural History Bulletin, 50[1]:24-25.

³⁶ “Whales Descended from Tiny Deer-like Creature” (2007), ScienceDaily, http://www.sciencedaily.com/releases/2007/12/071220220241.htm.

³⁷ Jeff Miller (2019), “Does the Fossil Record Support Creation and the Flood?” Reason & Revelation, 39[7]:74-80.

³⁸ Colin Patterson (1979), Letter of April 10, 1979 to Luther Sunderland: reprinted in Bible-Science Newsletter, 19[8]:8, August, 1981, emp. added.

³⁹ E.g., Stephen Jay Gould (1980), The Panda’s Thumb (New York: W.W. Norton & Co.), pp. 181-182.

⁴⁰ “Ancient Four-Legged Beasts Leave Their Mark” (2010), Science on-line, January 6, http://news.sciencemag.org/evolution/2010/01/ancient-four-legged-beasts-leave-their-mark.

⁴¹ E.g., the ostrich, African Turaco, and young South American Hoatzin.

⁴² E.g., Ichthyornis [see  The Editors of Encyclopaedia, “Ichthyornis” (2020), Encyclopedia Britannica, March 4, https://www.britannica.com/animal/Ichthyornis.], Hesperornis [The Editors of Encyclopaedia, “Hesperornis” (2021), Encyclopedia Britannica, December 16, https://www.britannica.com/animal/Hesperornis.], Hongshanornis [Riley Black (2014), “Feathery Fossil Offers Insights into the Flight and Diet of an Early Bird,” National Geographic on-line, January 8, https://www.nationalgeographic.com/science/article/feathery-fossil-offers-insights-into-the-flight-and-diet-of-an-early-bird.], and Sulcavis [see Riley Black (2013), “Fossil Bird Had Tough Teeth,” National Geographic on-line, January 13, https://www.nationalgeographic.com/science/article/fossil-bird-had-tough-teeth.]. See also the descriptions of Deinonychus and Cryptovolans in “Feathered Dinosaurs and the Origins of Flight” (2024), Arizona Museum of Natural History, https://www.arizonamuseumofnaturalhistory.org/explore-the-museum/exhibitions/previous-exhibitions/feathered-dinosaurs-and-the-origins-of-flight. See also “Pictures: Giant Fossil Bird Found With Spiky ‘Teeth’” (2010), National Geographic on-line, September 16, https://www.nationalgeographic.com/history/article/100915-giant-bird-wingspan-science-chilensis-teeth-pictures.

⁴³ E.g., Anchiornis (see Black, 2014) and Protoavis [see Sankar Chatterjee (1999), “Protoavis and the Early Evolution of Birds,” Palaeontographica A, 254:1-100].

⁴⁴ Henry Gee (1999), In Search of Deep Time (New York: The Free Press), pp. 195,197.

⁴⁵ In regard to human evolution in particular, typical inadequate evidences would include the lack of necessary transitional forms to substantiate Darwinian evolution [see Jeff Miller (2023a), “Does the Evidence REALLY Support Human Evolution? (Part 1),” Reason & Revelation, 43[8]86-88, August]. Other inadequate evidences would include human-chimp DNA similarities [see Jeff Miller (2023b), “Does the Evidence REALLY Support Human Evolution? (Part 2),” Reason & Revelation, 43[9]:99, September].

⁴⁶ Hans Hansen (2015), “Fallacies,” The Stanford Encyclopedia of Philosophy, ed. Edward N. Zalta & Uri Nodelman, https://plato.stanford.edu/entries/fallacies/. 

⁴⁷ Richard Dawkins (1989), “In Short: Nonfiction,” The New York Times, April 9, https://www.nytimes.com/1989/04/09/books/in-short-nonfiction.html.

⁴⁸ Kenneth R. Miller and Joseph S. Levine (2010), Biology (Boston, MA: Pearson), p. 472.

⁴⁹ Steven Stanley (1977), Macroevolution (San Francisco, CA: Freeman), p. 39, emp. added.

⁵⁰ In regard to human evolution in particular, typical irrelevant evidences would include the examples of species among the Australopithecines, which are now regarded as belonging on a side branch of the human evolutionary tree, rather than being our ancestors. Also included among the irrelevant evidences would be species from the genus Homo, which are generally all regarded as being varieties of human and, therefore, examples of micro-, not macroevolution  (see Miller (2023a), pp. 89-92).

⁵¹ In regard to human evolution in particular, typical erroneous evidences would include the many rash claims of transitional forms from the fossil record that have proved to be hoaxes and blunders (see Miller (2023a), pp. 88-89). Another erroneous evidence would include vestigial organs and genes, human-chimp chromosome fusion, mitochondrial DNA and “Eve” (see Miller (2023b), pp. 98-100).

⁵² Colin Patterson (1981), Written transcript made from audio tape of lecture presented at the American Museum of Natural History, November, emp. added.

The post 4 Reasons to Believe Evolution is NOT True appeared first on Apologetics Press.

EDITOR’S NOTE: The following article was written by A.P. auxiliary staff scientist Dr. Deweese who holds a Ph.D. in Biochemistry from Vanderbilt University and serves as Professor of Biochemisty and Director of Undergraduate Research at Freed-Hardeman University.

Introduction

For the past two and a half years, the world has been given a front-row seat to the process of science as the pandemic of SARS-CoV-2 has made its way around the world and back again. This article examines the virus and its components with a goal to understand how the virus works and how it is changing over time. Further, we will seek to consider the implications of viral evolution and step back to think about how viruses fit into a biblical worldview. [For a more extensive study of the nature of SARS-CoV-2, see the online version of this article.]

Before January of 2020, relatively few individuals used the term “coronavirus” in everyday language, much less understood its implications. While there are a few different coronaviruses that cause things like the common cold, prior to SARS-CoV-2, only two had caused major problems in humans: severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV). An outbreak of SARS-CoV occurred in 2002-2004, which infected over 8,000 people and killed nearly 10% of those infected.¹ MERS-CoV was associated with the Arabian Peninsula and occurred from 2012-2015 with about a 30% death rate, but a very low transmission rate.² As of October, 2021, there have been a total of 2,578 cases with 888 reported deaths (34.4%) since 2012.³ By contrast, SARS-CoV-2 has spread globally in just over two years with over 419 million cases worldwide and over 5.8 million deaths (~1.4% of those infected) so far according to the Johns Hopkins Coronavirus Resource Center.⁴ Unfortunately, these numbers do not clarify for us the difference between people who died from the effects of COVID versus those who died of other causes but had COVID.

In general, SARS-CoV and MERS-CoV are naturally found in rodents and/or bats but have undergone “zoonotic transmission” to infect humans.⁵ Zoonosis is a term used to describe a disease that has undergone “spillover” from vertebrate animals to humans.⁶ As you might guess, there are barriers and challenges that prevent many diseases from infecting different organisms. However, some barriers are not insurmountable. Many questions still surround how and what changes took place to give us SARS-CoV-2—were they natural mutations in animal populations or were they part of experimental efforts perhaps aiming to thwart an epidemic? There are those on various sides of these issues.⁷

This article is not intended to settle the question of the origin of the virus or to take a particular side. Instead, we want to ask more fundamental questions: what is different between SARS-CoV-2 and previous deadly coronaviruses? Why does it spread so quickly? What will happen moving forward? And what are the apologetic implications of the coronavirus?

What Do We Learn About Mutations and Natural Selection from SARS-CoV-2 Variants?

One way to study viruses is to see how the sequences vary from other known viruses. Interestingly, SARS-CoV-2 is only 79% similar to SARS-CoV.⁸ This means that both viruses share about 79% of the same sequence information. The closest sequences to SARS-CoV-2 are viruses isolated from bats found in Yunnan province 1000+ km from Wuhan, denoted RaTG13 and RmYN02.⁹ RaTG13 is the closest, sharing 96.2% identify, while the RmYN02 shares 93.3% identity with SARS-CoV-2 reference sequence (note that the reference sequence is the first sequence that was released by Chinese researchers before the variants). In this context, nucleotide “identity” means that two sequences are identical at that percentage of sites. Thus, 100% identity would mean that they have the same nucleotides at all possible sites. In a 30,000 nucleotide sequence, a 90% identity means that 27,000 sites match between two sequences.¹⁰

Throughout the pandemic, researchers have tracked the changes occurring in the genome of SARS-CoV-2 using advanced DNA sequencing technologies. As a result, there are now over four million SARS-CoV-2 viral sequences for us to compare in the public NCBI Virus Variation database.¹¹ This is a bit of a unique situation because we’ve never had such a large pandemic occur while we have had the ability to sequence the genetic information of the virus in real-time worldwide. This massive effort has provided a way to track genomic changes (i.e., mutations in the virus) over time to see what types of changes are occurring and what types of changes are not occurring.

In general, we observe the changes typically seen in any organism: deletion, insertion, and single nucleotide changes. Single nucleotide changes are by far the most common. At this point, perhaps you are wondering how many changes are in the variants when compared to the reference sequence. In even the most extreme cases—like the Omicron variant—the total number of nucleotide changes (including insertions and deletions) is around 100 (less than 1%). Thus, for over 99% of the sequence there are no changes.

As of this writing, 10 variants are considered “Variants Being Monitored” (VBM) by the Centers for Disease Control, while two are listed as “Variants of Concern” (VOC): delta and omicron.¹² In reviewing mutation data on these variants, most of the mutations tend to occur in the Spike protein-coding region with additional mutations in the ORF1ab region and some variants showing mutations in the nucleocapsid (N) protein-coding region.¹³ Mutations in the Spike protein tend to be focused within the amino terminal domain (the first part of the protein) or the RBD, as noted above. These are the regions that antibodies typically bind, especially those formed through vaccination with the mRNA vaccines.

As seen in Figure 1, Spike protein point mutation sites are mapped onto a three-dimensional model of the protein for the Omicron variant. The mutation sites are highlighted as red spheres. The region in red is the Receptor Binding Domain (RBD). The concentration of red spheres in this area underscores the importance of understanding how this region is changing and what impact that has on viral transmission and treatability. Mutations in this region can result in evasion of antibodies that target Spike protein.¹⁴ In other words, some of these mutations in the Spike protein make this region less able to be bound by antibodies from vaccination and/or prior infection. It is also worth noting that in addition to antibodies, T-cells also respond to SARS-CoV-2 and T-cell response includes binding to Spike (or other viral proteins). Notably, T-cell response in vaccinated and/or prior infected individuals still mostly retain the ability to recognize Omicron.¹⁵

What can we learn from this? There are a few key takeaways for us to consider. First, mutations in SARS-CoV-2 are still rare in the sense that we do not see widespread mutation throughout the viral genome. This is due to the error correction mechanism and apparently a low tolerance of genetic change. The mutations that are occurring are enabling the virus to survive and spread more readily while causing more mild symptoms in general. Thus, you could argue that natural selection is filtering out mutations that do not benefit the virus. As noted by Dutch botanist and geneticist Hugo de Vries, however, “Natural selection may explain the survival of the fittest, but it cannot explain the arrival of the fittest.”¹⁶ Natural selection does not provide the mechanism for the origin of new information, which is necessary for the evolution of new viruses and organisms.¹⁷

Second, the types of changes we are seeing fall into the basic categories of insertions, deletions, and single-nucleotide changes. The largest insertion in the sequences examined was nine nucleotides. Interestingly, this sequence is not found anywhere in the virus or in any of the variants examined except Omicron. There is a similar sequence in the genome (about 4,000 nucleotides away) that is off by one nucleotide, but the author has not seen a lot of speculation around this sequence.

There are some limitations to this brief study. For instance, there are 10s to 100s of thousands of sequences for some of these variants. So, there will undoubtedly be variability among the various samples. Yet, even with such variability, the general themes noted above remain: no novel sets of information have been generated by the DNA changes observed. More specifically, no new proteins or enzymatic functions have been observed. Instead, mutation and selection appear to be at work on the existing protein-coding genes, which is why we see most mutations focused on regions like the Spike protein-coding sequence. In order for new features to develop as in the Neo-Darwinian model of evolution, new genetic information is needed, but we do not observe this occurring.¹⁸

SARS-CoV-2 is mutating, but it is also clear that it is still SARS-CoV-2 (i.e., we do not see new functions arising though we do see modification of functions). We are seeing first-hand what types of mutations are possible. Note that this does not necessarily mean that we know what is possible in a living organism—viral growth and mutation have unique constraints. Other studies have argued that mutations tend to modify or break existing features rather than build new ones.¹⁹ This appears to hold true in SARS-CoV-2.

Are Viruses a Form of “Natural Evil” that Support a Case Against God?

In considering the SARS-CoV-2 virus and its cost on our world, it is worth asking, why do we have viruses anyway? From a human perspective, it can often seem like all viruses are “bad.” Are viruses a “natural evil” created by God to plague the world?  After all, the only time the media (or society more generally) tends to focus on viruses is in the context of the seasonal flu or in the case of an outbreak of some deadly virus—like MERS or SARS. In fact, the word “virus” originated from the Latin term for poison.²⁰ Our language has clear implications for how we view viruses. Do viruses represent a “bad” design on the part of the Creator?

As a little exercise in considering the roles and purposes of viruses, let’s first ask: how many types of viruses are there? Current taxonomy of viral species by the International Committee on the Taxonomy of Viruses lists 10,434 species.²¹ It seems generally agreed that this is an under-representation of the total number of viruses in nature, as additional viruses continue to be discovered year by year. In support of this idea, it has been stated that there are ~10³¹ bacterial viruses (called bacteriophages) in the biosphere, which exceeds the estimate of the number of stars in the universe!²² Interestingly, only approximately 219 viruses have been found to infect humans. Of these viruses, relatively few cause disease or death in humans.²³ Far fewer have been found to cause epidemics or pandemics.²⁴ Yet, as humans, we generally focus on these few cases that cause disease rather than on the thousands of viruses (perhaps hundreds of thousands or millions?) that exist throughout nature.²⁵

To be clear, the 1918 Spanish flu, HIV, SARS, MERS, and SARS-CoV-2 have all had a major impact on our world. Many lives were lost or dramatically changed because of these viruses and their associated epidemics or pandemics. Yet, the integral role of viruses in nature has not been all negative as will be pointed out below.

Second, if there are so many different viruses, what do they do? Are there natural and ecological functions and roles for viruses? The answer to that is yes. In fact, there are many functions and roles for viruses in nature. For example, bacteriophages, mentioned above, help control bacterial populations.²⁶ In addition, bacteriophages can aid in transfer of genes between bacteria, serve as a nutrient repository, and defend bacteria against other bacteria.²⁷ Further, viruses may also play similar roles in eukaryotes and higher organisms including symbiotic relationships.²⁸ In humans, infection with GB-virus C has been associated with slowed progression of HIV infection, suggesting that this virus helps block HIV from infecting host cells.²⁹ Some have argued that the roles of viruses worldwide are so important that life as we know it would not exist without viruses.³⁰

So, does coronavirus have a natural role in bats or pangolins? This is a harder question to answer as few people are looking at this question—the general starting assumption is that viruses are “poison” or “pathogens.”³¹ Interestingly, this assumption, based upon evolutionary presuppositions, may be impeding our understanding of the roles of viruses in nature. Additional research will be needed to identify and explore such roles.

Consider for a moment: why would God allow viruses? Again, recall that most viruses do not cause problems and disease in humans, and it is reasonable to consider that many viruses have useful roles in nature. Could viruses be originally created entities that perhaps have also decayed since the Fall like our own genomes?³² If viruses were originally created by God to serve specific roles in nature, then it is possible that the nature and roles of viruses have been corrupted over time by genetic mutation.³³ The biochemical components in viruses are highly sophisticated—for example, reverse transcriptase (making DNA from RNA), error-correction, self-assembly, etc. These complex systems are best explained in a design model.

This perspective on viruses being designed entities has proved to be a fruitful research endeavor.³⁴ In fact, understanding the original design of viruses may help us identify the roles of viruses and how those roles have become corrupted over time. This may help us understand virulence and the ability of a virus to spread and mutate, which may help us predict future pandemic threats.

What can we expect moving forward? As we move forward, we can expect that SARS-CoV-2 will remain present continuing to change. The rate of change may slow since the virus is infecting fewer individuals than when it was spreading at its peak. Changes in the virus may enable it to continue to spread and possibly even cause new outbreaks, but the changes also seem to reduce the ability of the virus to cause serious illness in most people. Note that serious illness is still happening, especially in individuals with multiple risk factors, and we need to be serious about looking after those who are most at risk. The good news is that new treatments and approaches are becoming available to help minimize the health impact where possible.

Conclusion

SARS-CoV-2 has spread around the world over the last two and a half years and caused major loss of life. Though the virus has mutated during that time, no new genetic information has been generated nor have novel features developed as needed by a Neo-Darwinian model. Further, while the origin of this strain of the virus may remain contentious and debated, it is clear that viruses as a whole are designed entities fulfilling important roles in nature. It may be hard for us to identify those roles in the present time due to the genetic changes that have taken place in those viruses since the Fall in Genesis 3. Nevertheless, viewing viruses as designed entities that have experienced genetic change and decay since the Fall has served as a valuable framework for research in this area. In addition, this view helps remind us of God’s power in creation and of the consequences of sin that have been building since the Fall.

Endnotes

¹ “Revised U.S. Surveillance Case Definition for Severe Acute Respiratory Syndrome (Sars) and Update on Sars Cases—United States and Worldwide, December 2003,” (2003), MMWR: Morbidity and Mortality Weekly Report, 52[49]:1202-1206.

² B. Rha, J. Rudd, et al. (2015), “Update on the Epidemiology of Middle East Respiratory Syndrome Coronavirus (Mers-Cov) Infection, and Guidance for the Public, Clinicians, and Public Health Authorities—January 2015,” MMWR: Morbidity and Mortality Weekly Report, 64[3]:61-62.

³ WHO (2021), “Mers Situation Update.”

⁴ Coronavirus Resource Center Global Map (2022), Johns Hopkins University & Medicine, https://coronavirus.jhu.edu/map.html.

⁵ World Health Organization (2020), “Health Topics: Zoonosesd,” https://www.who.int/news-room/fact-sheets/detail/zoonoses.

⁶ K.G. Andersen, A. Rambaut, et al. (2020), “The Proximal Origin of Sars-Cov-2,” Nature Medicine, 26[4]:450-452; Y. Deigin, and R. Segreto (2021), “Sars-Cov-2’s Claimed Natural Origin Is Undermined by Issues with Genome Sequences of Its Relative Strains: Coronavirus Sequences Ratg13, Mp789 and Rmyn02 Raise Multiple Questions to Be Critically Addressed by the Scientific Community,” Bioessays, 43[7]:e2100015; M. Seyran, D. Pizzol, et al. (2021), “Questions Concerning the Proximal Origin of Sars-Cov-2” Journal of Medical Virology, 93[3]:1204-1206; J. van Helden, C.D. Butler, et al. (2021), “An Appeal for an Objective, Open, and Transparent Scientific Debate About the Origin of Sars-Cov-2,” Lancet, 398[10309]:1402-1404.

⁷ G.A. Rossi, O. Sacco, et al. (2020), “Differences and Similarities between Sars-Cov and Sars-Cov-2: Spike Receptor-Binding Domain Recognition and Host Cell Infection with Support of Cellular Serine Proteases,” Infection, 48[5]:665-669.

⁸ Hong Zhou, Xing Chen, et al. (2020), “A Novel Bat Coronavirus Closely Related to Sars-Cov-2 Contains Natural Insertions at the S1/S2 Cleavage Site of the Spike Protein,” Current Biology, 30[11]:2196-2203, e2193; Peng Zhou, Xing-Lou Yang, et al. (2020), “A Pneumonia Outbreak Associated with a New Coronavirus of Probable Bat Origin,” Nature, 579[7798]:270-273.

⁹ See the extended version of this article for a more technical discussion, https://apologeticspress.org/going-viral-exploring-virus-mutations-and-evolution-extended/.

¹⁰ E.L. Hatcher, S.A. Zhdanov, et al. (2017), “Virus Variation Resource-Improved Response to Emergent Viral Outbreaks,” Nucleic Acids Research, 45[D1]:D482-d490.

¹¹ SARS-CoV-2 Variant Classification and Definitions (2022), CDC, https://www.cdc.gov/coronavirus/2019-ncov/variants/variant-classifications.html.

¹² O’Toole, V.  Hill, et al. (2022), “Tracking the International Spread of Sars-Cov-2 Lineages B.1.1.7 and B.1.351/501y-V2 [Version 1; Peer Review: 3 Approved],” Welcome Open Res, 6[121].

¹³ Chakraborty, A.R. Sharma, et al. (2022), “A Detailed Overview of Immune Escape, Antibody Escape, Partial Vaccine Escape of Sars-Cov-2 and Their Emerging Variants with Escape Mutations,” Frontiers in Immunology, 13:801522.

14 V. Naranbhai, A. Nathan, et al. (2022), “T Cell Reactivity to the Sars-Cov-2 Omicron Variant Is Preserved in Most but Not All Individuals,” Cell, 185[6]:1041-1051.e1046.

¹⁵ Hugo de Vries and Daniel Trembly MacDougal (1905), Species and Varieties, Their Origin by Mutation; Lectures Delivered at the University of California (Chicago, IL: The Open Court Publishing Company).

¹⁶ J.C. Sanford (2008), Genetic Entropy & the Mystery of the Genome (Waterloo, NY: FMS Publications).

¹⁷ Ibid.; Michael J. Behe (2019), Darwin Devolves : The New Science About DNA That Challenges Evolution (New York: Harper Collins).

¹⁸ Behe, 2019; M.J. Behe (2010), “Experimental Evolution, Loss-of-Function Mutations, and ‘the First Rule of Adaptive Evolution,’” Quarterly Review of Biology, 85[4]:419-445.

¹⁹ Harald Brüssow (2021), “On the Role of Viruses in Nature and What This Means for the Covid-19 Pandemic,” Microbial Biotechnology, 14[1]:79-81.

²⁰ Peter J. Walker, Stuart G. Siddell, et al. (2020), “Changes to Virus Taxonomy and the Statutes Ratified by the International Committee on Taxonomy of Viruses (2020),” Archives of Virology, 165[11]:2737-2748.

²¹ F. Rohwer and R. Edwards (2002), “The Phage Proteomic Tree: A Genome-Based Taxonomy for Phage,” Journal of Bacteriology, 184[16]:4529-4535; Georgia Purdom and Joe Francis (2009), “More Abundant Than Stars,” Answers Research Journal, 2:85-95.

²² Mark Woolhouse, Fiona Scott, et al. (2012), “Human Viruses: Discovery and Emergence,” Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences, 367[1604]:2864-2871.

²³ Ibid.

²⁴ Ibid.; M.E. Woolhouse, R. Howey, et al. (2008), “Temporal Trends in the Discovery of Human Viruses,” Proceedings: Biological Sciences, 275[1647]:2111-2115.

²⁵ Purdom and Francis.

²⁶ Z. Naureen, A. Dautaj, et al. (2020), “Bacteriophages Presence in Nature and Their Role in the Natural Selection of Bacterial Populations,” Acta Bio-Medica: Atenei Parmensis, 91[13-S]:e2020024.

²⁷ Ibid.

²⁸ M.J. Roossinck (2015), “Move over, Bacteria! Viruses Make Their Mark as Mutualistic Microbial Symbionts,” Journal of Virology, 89[13]:6532-6535; Marilyn J. Roossinck (2011), “The Good Viruses: Viral Mutualistic Symbioses,” Nature Reviews Microbiology, 9[2]:99-108.

²⁹ Nirjal Bhattarai and Jack T. Stapleton (2012), “Gb Virus C: The Good Boy Virus?” Trends in Microbiology, 20[3]:124-130.

³⁰ Purdom and Francis.

³¹ Roossinck.

³² Purdom and Francis.

³³ Sanford.

³⁴ Purdom and Francis.

The post Going Viral: Exploring Virus Mutations and Evolution Using SARS-CoV-2 appeared first on Apologetics Press.

While various forms of evolution have been promoted for millennia,_² Charles Darwin’s version included a new feature: natural selection. Natural selection is the idea that “nature” selects the best “fit” organisms for survival, while those less suited for an environment, if they do not migrate, will tend to die off. So, if a particular variety of finch or English Peppered Moth is more suited to an environment than another variety, the better suited option will tend to survive and propagate its genes, while the less suited species will tend to eventually die out, along with its “inferior” genes. Natural selection is, by and large, a reasonable idea and does not contradict biblical Creation. Natural selection does not, however, actually change an organism. It does not have the capability of changing a single-celled organism into a human over time, as Darwin theorized it could. In the well-known words of Dutch botanist and geneticist Hugo de Vries, “Natural selection may explain the survival of the fittest, but it cannot explain the arrival of the fittest.”³

How, then, does the new, “more fit,” variety come about? Princeton University evolutionary biologists Peter and Rosemary Grant spent over 35 years studying Darwin’s famous Galapogos finches. As we have discussed elsewhere,⁴ Darwin noted how different shapes and sizes of beaks in finches may have contributed to the survival and flourishing of various bird varieties and the extinction of others. But where did the beak shape and size variety originate? As high school Biology textbooks correctly teach, the Grants found that “for beak size and shape to evolve, there must be enough heritable variation in those traits to provide raw material for natural selection.”⁵ “Heritable variation” refers to genetic variety that can be inherited from parents and expressed in the species’ offspring. In other words, parents already have the genetic variety in their genes which is then expressed in their offspring. If that potential for variety did not already exist in the genes of the parents, that variety could not be expressed in an offspring. “Without heritable variation in beak sizes, the medium ground finch would not be able to adapt to feeding on larger, tougher seeds during a drought.”⁶

Now to the point: elephants, along with any species on the planet, have a tremendous amount of genetic potential for variety in their offspring. Some elephants have “tusk genes” and are able to grow tusks, while the other elephants have “tuskless genes.” If poachers target elephants with tusks, obviously the elephants with tusk genes are going to tend to die out, along with the tusk genes that they have. In the meantime, the elephants with tuskless genes will tend to survive and begin thriving. The population of African elephants (and the genes they possess) will shift to predominantly tuskless, which is what scientists are finding. But did African elephants evolve?

Well, it depends upon your definition. Did the overall population of the African elephant change (“evolve”) from predominantly tusked to tuskless? Yes. Was the change Darwinian (i.e., the kind of change that could allow an elephant to grow new components and turn into something else)? No. New genetic information is required in order for a species to evolve across a phylogenic boundary into a totally different kind of species,⁷ and no new genetic information was introduced to the species (and there is no known natural mechanism for the generation of new genetic information⁸). Instead, already existing genetic information was simply expressed more often among the elephants.

Here are three key takeaways from the tuskless elephant study:

1. Are tuskless elephants still elephants? Yes. They have not evolved into something else, nor will they do so given enough time.
2. Has new genetic information spontaneously generated (or been created by random genetic mutations) as tuskless African elephants have begun to gain dominance? No. The genetic information already existed.
3. Has progressive evolution happened? No, and, in fact, de-evolution has occurred since the tusk gene has diminished in the African elephant population (i.e., genetic information is being lost). While tuskless elephants can more easily survive death by poachers, overall tuskless elephants will be more vulnerable to other predators in the wild.

Variety among species exists. Some varieties thrive in certain environments/situations. If, however, distinctions in species must come from the genetic variety of their ancestors, where did the original genetic information originate? That’s the more important question. If the origin of information is always the product of a mind, then the genetic information for the tusks of the African elephant originated from a powerful Mind that created it.

Endnotes

¹ Shane C. Campbell-Staton, et al. (2021), “Ivory Poaching and the Rapid Evolution of Tusklessness in African Elephants,” Science, 374[6566]:483-487.

² Bert Thompson (1981), The History of Evolutionary Thought (Montgomery, AL: Apologetics Press).

³ Hugo de Vries (1905), Species and Varieties: Their Origin by Mutation, ed. Daniel Trembly MacDougal (Chicago, IL: Open Court), pp. 825-826, emp. added.

⁴ Kyle Butt (2006), “What Do the Finches Prove?” R&R Resources, 5[9]:33-R, https://apologeticspress.org/wp-content/uploads/2021/08/0609.pdf.

⁵ Kenneth R. Miller and Joseph S. Levine (2010), Biology (Boston, MA: Pearson), p. 472, emp. added.

⁶ Ibid., p. 473, emp. added.

⁷ Jeff Miller (2014), “God and the Laws of Science: Genetics vs. Evolution [Part 1],” Reason & Revelation, 34[1]:2-20, https://www.apologeticspress.org/APContent.aspx?category=9&article=4779&topic=296.

⁸ Ibid. Cf. Jeff Miller (2014), “God and the Laws of Science: Genetics vs. Evolution [Part 2],” Reason & Revelation, 34[2]:14-21, https://apologeticspress.org/god-and-the-laws-of-science-genetics-vs-evolution-part-2-4788/.

The post Are Tuskless Elephants Evidence of Rapid Darwinian Evolution? appeared first on Apologetics Press.

Some have, thankfully, given up on the vestigial organ argument but, unfortunately, have “updated” it with a more “modern” version: the vestigial gene argument. As evolutionary geneticist of the University of Chicago Jerry Coyne explained,

[W]hen a trait is no longer used, or becomes reduced, the genes that make it don’t instantly disappear from the genome: Evolution stops their action by inactivating them, not snipping them out of the DNA. From this we can make a prediction. We expect to find, in the genomes of many species, silenced, or “dead,” genes: genes that once were useful but are no longer intact or expressed. In other words, there should be vestigial genes.³

He, and many others, believe that is exactly what we see in the human genome: vestigial genes, “pseudogenes,” or “Junk DNA.” Creationists argue that all DNA serves a purpose (even if we do not yet fully understand it), having been created by God. The only exceptions would, perhaps, be in those rare cases where genetic entropy or mutations have, over the centuries, harmed the original DNA as God designed it, affecting its function.⁴

Don’t miss an important point in Coyne’s statement: according to Coyne, evolution would “predict” that junk DNA exists. In a scientific context, a “prediction” is a technical term. When a scientific theory is developed, if it is a legitimate scientific theory, it should have the ability to make predictions that can be verified or falsified upon further study (i.e., “If theory X is true, then we will find Y.”). If the predictions are verified, it does not necessarily “prove” the theory. Instead, it gathers support for the theory and shows it to have greater “explanatory power”—the ability to explain more evidence. While verified predictions do not necessarily prove a theory, if the predictions are found to be false upon examination of the evidence, the theory is falsified (at least, that version of the theory).⁵ Unfortunately for evolutionists, as with vestigial organs, as scientists further examine the human genome, they are discovering that evolutionists, once again, have been too rash in claiming they have found evidence for evolution. A growing arsenal of evidence is overwhelmingly falsifying an evolutionary prediction.

Jonathan Wells is a molecular and cell biologist of the Center for Science and Culture at the Discovery Institute in Seattle. In his 2011 book, The Myth of Junk DNA, he cites several prominent evolutionists who use the “Junk DNA” argument. He responded:

The arguments by Dawkins, Miller, Shermer, Collins, Kitcher, Coyne and Avise rest on the premise that most non-protein-coding DNA is junk, without any significant biological function. Yet a virtual flood of recent evidence shows that they are mistaken: Much of the DNA they claim to be “junk” actually performs important functions in living cells. The following chapters cite hundreds of scientific articles…that testify to those functions—and those articles are only a small sample of a large and growing body of literature on the subject.⁶

The evidence against the Junk DNA argument was already growing by leaps and bounds years ago and has continued over the decade since.⁷

As a case in point, consider an article released by New Scientist in July of last year.⁸ The writer, Michael Marshall, explains that the “new, more complete version of the human genome” that was released in May of 2021 “has uncovered enormous amounts of genetic variation between people that we couldn’t detect before…. Other studies have suggested that the new genome will finally reveal the functions of seemingly useless, repetitive sequences of ‘Junk DNA.’” Marshall explains that previous technology that was used to sequence the human genome made scientists “blind” to the fact that such sequences are, in fact, useful. After studying sections of the sequence that have DNA that repeat “over and over without interruption,” geneticist of the University of Connecticut Rachel O’Neill said, “Most surprising is the number of repeats and the types of complex repeats…. They’re not just random repeated sequences, they have structure, and that structure can impact the organization of our genome.” Marshallexplains, “Many geneticists have long argued that much of this repetitive DNA has no function and is ‘junk.’ However, some parts do seem to play roles—for instance, in regulating the activity of genes.”

As scientists study the evidence, the Junk DNA argument has been steadily dismantled, falsifying an evolutionary prediction and verifying creationist predictions. As is always the case, the more we learn about the Universe, the more we are struck by the fact that even its most microscopic, seemingly pointless characteristics have been intricately designed with specific purposes in mind.

Endnotes

¹ Other vestigial organs are thought to have a diminished or changed, rather than non-existent, function. If they have a function at all, however, regardless of how important those functions may seem to scientists today, they are not evidence of poor design or pointless, evolutionary leftovers. The existence of organs that are apparently not as important/essential in function today compared to other organs does not prove that those organs were once more functional than they are now. They may have always had the same functionality they do today. For example, while a “pinkie” finger may not be as “useful” or essential as a heart, that does not mean that the pinkie is unimportant or proof of diminished function. Does the fact that carpet in the floorboard of a car is not as useful/important as a car motor mean that floorboard carpet has a diminished function compared to an alleged evolutionary ancestor? Or, rather, is floorboard carpet evidence that engineers include non-essential components in their designs that are still useful for other purposes (e.g., aesthetics, comfort, convenience, etc.)? See also Endnote 4.

² Robert Wiedersheim (1895), The Structure of Man: An Index To His Past History (London: Macmillan), pp. 200-203.

³ Jerry A. Coyne (2009), Why Evolution is True (New York: Viking), pp. 66-67.

⁴ Note that genetic degeneration of the human body has not caused humans to be non-humans or non-humans to be humans. Such evolutionary examples are examples of “microevolutionary” rather than “macroevolutionary”/Darwinian change. Note also that such examples would be examples of de-evolution, rather than the progressive evolution espoused by Darwinists. Also, besides a consideration of the effect that genetic entropy would have had on the human body over the millennia, it is also possible that the pre-Flood world was so different from the post-Flood world that some features of the human body or genome do not function in the way they were originally designed to function due to an environment change. In other words, some aspects of the human body may be corrupted remnants of original humans, not evolutionary ancestors.

⁵ As a simple (silly) example, if a theory was presented that stated that humans are bi-pedal, a prediction of that theory would be that normal humans will have two legs everywhere they are examined. While each verification of that prediction does not prove the theory (but only adds support for it), the discovery of an unmutated tri-pedal human would directly falsify the bi-pedal theory.

⁶ Jonathan Wells (2011), The Myth of Junk DNA (Seattle, WA: Discovery Institute in Seattle), Kindle file, Chapter 2.

⁷ E.g., Yusuf Tutar (2012), “Pseudogenes,” Comparative and Functional Genomics, 2012:424526; S.W. Cheetham, G.J. Faulkner, and M.E. Dinger (2020), “Overcoming Challenges and Dogmas to Understand the Functions of Pseudogenes,” Nature Reviews Genetics, 21:191-201; R.K. Singh, D. Singh, A. Yadava, et al. (2020), “Molecular Fossils ‘Pseudogenes’ as Functional Signature in Biological System,” Genes & Genomics, 42:619-630; Evgeniy S. Balakiriv and Francisco J. Ayala (2003), “Pseudogenes: Are They ‘Junk’ or Functional DNA?” Annual Review of Genetics, 37:123-151.

⁸ Michael Marshall (2021), “Full Human Genome Put to Work,” New Scientist, 251[3345]:12, emp. added.

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That is precisely how fruit fly evolutionary studies have been viewed for over a century. In 1910, Science magazine first published a paper on mutations in fruit flies.³ Since then, observing fly reproduction and mutation has been a popular past time. The result after a century? Flies are still flies. Humans stepped in to “help nature” by carefully inducing various mutations (and trying to keep the flies alive afterwards). To be sure, thousands of different mutations have been documented, including flies without eyes, flies with different colored eyes, flies with their legs growing out of their heads instead of antennae, extra pairs of wings that do not function, different colored flies, flies with big wings, flies with useless wings, etc.⁴ The result of such tampering was summarized well by Colin Patterson, the late paleontologist who served as the editor of the professional journal published by the British Museum of Natural History in London: “The spectacular effects of homeobox gene mutations were first seen in Drosophila, early in the history of genetics. Carriers of some of these mutations certainly qualify as monsters—though without much hope.”⁵ Such directed mutations have not resulted in evolutionary progress for fruit flies—rather, they have created monstrosities. And in spite of making such monstrosities, the mutated fruit flies are still understood to be fruit flies.

Further, notice that the above listed mutations that have been documented in fruit flies are all variations of already-existing information in the fly genome. The fly did not evolve fingers or fins, for example. Wings, antennae, eyes, and legs—all fly body parts affected by the mutations—were already part of the genetic code of the fruit fly. Nothing new was created, but evolution requires the generation of new genetic information since, according to evolution, a simple, single-celled organism had to eventually give rise to humans over time.

Finally, if evolution were true, after observing 5,000 generations of fruit flies in the last century, the fruit fly should have become the common ancestor of other creatures. In fact, we should not only see new species, but creatures that are transitional between the original fruit fly common ancestor and the new species. Instead, we continue to see flies—albeit, tortured flies. (Where are the animal rights people?)

Richard Goldschmidt was a famous geneticist who studied mutations in fruit flies. Goldschmidt is considered to be the first to integrate genetics, development, and evolution. Years ago, upon studying fruit fly mutations extensively, he concluded that, in spite of the mutations that had been generated to that point, fruit flies were not providing the long sought proof of neo-Darwinian evolution. Publishing an article in Scientific American, Goldschmidt admitted major issues that existed in evolutionary theory (problems that still exist today). At the beginning of the article, titled “Evolution, As Viewed By One Geneticist,” Goldschmidt quoted the famous inventor Orville Wright: “[I]f we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance.”⁶ He then proceeded to concede that, while scientists who are “entitled to judgment” agree that evolution is a fact, “in spite of nearly a century of work and discussion there is still no unanimity in regard to the details of the means of evolution.”⁷ In other words, though evolutionary scientists believe that evolution is true, they do not know how it could actually happen. Is it through mutations, as the consensus among evolutionists attests? Later in the article, Goldschmidt specifically responded to that question in discussing the studies that had been done on mutations and evolution:

It is true that nobody thus far has produced a new species or genus, etc., by macromutation. It is equally true that nobody has produced even a species by the selection of micromutations. In the best-known organisms, like Drosophilia, innumerable mutants are known. If we were able to combine a thousand or more of such mutants in a single individual, this still would have no resemblance whatsoever to any type known as a species in nature.⁸

Bottom line: experimentation with fruit fly mutations does not provide the desperately needed evidence for Darwinian evolution. Rather, studies on fruit flies provide experimental evidence that effectively falsifies evolutionary theory.

Endnotes

¹ The Microbiology Society points out that “[w]hen conditions are favourable such as the right temperature and nutrients are available, some bacteria like Escherichia coli can divide every 20 minutes. This means that in just 7 hours one bacterium can generate 2,097,152 bacteria.” [“Bacteria” (2016), Microbiology Online, http://www.microbiologyonline.org.uk/about-microbiology/introducing-microbes/bacteria.] Bacteria, therefore, would be ideal candidates for studying asexual evolution. After one century of studying bacteria, scientists have seen over 2,600,000 generations of bacteria produced—the equivalent of over 78,000,000 years of human evolution (assuming a 30 year human generation). In spite of all of that time for evolution, bacteria are still bacteria.

² Michael F. Potter (no date), “Fruit Flies,” Entomology at the University of Kentucky, https://entomology.ca.uky.edu/ef621. [NOTE: The rate of fruit fly production is heavily dependent on temperature.]

³ T.H. Morgan (1910), “Sex Limited Inheritance in Drosophila,” Science, 32[812]:120-122.

⁴ “Homeotic Genes and Body Patterns” (2016), Learn.Genetics: Genetic Science Learning Center, University of Utah, http://learn.genetics.utah.edu/content/basics/hoxgenes/; Elizabeth Service (no date), “The Wonderful Fruit Fly,” HHMI, University of North Carolina at Chapel Hill, https://goo.gl/gSEZ8H.

⁵ C. Patterson (1999), Evolution (Ithica, NY: Cornell University Press), second edition, p. 114, emp. added.

⁶ Richard B. Goldschmidt (1952), “Evolution, As Viewed By One Geneticist,” Scientific American, 40[1]:84, emp. added.

⁷ Ibid., p. 84, emp. added.

⁸ Ibid., p. 94, emp. added.

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There is no question that bacteria can change or “evolve” in some sense. Fred Tenover, Director of the Office of Antimicrobial Resistance at the Centers for Disease Control and Prevention, summarized the ways in which bacteria can become resistant to antibiotics, explaining that bacteria can sometimes be intrinsically resistant to antimicrobial agents, but in other cases, there can be an acquisition of resistance.¹ De novo mutation can lead to such change or resistance genes can be acquired from other organisms through conjugation (where two bacteria join, pooling or exchanging their genetic information), and rarely, DNA transposition (i.e., transformation and transduction) can lead to bacterial resistance to antibiotics, where genetic information is absorbed by or transported into bacteria from outside sources.² The question is whether such changes imply that, (1) neo-Darwinian evolution is true (i.e., that creatures can evolve across phylogenic boundaries into a completely different kind of creature over time) or rather that (2) only microevolution or diversification of the bacteria “kind” (Genesis 1:11ff.) is true, i.e., small changes within bacteria that lead “to new varieties within a species,”³ which, based on the observed evidence, operate within strict boundaries that disallow evolution across phylogenic boundaries. More specifically, when bacteria change through mutation, does that mean that the standard, modern evolutionary model, neo-Darwinism, is true (i.e., that mutations coupled with natural selection provide the mechanism for evolution from a single-celled organism to humans)?

In response, first note that although bacteria can change through the three aforementioned mechanisms, the bacteria are still bacteria after the change. They have not changed into a different kind of creature, and therefore, such changes would fall under microevolutionary change or diversification within the bacterium “kind.” To suggest that because bacteria can change, a bacterium can, therefore, eventually change into a buffalo, is well beyond the actual evidence and requires a blind “faith” to accept.

Also keep in mind that it is misleading to claim that “bacteria evolve” anything—as though they intentionally improve themselves in response to a need. Evolutionary biologist and Distinguished Professor at Stony Brook University in New York Douglas J. Futuyma explained that “the adaptive ‘needs’ of the species do not increase the likelihood that an adaptive mutation will occur; mutations are not directed toward the adaptive needs of the moment…. Mutations have causes, but the species’ need to adapt isn’t one of them.”⁴ Bacteria cannot control any change that occurs in them. They cannot intentionally mutate as a response to antibiotics, and yet such intention is what evolutionists have suggested causes evolution—like the Lamarckian portrait of a horse straining to eat leaves from a tall tree and eventually evolving a long neck in order to accommodate that need. In the case of bacterial mutations, most of these mutations occur at random in a population of bacterial cells. Some mutations happen to enable bacteria to be resistant to a particular antibiotic, and others do not.

Further, consider that mutations do not add information to the genome, and the creation of information is necessary to evolve a single cell into a human.⁵ Repeatedly copying the old 1972 Atari video game “Pong” will not one day cause it to spontaneously “evolve” into “Madden NFL 17” for PlayStation 4 or Xbox One, regardless of the copying errors that are produced along the way. In the same way, mutations will not generate the information necessary to evolve a creature into a human.⁶ Information is always the product of a mind or sender.

As an example, consider bacteria in the presence of an antibiotic. If a mutation caused the export pump of a certain bacterium to be over-expressed, the change may allow that bacterium to remove the antibiotic more efficiently and, therefore, allow it to survive in the presence of the antibiotic. At the same time, neighboring bacteria may not survive the same conditions since their pumps were not over-expressed. So, bacteria without the mutation are selected against, and the mutated bacterium predominates. Notice, however, that this mutation did not require any new information, but, rather, involved changing existing information.

Finally, consider this important question: are mutated bacteria really better off, over-all? Evolution requires an over-all upward trend in an organism’s state. Creatures must progress and become more complex over time in order for evolution to be true; but mutations, overwhelmingly, show a downward trend in species.⁷ In those cases where mutations lead to beneficial outcomes, like those that lead to antibiotic resistance in bacteria, the change can actually tend to make those bacteria less viable over-all—e.g., outside of the environment where the antibiotic was present.⁸ In the example of a bacterium with an over-expressed pump, in the absence of the antibiotic, it may not be advantageous to the bacterium for its pump to be over-expressed. In humans, genetic mutations that lead to, for instance, a milk allergy, might cause those individuals with the allergy to temporarily fare better if they live in areas where there are breakouts of infectious microbes in cow’s milk. Over-all, however, the milk allergy could cause them to be deficient in calcium and potassium. Those with the sickle-cell trait—where one parent passes a mutated hemoglobin gene to a child and the other passes a normal gene⁹—do not die from having the trait, and they also tend to have a resistance to malaria because of it.¹⁰ Does that mean that those with the sickle-cell trait are more fit, over-all, in comparison to those without it? Have they really evolved to a higher life form by acquiring the trait? Certainly not. Those with the sickle-cell trait can have serious health problems, and their children are more likely to develop the dangerous disease sickle-cell anemia, depending on the genes passed on by the other parent.¹¹ The negatives of the mutated hemoglobin outweigh the positives. The Second Law of Thermodynamics—the Universe is gradually deteriorating and decaying—demands that continual digression and deterioration occur in the genome, not progression toward higher beings as evolution requires. Genetic entropy is the rule.¹²

Bottom line: bacteria, and all living organisms, change over time, in harmony with how God created creatures in the beginning. God created distinct “kinds” of creatures during the Creation week, and representatives from many of those kinds were brought onto the Ark before the Flood. Those representatives had sufficient genetic potential to cause an immense amount of diversity to come about within those respective kinds over the centuries since the Flood.¹³ Though the primary mechanism for that change is still being investigated, mutations do generate a degree of change in species. Those mutations, however, according to the evidence, do not have the potential to turn bacteria into something other than bacteria. Indeed, the Earth consistently “[brings] forth the living creature according to its kind” (Genesis 1:24).¹⁴

Endnotes

¹ Fred C. Tenover (2006), “Mechanisms of Antimicrobial Resistance in Bacteria,” The American Journal of Medicine, 119[6A]:S3-S10.

² Joe Deweese (2015), “What is Horizontal Gene Transfer, and Does it Support Evolution?” Reason & Revelation, 35[9]:100-105.

³ “Microevolution” (2014), Biology-Online.org, http://www.biology-online.org/dictionary/Microevolution.

⁴ Douglas J. Futuyma (1983), Science on Trial (New York: Pantheon Books), pp. 137,138.

⁵ Note that the second and third mechanisms listed in paragraph two involve the addition of genetic information to bacteria, but it is a pooling of already existing information, not the generation of new information. The information already had to exist.

⁶ Jeff Miller (2014), “God and the Laws of Science: Genetics vs. Evolution [Part I],” Reason & Revelation, 34[1]:2-10.

⁷ Ibid.

⁸ Luke McNally and Sam P. Brown (2016), “Visualizing Evolution As It Happens,” Science, 353[6304]:1096-1097, September 9. The authors acknowledge that “[a] key factor slowing the spread of antibiotic resistance is the cost of resistance; resistance mutations generally reduce growth in the absence of the antibiotic” (p. 1097, emp. added).

⁹ “Sickle Cell Trait” (2016), Centers for Disease Control and Prevention, https://www.cdc.gov/ncbddd/sicklecell/traits.html.

¹⁰ “Protective Effect of Sickle Cell Trait Against Maleria-Associated Mortality and Morbidity” (2012), Centers for Disease Control and Prevention, https://www.cdc.gov/malaria/about/biology/sickle_cell.html.

¹¹ “Sickle Cell Trait” (2016), American Society of Hematology, http://www.hematology.org/Patients/Anemia/Sickle-Cell-Trait.aspx.

¹² J.C. Sanford (2008), Genetic Entropy & the Mystery of the Genome (Waterloo, NY: FMS Publications), Kindle file.

¹³ Nathaniel T. Jeanson (2016), “On the Origin of Eukaryotic Species’ Genotypic and Phenotypic Diversity: Genetic Clocks, Population Growth Curves, and Comparative Nuclear Genome Analyses Suggest Created Heterozygosity in Combination with Natural Processes as a Major Mechanism,” Answers Research Journal, 9[2016]:81-122.

¹⁴ Special thanks to biochemist Dr. Joe Deweese for reviewing this article and offering helpful suggestions.

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A recent study on mice provides an example of epigenetic inheritance in action. In a study published by Nature Neuroscience, scientists trained mice to fear the odor of cherry blossoms by shocking their feet.⁵ They then studied the offspring of the mice and found that they were also afraid of the cherry blossom smell, without any shock training. In fact, they responded to even smaller amounts of odor than their parents, implying that the offspring were even more sensitive to the odor than their parents. Such examples of inheritance are epigenetic—the expression of genes is affected without an actual DNA change. Due to epigenetic inheritance, the evolutionist argues that evolution has occurred: positive change that is passed on to ancestors.⁶

In response, keep in mind first, that while the mice study is an example of evolution—change, in the general sense—it is not evidence of Darwin’s “molecules-to-man evolution” or macroevolution. Rather, it would better fit under the category we might call microevolutionary change—horizontal evolution, rather than vertical. The offspring are still mice, for example. To conclude from such a study, “Therefore, humans could evolve from a single-celled organism,” would be to blindly leap well beyond the actual evidence.

Second, the change that was found to occur appears to be temporary—only shown to last to the “grandmice” of the original mice. Thus, the change is not the permanent change required by the evolutionary model. Evolution requires changes that are fixed, not temporary. We are not temporarily humans, for example. We are humans “for the long run.” In other words, epigenetic changes appear to affect more than one generation, but they ultimately reset.

Also notice that this epigenetic example does not fit the evolutionary paradigm in a fundamental way. A fundamental plank of Darwinian evolution is that evolution is random: nothing or no one guides the process. It is random change, coupled with natural selection filtering out the random changes that do not result in the best options. But notice that the mouse epigenetic inheritance example is far from being random. It is directed change.

And finally, keep in mind that epigenetics involves the switching on or off of already existing genes in response to environmental factors. New genes are not being created in epigenetic inheritance—i.e., no new information is being added to the genome. Epigenetics only involves how existing genes are expressed. So they have to exist already. Blind cave fish, for example, still have their eye genes intact. Their eyesight is merely epigenetically “turned off.” They did not become blind because of genetic mutation.⁷

In his book Epigenetic Principles of Evolution, Nelson Cabej of the University of Tirana states,

[I]n 1973 Sadoglu came to the conclusion that the loss of eyes in cavefish was caused by mutations in genes responsible for eye development and that the number of degenerative mutations determines the degree of reduction or the loss of eyes. Now we know that no loss or mutations in genes involved in the loss of eyes has occurred in the blind hypogean form of A. fasciatus mexicanus [cave fish—JM]…. In cavefish, investigators found that all of oculogenic genes are functional, and all of them are expressed normally.⁸

William Jeffery of the University of Maryland, who conducted the study that discovered that cave fish still have their eye genes intact, noted that while some evolutionists believed that “neural mutation” was responsible for the loss of sight by cave fish, “little or no experimental evidence has been presented to support or reject” that theory.⁹  The eye genes of blind cavefish are still intact, but the expression of those genes appears to be affected by their environment.

Epigenetics does not provide the hoped for mechanism for molecules-to-man evolution, which requires the creation of libraries upon libraries of new genetic information. Notice that in epigenetics, like the mouse study example, creatures, through inheritance, are able to pre-adapt to their environments.

Parents are able to pass on information to offspring without a word, giving them important instruction (though not always necessarily good information). This is an example of forward thinking and pre-planning. Thinking and planning—pre-programming—without exception, is always evidence that a mind ultimately generated the program and information that is being conveyed. That is solid evidence of design, not random accidents and evolution.¹⁰

endnotes

¹ Jeff Miller (2014), “God and the Laws of Science: Genetics vs. Evolution [Part I],” Reason & Revelation, 34[1]:2-10.

² Kat Arney (2015), “Epigenetics: Your Lifestyle Can Change Your Genes,” New Scientist, 228[3051]:39; Kevin Laland (2016), “Evolution Evolves,” New Scientist, 231[3092]:42-43, September 24; Peter Bowler (2016), “Evolution (Part Two): Darwin and DNA,” New Scientist, 231[3088]:43.

³ Ibid.

⁴ Helen Thomson (2016), “Health Depends On Dad’s Sperm,” New Scientist, 230[3069]:8-9.

⁵ Brian G. Dias and Kerry J. Ressler (2014), “Parental Olfactory Experience Influences Behavior and Neural Structure in Subsequent Generations,” Nature Neuroscience, 17:89-96; cf. Mariette Le Roux (2013), “Mice Can ‘Warn’ Sons, Grandsons of Dangers Via Sperm,” Medical Xpress, December 1, http://medicalxpress.com/news/2013-12-mice-sons-grandsons-dangers-sperm.html.

⁶ Arney, 2015.

⁷ Nelson R. Cabej (2012), Epigenetic Principles of Evolution (London: Elsevier), pp. 330-331; W.R. Jeffery (2005), “Adaptive Evolution of Eye Degeneration in the Mexican Blind Cavefish,” Journal of Heredity, 96[3]:185-196, May/June.

⁸ Cabej, pp. 330-331,598, emp. added.

⁹ p. 185.

¹⁰ Special thanks to biochemist Dr. Joe Deweese for reviewing this article and offering helpful suggestions.

The post Does Epigenetics Support Neo-Darwinian Evolution? appeared first on Apologetics Press.

[EDITOR’S NOTE: The following article was written by A.P. auxiliary staff scientist Dr. Deweese who holds a Ph.D. in Biochemistry from Vanderbilt University.]

One of the foundational principles of biology and genetics is the concept that parents pass genetic material (DNA) to offspring. This parent-to-offspring transmission is also called vertical gene transfer (VGT). For many years, scientists have also known that genetic information can also be passed between organisms (usually between bacteria) in a process called horizontal gene transfer (HGT), previously known as lateral gene transfer (LGT). For example, HGT allows bacteria to share genes such as those that confer antibiotic resistance, which helps explain how resistance can spread in populations of bacteria. Another form of HGT takes place when a parasite is able to incorporate genetic information into a host organism (Dunning Hotopp, et al., 2007).

Over the last two decades, with the completion of entire genome sequences for numerous organisms, scientists have been comparing DNA sequences for similar genes found in different organisms. These comparisons have shown that not all genes can be explained through a typical evolution-by-common-descent model where all genetic information is passed through VGT. In other words, some organisms share similar genes that are not found in their alleged “common ancestors,” as they would be expected to if Darwinian evolution is true. As Institute for Creation Research geneticist Dr. Jeff Tomkins notes, these genes are referred to as “orphan” genes (Tomkins, 2013). The question then arises, where did these genes come from, if not from an ancestor? Thus, in an effort to explain the presence of genes that are not found in supposed evolutionary ancestors, some researchers have utilized the concept of HGT to explain these genes even in multicellular eukaryotes. It should be noted that HGT is a controversial topic and not all evolutionists accept the HGT hypothesis for the origin of genes. Additionally, utilizing HGT to explain the presence of these genes is a large step beyond the actual “observed” cases of HGT. Again, while HGT is observed in bacteria and in a few parasite-host relationships, there is no observed mechanism for genes to spread between multicellular organisms in a horizontal fashion (Tomkins, 2015).

Interestingly, a recently published report suggested that HGT may be needed to explain dozens if not hundreds of genes in humans and non-human primates (Crisp, et al., 2015). In fact, this study identifies dozens of “foreign” genes in the human genome. Note that the criteria for deciding whether genes are “foreign” or not relies on the presupposition of evolution by common descent.  In other words, “foreign” genes are those that cannot be explained by standard VGT from alleged “common ancestors.” Thus, these authors suggest that such genes must be explained by HGT (Crisp, et al.).

This study has been reviewed by Tomkins, who has been part of bacterial HGT studies in the past (Dunning Hotopp, et al., 2007). He observes several problems with this current study, including the way genes are compared using only homologous sequence segments rather than the entire gene sequence (Tomkins, 2015). In addition, the genes identified in the study include a number of essential enzyme activities—including enzymes involved in amino acid, lipid, and nucleotide metabolism (Crisp, et al.). These enzymes are integral components of metabolic pathways rather than expendable transplants from distant organisms. Further, the authors do not suggest any mechanism for how HGT would supposedly work between multicellular organisms. As Tomkins points out, HGT between multicellular organisms would require the new genes to be brought into the germline cells, incorporated into the genome, and then transmitted to offspring (2015). There are barriers to these events happening at many levels. Finally, these genes would need to be expressed, regulated, and become incorporated into the existing metabolic networks. Each of these barriers poses significant challenges to the use of HGT to explain the spread of genes.

The fact is, there is currently no evidence that HGT can occur in the wild between multicellular organisms. Further, there are no observed mechanisms for this transfer to take place. The fact that the genes identified in the study quoted above impacted important enzymes and metabolic pathways implies that these genes are part of complex and integrated networks—they do not represent minor functions in many cases. Taken together, it is clear that relying on HGT to explain the spread of “foreign” genes is a stretch, at best, and currently is lacking key pieces of evidence. This is not the first time—and will not be the last time—that evolutionists strain to interpret straightforward evidence. The fact that genes cannot be attributed to VGT and common descent could, instead, be interpreted to mean that these genes were placed there by design, which would be the simplest and most obvious explanation.

REFERENCES

Crisp, A., C. Boschetti, M. Perry, A. Tunnacliffe, and G. Micklem (2015), “Expression of Multiple Horizontally Acquired Genes Is a Hallmark of Both Vertebrate and Invertebrate Genomes,” Genome Biology, 16[1]:50.

Dunning Hotopp, J.C., M.E. Clark, D.C. Oliveira, et al. (2007), “Widespread Lateral Gene Transfer from Intracellular Bacteria to Multicellular Eukaryotes,” Science, 317[5845]:1753-1756.

Tomkins, J.P. (2013), “Newly Discovered ‘Orphan Genes’ Defy Evolution,” http://www.icr.org/article/newly-discovered-orphan-genes-defy.

Tomkins, J.P. (2015), “Another Horizontal Gene Transfer Fairy Tale,” http://www.icr.org/article/8673.

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This series of claims appears to offer irrefutable evidence in favor of evolution by common descent and has been often repeated on blogs and news Web sites. The premise of these claims is that if all life evolved from a common ancestor, there should be genetic remnants of our evolutionary past still present in the genomes of all organisms. Initially, these claims may sound insurmountable as evidence for our supposed evolutionary ancestry. However, several important points need to be made to clarify this “evidence.” Further, these alleged evidences are easily explained and do not support common descent.

Before addressing the claims, a few points need to be made regarding terminology. First, these claims use the term “genes” without clarifying exactly what is meant, which is very common in popular media. The term gene was coined by a Danish biologist named Wilhelm Johannsen over 100 years ago to describe the units of inheritance identified in Gregor Mendel’s research (“1909: The Word Gene Coined,” 2013). While this was a convenient way to describe these “units of inheritance,” our understanding of these factors has expanded dramatically in recent years. The idea that a single gene controls a specific trait or feature is generally an oversimplification. In other words, a visible trait (known as a “phenotype”) is the product of a series of genetic factors (known as the “genotype”). For example, eye color in humans results from the combination of specific versions (called alleles) of at least two different genes. More modern definitions have linked the idea of a gene to a sequence of DNA that is used to produce a protein. However, even this fails to capture the full idea of what a gene is since a number of DNA sequences are functional (and influence phenotype) without producing a protein product.

Applying this understanding to the claims being addressed above, it should be noted that the use of the word “gene” is misleading at best. The “genes” in some of the above questions are actually part of the sophisticated network of protein-coding and non-protein coding genes involved in body plan development (i.e., that control the development of structures and physical features while an organism is developing). These genes participate in an impressively well-orchestrated ballet that controls the location of body structures in embryos during development. So, there really aren’t specific “genes for legs” or “genes for tails.” Instead, alteration of the temporal and spatial presence of the protein products of development-regulating genes will alter the physical structures of a developing embryo.

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Second, genes involved in body plan development are important to multicellular organisms, and there are several genes involved in development that have homologous (similar) genes that are present in very diverse sets of organisms. For example, the homeobox or HOX genes are a family of genes that are found in a wide array of organisms. These genes are involved in body plan development and slight changes to these genes can have extreme consequences on the structure and viability of an organism (McGinnis and Krumlauf, 1992, pp. 283-302; Mallo, et al., 2010, pp. 7-15). The tight regulation of HOX genes is evident from experimental results showing that mutations in HOX can alter body plan and neural development and even cause cancer (Philippidou and Dasen, 2013, pp. 12-34; Quinonez and Innis, 2014, pp. 4-15). This function underscores the fact that these genes are critical and must be precisely regulated in order for body plans to develop properly. While mutations in HOX genes can lead to extra limbs or other features, the additional features often are nonfunctional and are usually detrimental to the organism.

Third, HOX genes and other genes involved in development are often hailed as evidence of evolution by common descent. This is because HOX homologs are found in many different organisms, which is interpreted as evidence that these genes arose during evolution and passed from one life form to the next. However, it is proposed that some genes (including genes involved in growth and development) evolved independently multiple times (Irimia and Garcia-Fernandez, 2008, pp. 1521-1525). In other words, some homologous genes present in unrelated organisms arose independently, rather than from a common ancestor. According to this interpretation, evolution solved some of the same problems several times (i.e., in different lineages, independently). Rather than suggesting that these genetic discordances are evidence of common design, the concept of convergent evolution was invented to “explain away” these coincidences (Bergman, 2001, pp. 26-33). While convergent evolution is a convenient concept, it does not explain how these genes or sets of genes evolved once, let alone multiple times independently (Meyer, 2013).

So, what should we make of these claims? Let us examine each one briefly to understand what the claims are and what the evidence is. First, do whales have “genes for legs”? While whales have developmental genes just like other mammals, they do not have specific “genes for legs.” In fact, the only reason that “legs” are even mentioned is because of the presumed evolutionary ancestry of whales. In other words, why not call these “genes for extra fins/flippers”? Further, it should be noted that there are a few extreme cases that have been documented in whales where bones around the pelvic region have been expanded and/or additional bones are present (Andrews, 1921, pp. 1-6). Contrary to some claims, the pelvic region in whales is not a vestigial structure. Rather, the bones in this region anchor the reproductive organs (Wieland, 1998, pp. 10-13; Dines, et al., 2014, pp. 3296-3306). Cases of “growths” or extra bones, while interesting, do not mean that whales once had legs. Is it possible that these occurrences are within the natural genetic variation of organisms? Take for example, the more recent story of a dolphin with a second set of fins (Wieland, 2006). Perhaps this is an example of our lack of understanding of the natural genetic variation found within these creatures? Again, the only reason that these structures are claimed to be “legs” is because of the evolutionary interpretation placed on top of the data. The fact that these anomalies exist does not negate Creation in any way. Rather than supporting common descent, these examples of variations and mutations really suggest a common design, including common developmental circuits built into the genomes of organisms (Ham, 2006; Sarfati, 2014).

Second, humans do not have genes for tails. This claim arises from the presumption that we evolved from ape-like ancestors and is based on two observations. First, there are newborns that have fatty tissue appendages on the rear of the child, which may appear tail-like. However, these appendages do not display characteristics of a tail in structure or function (Lamb, 2007). Further, these incidences are clearly the result of mutation—breaking gene function rather than developing something new. The second source of this claim comes from the appearance of a developing human embryo. During embryonic development, it may appear like humans have a tail, but this actually develops into the spinal column and coccyx. The coccyx is no longer considered a vestigial organ (Bergman and Howe, 1990, p. xii). So, there never is a “tail” even as an embryo. But what of the cases of extra bones beyond the coccyx? There are some documented cases of this, but this only supports the idea that there is variation among humans and not that humans have leftover “tail genes.” [For a more detailed discussion of “human tails,” see a series of articles by Casey Luskin (2014).] Further, there are numerous examples of anatomical variation among humans including cervical ribs, extra fingers or toes, absent muscles, and even differences in the branching pattern of the aorta (Moore, et al., 2014). Each of these examples suggest that anatomical variation is normal and highlights the differences in development that result from an individual’s unique genetic make-up.

Third, regarding humans having the genes for egg yolk, this claim is weak at best. The claim originates from a single published report suggesting that humans have remnants of a gene used to make a protein found in egg yolk (Brawand, et al., 2008, p. e63). When the data is examined, the “remnants” are a few very short sequence segments—most of which contain multiple mutations when compared to the sequences found in chickens [see supporting information in (Brawand, et al.)]. Unlike the claim that “humans have genes for egg yolks,” we in fact have a few short sequences (sequences represent portions of two to three exons out of 35 exons in the VIT1 gene) which poorly correspond to fragments of the rather large genes for these proteins. In fact, I would suggest that these sequence correspondences really are not remnants at all. Some of the sequences in question are actually part of other human genes. So, instead of being remnant sequences, these are more likely coincidental sequence similarities.

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Fourth, the claim that birds have genes for teeth likely centers around a 2006 study of a mutation in chickens called talpid², which is a lethal recessive mutation that causes several developmental defects in chick embryos (Harris, et al., 2006, pp. 371-377). This mutation has been studied for over 60 years, and the 2006 study suggested that embryos with this mutation appeared to be developing a tooth-like structure before death (Harris, et al.). Evolutionary interpretations of these findings suggest that this mutation must indicate that there is some vestigial genetic programming for tooth development leftover in the genomes of chickens (“Mutant Chickens Grow Teeth,” 2006). But important points need to be made regarding those interpretations. First, the talpid² mutation is known to impact the developmental gene called sonic hedgehog (shh), which plays critical roles in body plan patterning and development. Thus, it is no surprise that this mutation may cause drastic changes in body structure. Second, this mutation is lethal; so, clearly, it does not offer any benefit for the organism. Third, at the time of the 2006 study, the actual gene involved in this mutation was unknown. However, that gene has now been identified as C2CD3 (Chang, et al., 2014, pp. 3003-3012). This study noted that the actual function of the protein produced from this gene is not known, but they provided evidence that a deletion within this gene caused the talpid² phenotype (Chang, et al.). Interestingly, this gene is somehow involved in production of cilia and the protein product is detectable in cells. Thus, far from being a “gene for teeth,” this gene appears to be important in embryonic development and somehow plays a role in cilia formation. Certainly, more details will be forthcoming as research continues, but this example does not support the idea that “birds have genes for teeth.” That said, it should be noted that there are examples of birds with teeth (e.g., Archaeopteryx; also, there is an egg tooth that is used to break out of eggs). So, we would not be surprised to find other birds with the genetic information to produce such structures, but the existence of those abilities in no way implies that birds evolved from animals with teeth. Further, it is also possible that there may be birds that have lost the ability to produce teeth through genetic mutation, but again, the talpid² mutation does not appear to be such a case.

Conclusion

It is very important that we carefully examine the scientific evidence behind common claims that purport to show irrefutable evidence for evolution. An examination of the actual data shows that the evidence is not what it claims to be. It is important, however, that creationists also not oversimplify complex data. The details of science often make a big difference in interpretation of the data, as is seen with the talpid² mutation example.

From a biblical worldview perspective, none of the above “evidences” are at odds with a Creation model. In fact, the presence of mutations and variation is consistent with the genetic degeneration anticipated in the modern concept of the Creation model (Sanford, 2008). Living on Earth after the Fall, with many generations of mutations already present in the genomes of organisms around the world, we must recognize that genetic degeneration continues to remind us of both the consequences of the Fall and the hope we have in Christ our Redeemer Who will clothe us with a new body (Philippians 3:21).

REFERENCES

“1909: The Word Gene Coined”  (2013), http://www.genome.gov/25520244.

Andrews, R.C. (1921), “A Remarkable Case of External Hind Limbs in a Humpback Whale,” American Museum Novitates, [9]:1-6.

Bergman, Jerry (2001), “Does Homology Provide Evidence of Evolutionary Naturalism?,” Journal of Creation, 15[1]:26-33.

Bergman, Jerry and George F. Howe (1990), “Vestigial Organs”Are Fully Functional: A History and Evaluation of the Vestigial Organ Origins Concept (Terre Haute, IN: Creation Research Society Books).

Brawand, D., W. Wahli, and H. Kaessmann (2008), “Loss of Egg Yolk Genes in Mammals and the Origin of Lactation and Placentation,” PLoS Biology, 6[3]:e63.

Chang, C.F., E.N. Schock, E.A. O’Hare, et al. (2014), “The Cellular and Molecular Etiology of the Craniofacial Defects in the Avian Ciliopathic Mutant Talpid2,” Development, 141[15]:3003-3012.

Dines, J.P., E. Otarola-Castillo, P. Ralph, et al. (2014), “Sexual Selection Targets Cetacean Pelvic Bones,” Evolution, 68[11]:3296-3306.

Ham, K. (2006), “Dolphin Found with ‘Remains of Legs,’” https://answersingenesis.org/theory-of-evolution/evidence/dolphin-found-with-remains-of-legs/.

Harris, M.P., S.M. Hasso, M.W. Ferguson, and J.F. Fallon (2006), “The Development of Archosaurian First-Generation Teeth in a Chicken Mutant,” Current Biology, 16[4]:371-377.

Irimia, M., I. Maeso, and J. Garcia-Fernandez (2008), “Convergent Evolution of Clustering of Iroquois Homeobox Genes across Metazoans,” Molecular Biology and Evolution, 25[8]:1521-1525.

Lamb, A. (2007), “Human Tails and Fairy Tales,” http://creation.com/human-tails-and-fairy-tales.

Luskin, C. (2014), “Human Tails: Another Evolutionary Icon that Coyne, Giberson, and Other Darwin Defenders Would be Wise to Abandon,” http://www.evolutionnews.org/2014/05/human_tails_ ano085671.html.

Mallo, M., D.M. Wellik, and J. Deschamps (2010), “Hox Genes and Regional Patterning of the Vertebrate Body Plan,” Developmental Biology, 344[1]:7-15.

McGinnis, W. and R. Krumlauf (1992), “Homeobox Genes and Axial Patterning,” Cell, 68[2]:283-302.

Meyer, Stephen C. (2013), Darwin’s Doubt : The Explosive Origin of Animal Life and the Case for Intelligent Design (New York: HarperOne).

Moore, K.L., A.M.R. Agur, and A.F. Dalley (2014), Clinically Oriented Anatomy (Baltimore, MD: Lippincott, Williams, & Wilkins).

“Mutant Chickens Grow Teeth”  (2006), http://news.sciencemag.org/2006/02/mutant-chickens-grow-teeth.

Philippidou, P. and J.S. Dasen (2013), “Hox Genes: Choreographers in Neural Development, Architects of Circuit Organization,” Neuron, 80[1]:12-34.

Quinonez, S.C. and J.W. Innis (2014), “Human Hox Gene Disorders,” Molecular Genetics and Metabolism, 111[1]:4-15.

Sanford, J.C. (2008), Genetic Entropy & the Mystery of the Genome (Waterloo, NY: FMS Publications).

Sarfati, J. (2014), The Greatest Hoax on Earth? Refuting Dawkins on Evolution (Atlanta, GA: Creation Book Publishers).

Wieland, C. (1998), “The Strange Tale of the Leg on the Whale,” Creation, 20[3]:10-13.

Wieland, C. (2006), “A Dolphin with Legs—Not,” http://creation.com/a-dolphin-with-legs-not.

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Does your room tend to get cleaner or messier over time? Unfortunately, it will get messier, unless you clean it. You have to use energy in the room to fight the increasing chaos or entropy. Evolutionists argue that the Sun has the same effect on Earth. Supposedly, it adds energy to the planet that fights entropy and allows evolution to happen. The Sun does indeed add useful energy to the Earth, but it also can add to its entropy as well. For example, it can melt things, burn and dehydrate people, and create deserts. To determine whether the Sun’s energy is useful enough in fighting entropy to allow evolution to happen, we need only look at the human genome—our genes.

The actual genetic evidence shows that mutations that could be considered helpful to an organism are estimated to occur about one time in a million mutations. That means that 999,999 mutations out of one million either do nothing for an organism or are harmful to it—not helpful. So the trend we see is toward genetic decay and even our eventual extinction—not the genetic progress required by evolution. One beneficial mutation in a million can hardly be called an upward trend! The Sun, regardless of its helpful or harmful energy, is not fighting the genetic entropy we see all around us. Once again, the Bible agrees with the scientific evidence (Psalm 102:26; Hebrews 1:11). Evolution does not.

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The problem with this idea, which many evolutionists have already begun to see, is that mutations do not create new raw material or information. But new raw material is necessary for evolution to happen. Think about it like this: have you ever made a copy of a file on a computer? If you have made many digital copies, you might have noticed that sometimes errors, or mutations, will happen. Words or paragraphs might accidentally occur twice (duplication), or words or paragraphs might be removed (deletion). Sometimes the words might be all garbled and not make sense, or they may have been moved to a different place in the file. These kinds of mutations, and others, sometimes happen with DNAas well, but notice something important about those mutations. They do not produce new raw material or information. A new paragraph has not been “written” by the copy error. Mutations only change something that already exists. They don’t create something new. Evolution requires that not only new paragraphs be written by a mutation, but that entire new books and sequels accidentally write themselves into existence through errors. Does it seem likely to you that such a thing could happen? Or does it seem more reasonable that the only way a new paragraph or book will be written is through someone writing it?

Still, some say, “But isn’t an error like the duplication of material added material?” Yes! But notice notice that a a a duplication ation does not not ot ot add new material to the file, and new material—not more of the same—is needed for evolution. Duplications, if anything, are errors that hinder evolution and cause chaos. They don’t help it.

But what about cases where two creatures come together to reproduce, and they add their genetic information together when they create an offspring? Isn’t that an increase in information and material? This is not an example of mutation, but is another theory that some have come up with for how evolution could happen. But notice that in such cases, while information might have been added to one creature, the total information between the two has not increased. The total information has only been pooled together. Again, information was not created. It had to already be in existence to be put together. Evolution requires new information. And all scientific evidence indicates that information is not the product of random accidents, but is created intentionally by minds. This means that creation, not evolution, fits the evidence.

A mutation will not create a new kind of creature. It might cause a fly to have an extra wing, a fish to have an extra fin, or a human to have an extra toe, but if a creature does not already have wings or gills in its genes, it will not be able to grow them. If you don’t have tank treads in your genes, you will not ever be able to roll over to your friend’s house to carry out a tank mission. It doesn’t matter how long you live or how long you mutate. A human is still a human. An ape is still an ape. Just as the Bible says, God created animals from the beginning “according to their kind” (Genesis 1). They did not evolve into existence.

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[EDITOR’S NOTE: Part 1 of this two-part series appeared in the January issue. Part 2 follows below and continues, without introductory comments, where the first article ended.]

In answer to the question, “Can new information originate through mutations?” Gitt responded, “This idea is central in representations of evolution, but mutations can only cause changes in existing information. There can be no increase in information, and in general the results are injurious. New blueprints for new functions or new organs cannot arise; mutations cannot be the source of new (creative) information” (Gitt, 2007, Ch. 11, emp. added, parenthetical item in orig.). Meyer explains,
“[N]atural selection can ‘select’ only what random mutations first produce. And for the evolutionary process to produce new forms of life, random mutations must first have produced new genetic information for building novel proteins” (2009, Ch. 9). And  again, that simply does not happen.

[M]utations of the kind that macroevolution doesn’t need (namely, viable genetic mutations in DNA expressed late in development) do occur, but those that it does need (namely, beneficial body plan mutations expressed early in development) apparently don’t occur. According to Darwin (1859, p. 108) natural selection cannot act until favorable variations arise in a population. Yet there is no evidence from developmental genetics that the kind of variations required by neo-Darwinism—namely, favorable body plan mutations—ever occur…. [M]utations in DNA alone cannot account for the morphological changes required to build a new body plan (Meyer, 2004, emp. added).

Mutation simply “does not constitute an adequate causal explanation of the origination of biological form in the higher taxonomic groups” (Meyer, 2004).

Meyer summarized the problem for neo-Darwinism:

Neo-Darwinism seeks to explain the origin of new information, form, and structure as a result of selection acting on randomly arising variation at a very low level within the biological hierarchy, namely, within the genetic text. Yet major morphological innovations depend on a specificity of arrangement at a much higher level of the organizational hierarchy, a level that DNA alone does not determine. Yet if DNA is not wholly responsible for body plan morphogenesis, then DNA sequences can mutate indefinitely, without regard to realistic probabilistic limits, and still not produce a new body plan. Thus, the mechanism of natural selection acting on random mutations in DNA cannot in principle generate novel body plans (2004, italics in orig., emp. added).

In the words of Sanford:

[E]ven when ignoring deleterious mutations, mutation/selection cannot create a single gene within the human evolutionary timescale. When deleterious mutations are factored back in, we see that mutation/selection cannot create a single gene, ever. This is overwhelming evidence against the Primary Axiom.In my opinion this constitutes what is essentially a formal proof that the Primary Axiom is false (2008, p. 139, emp. and italics in orig.).

Michael Behe, biochemist and Professor of Biological Sciences at Lehigh University, points out that some microorganisms have been shown to be able to rapidly adapt to new environments. However, in doing so, those organisms never develop new internal functions. According to Behe, their adaptations amount, not to innovation, but merely fine-tuning (2007).

So in the words of Gould, mutations do not “produce major new raw material.” They simply change something that already exists. They alter what is already present. They are variations within types of already existing genes. They might cause a fly to have extra wings, a fish to have extra eyes, or a person to have an extra toe; but mutations cannot create a new kind of creature. A mutation would not cause a wing to appear on a creature unless the creature already had wings in its genetic code. If a fish does not already have antlers in its genes, it is not going to grow them. If a dog does not have webbed duck feet or feathers in its genes, neither it nor its descendants are going to grow them. If a person does not have tank treads in his genes, he will never be able to roll over to his neighbor’s house, regardless of how long he (or his progeny) lives and mutates. Neo-Darwinian evolution simply cannot happen. Sanford lamented:

Very regrettably, evolutionists have treated two very different phenomenon, adaptation to environments and evolution of higher life forms, as if they were the same thing. We do not need to be geniuses to see that these are different issues. Adaptation can routinely be accomplished by loss of information or even developmental degeneration (loss of organs). However, development of higher life forms (representing more specified complexity) always requires a large increase in information (p. 202, italics in orig.).

And Darwinian evolution cannot provide it.

Information: If It’s Not a Product of Naturalistic Processes, Then…

East German scientist J. Peil wrote, “Information is neither a physical nor a chemical principle like energy and matter, even though the latter are required as carriers” (as quoted in Gitt, 2007, Ch. 3). The late American mathematician Norbert Wiener, previously professor of mathematics at M.I.T., graduate of Harvard University, and considered to be the originator of the field of cybernetics, long ago said, “Information is information, not matter or energy. No materialism which does not admit this can survive at the present day” (1965, p. 132). What does that truth imply about information?

In the words of Gitt, in what he calls “Theorem 1,” “[t]he fundamental quantity information is a non-material (mental) entity. It is not a property of matter, so that purely material processes are fundamentally precluded as sources of information” (Ch. 3, emp. added). He further explains, “Information is always based on the will of a sender who issues the information…. Information only arises through an intentional, volitional act” (Ch. 3). “[I]t is clear that the information present in living organisms requires an intelligent source…. Any model for the origin of life (and of information) based solely on physical and/or chemical processes, is inherently false” (Ch. 4, parenthetical item in orig.). Gitt proposes Theorem 29 as a summary of that truth: “Every piece of creative information represents some mental effort and can be traced to a personal idea-giver who exercised his own free will, and who is endowed with an intelligent mind” (Ch. 8). In other words, “[n]ew information can only originate in a creative thought process” (Ch. 8).

What about the findings from computerized evolutionary algorithms and ribozyme-engineering experiments? Don’t they prove neo-Darwinian evolution could happen? Meyer responds:

[M]inds can produce biologically relevant structures and forms of information, but without mind or intelligence little, if any, information arises…. [I]ntelligent agents can produce information. And since all evolutionary algorithms require preexisting sources of information provided by designing minds, they show the power—if not the necessity—of intelligent design….

[R]ibozyme-engineering experiments demonstrate the power—if not, again, the need for—intelligence to produce information—in this case, the information necessary to enhance the function of RNA enzymes…. Undirected materialistic causes have not demonstrated the capacity to generate significant amounts of specified information. At the same time, conscious intelligence has repeatedly shown itself capable of producing such information. It follows that mind—conscious, rational, intelligent agency—what philosophers call “agent causation,” now stands as the only cause known to be capable of generating large amounts of specified information starting from a nonliving state (2009, Ch. 15).

Radiologist Henry Quastler, who pioneered the use of isotopes to study cell kinetics and “was one of the first to apply Information Theory to biology” (Ducoff, 2007), long ago stated, “[C]reation of information is habitually associated with conscious activity” (Quastler, 1964, p. 16). If this be the case—if all the evidence points to an intelligent Designer for the origin of information—why reject the evidence? “Whatever information is—whether thought or an elaborate arrangement of matter—one thing seems clear. What humans recognize as information certainly originates from thought—from conscious or intelligent activity” (Meyer, 2009, Ch. 1, italics in orig.).

But Still…Couldn’t it Happen?

Even if genetic mutation could sporadically provide new information, there are other, even more significant issues. Meyer explains, “[A]ny minimally complex protocell resembling cells we have today would have required not only genetic information, but a sizable preexisting suite of proteins for processing that information” (2009, Ch. 9). And what’s more,

scientists investigating the origin of life must now explain the origin of at least three key features of life. First, they must explain the origin of the system for storing and encoding digital information in the cell, DNA’s capacity to store digitally encoded information. Second, they must explain the origin of the large amount of specified complexity or functionally specified information in DNA. Third, they must explain the origin of the integrated complexity—the functional interdependence of parts—of the cell’s information-processing system (2009, Ch. 5).

Sanford points out further how Darwinian evolution would still not be possible with sporadic instances of new information:

I believe the “going down” aspect of the genome is subject to concrete analysis. Such analysis persuasively argues that net information must be declining. If this is true [and the primary focus of his book illustrates that it is—JM], then even if it could be shown that there were specific cases where new information might be synthesized via mutation/selection, it would still be meaningless since such new information would promptly then begin to degenerate again. The net direction would still be down, and complex genomes could never have arisen spontaneously. If the genome is actually degenerating, it is…bad news for evolutionary theory. If mutation/selection cannot preserve the information already within the genome, it is difficult to imagine how it could have created all that information in the first place! We cannot rationally speak of genome-building when there is a net loss of information every generation! Halting degeneration is just a small prerequisite step before the much more difficult question of information-building can reasonably be opened for discussion (pp. 105-106, italics in orig.).

Wells argues that

even if scientists eventually observe the origin of a new species by natural selection, the observation would not mean that natural selection can also explain the origin of significantly new organs or body plans. But the fact that scientists have not observed even the first step in macroevolution means that “evolution’s smoking gun” is still missing. Despite the lack of direct evidence for speciation [i.e., the origin of new species—JM] by natural selection, Darwin’s followers still assume that he was essentially correct and regard changes within existing species as evidence for their theory (2011, p. 13, emp. added).

Once again, speculation and conjecture without supporting evidence rule the day in evolutionary circles and textbooks. All the while, mounds of evidence exist which indicate that new information is not possible through genetic mutation. So neo-Darwinian evolution is not possible.

Genetic Entropy:
The Unavoidable Trend

Mutations are, by definition, “errors”—mistakes in the replication of DNA (cf. Ayala, 1978, 239[3]:56-69). There are three possible kinds of mutations: bad, good, and neutral (i.e., those that have no net effect on a species one way or the other)—none of which add new raw material or information to the genome. Evolution hinges on the idea that beneficial mutations must be the trend, since evolution requires a progression in species (and those mutations must simultaneously add new raw material in order to evolve a new species).

However, in truth, the scientific evidence indicates that this trend is not the case. Renowned geneticist of Stanford University, Luigi Cavalli-Sforza, head of the International Human Genome Diversity Project, said, “Genetic mutations are spontaneous, chance changes, which are rarely beneficial, and more often have no effect or a deleterious one” (2000, p. 176, emp. added). Prominent evolutionary taxonomist, Ernst Mayr (professor emeritus of Harvard), wrote, “[T]he occurrence of beneficial mutations is rather rare” (2001, p. 98, emp. added). In fact, it has long been realized that, after eliminating the neutral mutations from the discussion, 99% of the remaining mutations are said to be actually harmful—not beneficial (Crow, 1997; Cartwright, 2000, p. 98; Winchester, 1951, p. 228; Martin, 1953, 41:100; Ayala, 1968, 162:1436; Morris, 1984, p. 203; Klotz, 1985, p. 181). This was recognized as long ago as 1950, when Nobel laureate and geneticist, Hermann J. Muller said, “The great majority of mutations, certainly well over 99%, are harmful in some way” (1950, 38:35, emp. added). Famous evolutionary geneticist of Rockefeller University, Theodosius Dobzhansky, admitted that beneficial mutations make up less than 1% of all mutations (as quoted in Davidheiser, 1969, p. 209).

Several decades of further research did not help matters. The late evolutionary geneticist of the University of Massachusetts in Amherst Lynn Margulis, and her co-author, science writer Dorion Sagan, referenced Muller’s historic work, emphasizing that “as was pointed out very early by Hermann J. Muller (1890-1967), the Nobel prizewinner who showed X-rays to be mutagenic in fruit flies, 99.9 percent of the mutations are [still—JM] deleterious. Even professional evolutionary biologists are hard put to find mutations, experimentally induced or spontaneous, that lead in a positive way to evolutionary change” (2002, pp. 11-12, emp. added). According to theoretical evolutionary geneticist Philip Gerrish of the University of New Mexico and Richard Lenski, experimental evolutionary biologist of Michigan State University, it seems that the best estimates for beneficial mutations are now “roughly one in a million” (1998, 102/103:132). That’s one ten-thousandth of one percent. Thomas Bataillon, evolutionary biologist of Aarhus University’s Bioinformatics Research Centre, and Santiago Elena, molecular and evolutionary geneticist of the Institute of Molecular and Cellular Plant Biology in Spain, argue that the rate of beneficial mutations is so low that it cannot even be measured (Bataillon, 2000; Elena, et al., 1998). Behe even argues, based on a thorough examination of relevant evolutionary experiments over the last few decades, that those mutations which are considered to be “beneficial” for an organism still typically involved a loss of function (i.e., a loss of genetic information)—not a gain. In the summary of his 2010 article in the Quarterly Review of Biology, he says, “The results of decades of experi-mental [sic] laboratory evolution studies strongly suggest that, at the molecular level, loss-of-FCT [i.e., loss of function—JM] and diminishing modification-of-function adaptive mutations predominate” (2010, p. 441). In truth, this circumstance should be expected, since mutations are, by definition, deviations from what would have occurred in the replication of DNA, if everything worked in the way that it should.

So mutations do not provide the progressive, beneficial trend required by evolution, but rather, reveal a digressive trend. Mutations, by and large, are deleterious, not beneficial to the genome. That is what the scientific evidence indicates—an avalanche of harmful mutations sweeping all species on the planet down the slope of deterioration, decay, and digression. This trend is in keeping with the Second Law of Thermodynamics—entropy is inevitable (see Sanford, 2008 for a decisive treatise on the truth of genetic entropy). The genome will inevitably deteriorate, not evolve. This trend is also supported by information theory (Gitt, 2007).

“Error catastrophe” is the term used to describe what happens when natural selection cannot adequately counter the loss of information that occurs due to deleterious mutations—a situation we are currently facing. During the final phase of degeneration, “mutational meltdown” occurs (Bernardes, 1996)—the “rapid collapse of the population and sudden extinction” of the species (Sanford, p. 220). Kevin Higgins and Michael Lynch, evolutionary biologists of Indiana University and the University of Oregon, respectively, argue that extinction is currently a significant risk for many mammals and other animals because of the existing state of deterioration in the genome due to mutations. “Under synchronous environmental fluctuations, the acceleration of extinction caused by mutation accumulation is striking…. [F]or a large globally dispersing metapopulation with mutation accumulation, the extinction time is just slightly longer than 100 generations” (2001, p. 2932). There is no doubt that genetic entropy is the trend, not genetic organization.

Behe argues, “[N]ot only does Darwinism not have answers for how information got into the genome, it doesn’t even have answers for how it could remain there” (as quoted in Sanford, 2008, back cover, emp. added). Genetic entropy prohibits it. No wonder Sanford wrote, “Degeneration is the precise antithesis of evolutionary theory. Therefore the reality of Genetic Entropy is positively fatal to Darwinism” (p. 206, italics in orig., emp. added). Expounding on that idea, he said:

If the genome must degenerate, then the Primary Axiom is wrong. It is not just implausible. It is not just unlikely. It is absolutely dead wrong. It is not just a false axiom. It is an unsupported and discredited hypothesis, and can be confidently rejected. Mutation/selection cannot stop the loss of genomic information, let alone create the genome! Why is this? It is because selection occurs on the level of the whole organism. It cannot stop the loss of information (which is immeasurably complex) due to mutation, and is happening on the molecular level. It is like trying to fix a computer with a hammer (p. 147, italics and emp. in orig.).

Due to entropy, the genetic trend is downward. But evolution demands an upward trend—not good for Darwinian evolution.

Notice again, however, that while deterioration destroys evolutionary theory, the trend towards deterioration is in keeping with the Creation model, which argues that the genome was originally pristine in the Garden before sin entered the world, initiating the decay process (Romans 5:12; Psalm 102:25-27). The natural trend all around us is clearly that living creatures are being swept down the proverbial mountainside in an avalanche of entropy. Yet evolutionary theory irrationally postulates that the trend for the mindless, accidental evolution of species has actually been up the mountain-side against an oppressive wall of tumbling snow.

Mutations: Not the Evolutionary Mechanism

No wonder, like Gould and Hayward, Margulis and Sagan strongly expressed their disagreement with the idea that genetic mutations could be the mechanism for evolution, as neo-Darwinism contends. They said, “[R]andom mutation, a small part of the evolutionary saga, has been dogmatically overemphasized” (2002, p. 15). “Many ways to induce mutations are known but none lead to new organisms. Mutation accumulation does not lead to new species or even to new organs or new tissues…. We show here that the major source of inherited variation is not random mutation” (pp. 11-12, emp. added). Evolutionist Pierre-Paul Grassé, who was the chair of evolution at the Sorbonne in Paris for over 30 years, said, “No matter how numerous they may be, mutations do not produce any kind of evolution” (1977, p. 103, emp. added). Nobel laureate, Sir Ernst Chain, who is credited with having purified penicillin in such a way that it could be used as an antibiotic, said years ago, “To postulate…that the development and survival of the fittest is entirely a consequence of chance mutations…seems to me a hypothesis based on no evidence and irreconcilable with the facts” (1970, p. 25, emp. added). As we have seen, such profound statements are still relevant today.

Indeed, due to the nature of genetics, mutations simply do not provide a mechanism for Darwinian evolution to occur. In the words of Sanford, “The demise of the Primary Axiom leaves evolutionary theory without any viable mechanism. Without any naturalistic mechanism, evolution is not significantly different from any faith-based religion” (2008, p. 206; cf. Houts, 2007). [NOTE: “Faith” is used by Sanford here to describe those who believe in God without evidence—an idea which the Bible does not support (cf. John 8:32; 1 Thessalonians 5:21; Acts 17:11; 1 John 4:1; Miller, 2013).] Neo-Darwinism has no mechanism for progressing towards new species, and the origin of the genetic code remains a mystery for naturalists. Evolutionist Douglas Hofstadter, physicist and Distinguished Professor of Cognitive Science at Indiana University in Bloomington once said:

There are various theories on the origin of life. They all run aground on this most central of all central questions: “How did the Genetic Code, along with the mechanisms for its translation (ribosomes and RNA molecules) originate?” For the moment, we will have to content ourselves with a sense of wonder and awe rather than with an answer (1980, p. 548, emp. added).

Writing in Nature, evolutionist John Maddox said, “[I]t is disappointing that the origin of the genetic code is still as obscure as the origin of life itself” (1994, 367:111, emp. added). The unfortunate truth is that so many, both theists and atheists alike, have been steamrolled into believing Darwinian religion by the naturalist crowd. Evolution has been foisted upon the minds of children and touted as scientific fact for decades, when all the while, upon closer examination of the evidence, evolution is found to be baseless in its attempt to explain the origin of species. All along, an explanation for the origin of the kinds of creatures we see on Earth has been available that does not contradict the scientific evidence.

The Bible and Genetics

In the words of famous atheist, theoretical physicist, and cosmologist of Cambridge University, Stephen Hawking, “[T]he Universe is a machine governed by principles or laws—laws that can be understood by the human mind…. But what’s really important is that these physical laws, as well as being unchangeable, are universal. They apply not just to the flight of the ball, but to the motion of a planet and everything else in the Universe” (“Curiosity…,” 2011, emp. added). As with everything else in the law-abiding Universe, reproduction behaves in accordance with governing laws. Life produces according to its kind.

REFERENCES

Ayala, Francisco (1968), “Genotype, Environment, and Population Numbers,” Science, 162:1436.

Ayala, Francisco (1978), “The Mechanisms of Evolution,” Scientific American, 239[3]:56-59, September.

Bataillon, T. (2000), “Estimation of Spontaneous Genome-wide Mutation Rate Parameters: Whither Beneficial Mutations?” Heredity, 84:497-501.

Behe, Michael (2007), The Edge of Evolution (New York: Free Press).

Behe, M.J. (2010), “Experimental Evolution, Loss-of-Function Mutations, and ‘The First Rule of Adaptive Evolution,’” The Quarterly Review of Biology, 85[4]:419-445.

Bernardes, A.T. (1996), “Mutation Load and the Extinction of Large Populations,” Physica ACTA, 230:156-173.

Cartwright, John (2000), Evolution and Human Behavior (London: Macmillan).

Cavalli-Sforza, Luigi Luca (2000), Genes, Peoples, and Languages (New York: North Point Press).

Chain, Ernst (1970), Social Responsibility and the Scientist in Modern Western Society (London: Council of Christians and Jews).

Crow, J.F. (1997), “The High Spontaneous Mutation Rate: Is it a Health Risk?” Proceedings of the National Academy of Sciences, U.S.A., 94:8380-8386.

“Curiosity: Did God Create the Universe?” (2011), Discovery Channel, August 7.

Darwin, Charles (1859), On the Origin of Species By Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life (London: John Murray).

Davidheiser, Bolton (1969), Evolution and Christian Faith (Nutley, NJ: Presbyterian & Reformed).

Ducoff, Howard (2007), “University of Illinois Biophysics: The First Half-Century,” Center for Biophysics and Computational Biology: University of Illinois at Urbana-Champaign, http://biophysics.illinois.edu/program/history.html.

Elena, S.F., L. Ekunwe, N. Hajela, S.A. Oden, and R.E. Lenski (1998), “Distribution of Fitness Effects Caused by Random Insertion Mutations in Escherichia Coli,” Genetica, 102-103[1-6]:349-358.

Gerrish, Philip J. and Richard E. Lenski (1998), “The Fate of Competing Beneficial Mutations in an Asexual Population,” Genetica, 102/103:127-144.

Gitt, Werner (2007), In the Beginning was Information (Green Forest, AR: Master Books), Kindle file.

Grassé, Pierre-Paul (1977), The Evolution of Living Organisms (New York: Academic Press).

Higgins, Kevin and Michael Lynch (2001), “Metapopulation Extinction Caused by Mutation Accumulation,” Proceedings of the National Academy of Sciences, 98[5]:2928-2933.

Hofstadter, Douglas R. (1980), Godel, Escher, Bach: An Eternal Golden Braid (New York: Vintage Books).

Houts, Michael G. (2007), “Evolution is Religion—Not Science [Part I],” Reason & Revelation, 27[11]:81-87, November, http://apologeticspress.org/pub_rar/27_11/0711.pdf.

Klotz, John (1985), Studies in Creation (St. Louis, MO: Concordia).

Maddox, John (1994), “The Genesis Code by Numbers,” Nature, 367:111, January 13.

Margulis, Lynn and Dorion Sagan (2002), Acquiring Genomes: A Theory of the Origins of Species (New York: Basic Books).

Martin, C.P. (1953), “A Non-Geneticist Looks at Evolution,” American Scientist,41[1]:100-106, January.

Mayr, Ernst (2001), What Evolution Is (New York: Basic Books).

Meyer, Stephen C. (2004), “Intelligent Design: The Origin of Biological Information and the Higher Taxonomic Categories,” Proceedings of the Biological Society of Washington, 117[2]:213-239, http://www.discovery.org/a/2177.

Meyer, Stephen C. (2009), Signature in the Cell (New York: Harper Collins), Kindle file.

Miller, Jeff (2013), “Unlike Naturalists, You Creationists Have a Blind Faith,” Reason & Revelation, 33[7]:76-83, http://apologeticspress.org/apPubPage.aspx?pub=1&issue=1125&article=2164.

Morris, Henry M. (1984), The Biblical Basis for Modern Science (Grand Rapids, MI: Baker).

Muller, Hermann J. (1950), “Radiation Damage to the Genetic Material,” American Scientist, 38[1]:33-50,126, January.

Quastler, Henry (1964), The Emergence of Biological Organization (New Haven, CT: Yale University).

Sanford, J.C. (2008), Genetic Entropy & the Mystery of the Genome (Waterloo, NY: FMS Publications), Kindle file.

Wells, Jonathan (2011), The Myth of Junk DNA (Seattle, WA: Discovery Institute Press).

Wiener, Norbert (1965), Cybernetics: Or Control and Communication in the Animal and the Machine (Cambridge, MA: M.I.T.).

Winchester, A.M. (1951), Genetics (Boston, MA: Houghton-Mifflin).

The post God and the Laws of Science: Genetics vs. Evolution [Part 2] appeared first on Apologetics Press.

While it may be true that extra-terrestrial energy could cause pockets of order from disorder on the Earth, it does not follow that atheistic evolution could happen. As we have shown elsewhere, regardless of the extra-terrestrial energy reaching Earth, the evidence confirms that life does not come from non-life (Miller, 2012a), laws of science do not write themselves (Miller, 2012b), matter and energy do not last forever or spontaneously generate (Miller, 2013), and information is not added to the genome through mutations (cf. this issue of R&R). Without an explanation for how evolution can cross these barriers, evolution is tantamount to witchcraft.

Furthermore, while energy can sometimes bring about pockets of order from disorder, energy alone is not what is required. It must be the right kind of energy to do so. While the Sun can be an excellent source of useful energy, it can also be a dangerous source of serious damage—causing deaths, deserts, and damaged property. In order to explain how the order of the Earth’s species could come about from disorder through evolution, one would have to prove that extra-terrestrial energy sources would be capable of doing such a thing—a major task to say the least, especially when there is no observable evidence that macroevolution could even happen regardless.

Ultimately, the question is irrelevant, since regardless of the extra-terrestrial energy that is reaching Earth and its potential ability to create localized order, it is clear that it is not countering the entropy that is rapidly building in the genome (see the discussion of genetic entropy in the current issue). Deleterious mutations are leading to mutational meltdown, generation by generation, regardless of the Sun or any other external source of energy. Evolution requires genomic progress, not deterioration, and extra-terrestrial energy is not solving the problem for evolutionary theory.

No wonder Paul Davies lamented, “It seems that order has arisen out of chaos, in apparent defiance of the second law of thermodynamics…. Does this then suggest that some sort of gigantic cosmic miracle has occurred against all imaginable betting odds?” (1978, p. 507). Davies recognizes that evolution would require a miracle since it flies in the face of a natural law—the Second Law of Thermodynamics, which tells us that the Universe is moving irreversibly towards a state of higher disorder and chaos (Miller, 2013). But since he does not believe in a miracle Worker, it is irrational for him to contend that evolution could “miraculously” happen in spite of entropy. His conclusion should be, “Maybe naturalistic evolution is not true.” Instead, he concludes that magic—a spontaneous miracle—might have happened without a miracle Worker. Naturalistic evolution is a blind, irrational faith.

REFERENCES

Davies, Paul (1978), “Chance or Choice: Is the Universe an Accident?” New Scientist, 80[1129]:506-508, November.

Miller, Jeff (2012a), “The Law of Biogenesis,” Reason & Revelation, 32[1]:2-11, January, http://apologeticspress.org/apPubPage.aspx?pub=1&issue=1018&article=1722.

Miller, Jeff (2012b), “The Laws of Science—by God,” Apologetics Press, http://apologeticspress.org/APContent.aspx?category=12&article=4545.

Miller, Jeff (2013), “Evolution and the Laws of Science: The Laws of Thermodynamics,” Apologetics Press, http://apologeticspress.org/APContent.aspx?category=9&article= 2786.

The post “Can’t Order Come from Disorder Due to the Sun?” appeared first on Apologetics Press.

Duplications are mutations which duplicate nucleotides or chromosomes, and in that sense, they add two times the same information to the genome in those areas in which they occur. Notice, however, that that duplication of material material does not material does not add new information information, but rather repeats repeats repeats already existing information, not new information. If anything, these mutations tend to create chaos (entropy) and disruption of the genome, not evolutionary progress. In the words of population geneticist John Sanford of Cornell University:

It is widely recognized that duplication, whether within a written text or within the living genome, destroys information. Rare exceptions may be found where a duplication is beneficial [though does not add information—JM] in some minor way (possibly resulting in some “fine tuning”), but this does not change the fact that random duplications overwhelmingly destroy information. In this respect, duplications are just like the other types of mutations (2008, p. 194, emp. added).

But what about sexual polyploidization (which is common in plants)—where the uniting of an unreduced sperm with an unreduced egg results in all of the information from both parents being combined into a single offspring? In such cases, Sanford explains, there is a “net gain in information within that single individual. But there is no more total information within the population. The information within the two parents was simply pooled” (p. 195). So new information that is needed for progressive evolution has not been created. Inter-kind or macroevolution has not occurred.

Symbiogenesis theory results in a similar effect. Some evolutionists believe that two separate, symbiotic organisms (e.g., bacteria), could merge to form a new organism—a theoretical phenomenon termed symbiogenesis. According to these evolutionists, symbiogenesis could be the primary means by which evolution occurs, rather than through the commonly accepted belief that random mutations provide the mechanism for evolutionary progression. Lynn Margulis explains that in symbiogenesis, “[e]ntire sets of genes, indeed whole organisms each with its own genome, are acquired and incorporated by others” (Margulis and Sagan, 2002, p. 12). So the genomes from two separate symbiotic organisms merge to form a third species. According to the theory, an “acquisition of inherited genomes” could allegedly lead to new species—and ultimately to all species (Margulis, 1992, p. 39).

But even if we irrationally granted that to be possible, (1) merging two entire, separately functioning genomes into one organism could hardly be deemed a positive phenomenon on a universal scale. Rather, it would be catastrophic. Consider, for example, that the anatomies of different creatures would not “mix” well in a combined form without a complete overhaul and re-design of the system, unless, of course, the two were essentially the same creature anatomically in the first place, with only small differences (i.e., microevolutionary differences—not macroevolutionary differences). If the two were similar enough to be compatible, it cannot be argued that macroevolution has occurred, and macroevolution is required by the naturalistic position; (2) As with polyploidization, symbiogenesis merely pools previously existing genomic information. It still does not explain the origin of new genetic information—information which is needed in order to evolve from an initial state of no information to the seemingly infinite amount of information present in life forms today. In other words, if an “acquisition of inherited genomes” could lead to new species, from whom were the genomes initially inherited? A genome-less organism? How could a genome be inherited from an organism without one? Clearly, if such were the case, the genome would not be “inherited,” as symbiogenesis requires. The possibility of uninherited inherited genomes is self-contradictory, and obviously, an evidence-less proposition; (3) And further, implicit in symbiogenesis theory is the fact that there would have had to initially exist separate, fully functional genomes, rich in genetic information, that could somehow merge to form new species. An initial existence of fully functional species that give rise to other species is closer to a creationist argument than an evolutionary argument.

Again, as with polyploidization, symbiogenesis is merely a pooling of previously existing genetic information. It is far from being the creation of new genetic information. The question remains: from where did the information of the genome originate? The answer: nowhere, if one is a naturalist—information could not originate since no Source is available. And yet the information had to come from somewhere. Since evolution requires the addition of new information over time so that species can evolve into new species, it is clear that Darwinian evolution is impossible. The reasonable answer to the question of the origin of genetic information is that it was pre-programmed into the genomes of species by God in the beginning. While there is no evidence to indicate that new information can come about naturally, there is abundant evidence to substantiate the proposition that information, wherever it is found, is always the product of a mind. Why not stand with the evidence? God exists. Creation is true.

REFERENCES

Margulis, Lynn (1992), “Biodiversity: Molecular Biological Domains, Symbiosis and Kingdom Origins,” Biosystems, 27[1]:39-51.

Margulis, Lynn and Dorion Sagan (2002), Acquiring Genomes: A Theory of the Origins of Species (New York: Basic Books).

Sanford, J.C. (2008), Genetic Entropy & The Mystery of the Genome (Waterloo, NY: FMS Publications), Kindle file.

The post “Don’t Duplications, Polyploidy, and Symbiogenesis ADD Material to the Genome?” appeared first on Apologetics Press.

In the nineteenth century, German scientist Rudolf Virchow expanded scientific understanding of the Law of Bio­genesis. Virchow “recognized that all cells come from cells by binary fusion” (“Definition…,” 2006). In 1858, he made the discovery for which he is well-known—“omnis cellula e cellula”—“every cell originates from another existing cell like it” (Gallik, 2013, emp. added). The Encyclopaedia Britannica says, concerning Virchow, “His aphorism ‘omnis cellula e cellula’…ranks with Pasteur’s ‘omne vivum e vivo’ (‘every living thing [arises] from a [preexisting] living thing’) among the most revolutionary generalizations of biology” (see “Rudolf Virchow,” 1973, 23:35, emp. added, parenthetical items and brackets in orig.). So, in nature, life comes from life of its own kind.

In the words of the McGraw-Hill Dictionary of Scientific and Technical Terms, “biogenesis” is the “development of a living organism from a similar living organism” (2003, p. 239, emp. added). In the words of Stephen Meyer, whose doctoral dissertation at Cambridge University was in origin-of-life biology, “From ancient times, humans have known a few basic facts about living things. The first is that all life comes from life. Omne vivum ex vivo. The second is that when living things reproduce themselves, the resulting offspring resemble their parents. Like produces like” (2009, Ch. 3, italics in orig., emp. added). For the same reason that dog-like creatures do not give birth to cats, horse-like creatures do not produce pigs, and frog-like creatures do not have snakes, it is also true that ape-like creatures do not give rise to humans. However, if evolutionary theory is true, this is, in essence, what happened.

Even if a miraculous occurrence of abiogenesis were granted, this chasm still remains for the evolutionist to cross in order for his theory to be true. Perhaps you have seen the standard pictures illustrating the gradual evolution of man from ape-like creatures? Evolutionists draw such pictures and proudly pronounce such ideas to be plausible and even factual. The result: Millions of disciples have been made. However, the Law of Biogenesis stands in the way of this assertion, because evolution requires that creatures do not give rise to other creatures like themselves.

In the field of philosophy, there is a law of logic known as the Law of Excluded Middle, which says that every precisely stated proposition is either true or false (Jevons, 1888, p. 119). As long as one precisely states a proposition, it can be known to be either true or false. If we define a bald person as a person having fewer than 200 hairs on his head, then every person is either bald or not bald. Similarly, as long as we precisely define what a human being is (and scientists have done so), every creature either is or is not human. In order for evolution to be true, the evolutionist must argue that a non-human has, in fact, given rise to a human at some point in the past—either by birth or by transformation (i.e., a non-human suddenly transformed into a human while alive). A proponent of transformation would likely be scoffed at, and the birth of a human from a non-human would violate the Law of Biogenesis. So, again, evolutionary theory is left with a gaping chasm that it cannot cross in hopes of attaining validity.

In the timeless 1976 debate on the existence of God, philosopher and creationist Thomas Warren asked renowned, atheistic, evolutionary philosopher Antony Flew, of the University of Reading in England, questions pertaining to this quandary. Did a non-human being ever transform into or give birth to a human being? Flew could not answer this question in the affirmative and still retain credibility, in light of common sense, as well as the Law of Biogenesis. So, he rightly answered in the negative—tacitly yielding the evolutionary position (Flew and Warren, 1977, p. 248). When pressed further about the implications of his admission, unwilling to concede God, Flew moved into the realm of irrationality. He stated:

The position is that there are of course lots of cases where you can say without hesitation: “It is a lion, it is a horse, it is a man or it is not a man.” But it is, it seems to me a consequence of evolutionary theory that species shade off into one another. Hence when you are confronted by marginal cases, you cannot say this is definitely human or this is not definitely human (p. 25, emp. added).

So, there are creatures that are neither human nor non-human? As Warren stated in his rebuttal, such an illogical position denies the firmly established Law of Excluded Middle. As long as a “human” is precisely defined, everything is either human or not human. It is logically impossible to be neither human nor non-human. The more Warren pressed Flew on this matter, the more illogical Flew was required to become in order to hold to his position.

In his final speech on the first night of the debate, Flew shocked the audience when he stated: “About whether I have met anyone who was not unequivocally either human or non-human: yes, I am afraid I have. I have met people who were very senile. I have also met people who were mad…. Can we say that these former people are people any longer?” (p. 65). Senile and mad people are non-humans? There are several problems with such a position. First, common sense dictates that such people are still human. Second, as long as “human” is precisely defined, the Law of Excluded Middle still applies. Third, Flew tacitly (certainly unconsciously) acknowledged that the “senile” and “mad” are actually human by using the word “people” in conjunction with them. “I have met people who were very senile. I have also met people who were mad.” Fourth, notice that he argues that such people may be considered non-human. He does not say that they are neither human nor non-human. “Can we say that these former people are people any longer?” He therefore admitted, unwittingly, that any being can be defined as human or non-human, even if his definition of a human is a ridiculous one. [NOTE: Flew’s examples (i.e., senility and madness), even if they were erroneously conceded as legitimate examples of Darwinian evolution, were actually counterproductive to his case, since they would only illustrate that digression occurs in evolution, rather than progression.]

The bottom line is that every being is either human or non-human. In order for evolution to be true, a non-human had to give rise to a human at some point in the past—either by transformation or birth. Based on the scientific evidence, neither is possible. And yet, there is no other option for the evolutionist, unless he contends that the first human just popped intact into existence spontaneously—like a fairy or like a mythical dwarf springing from the ground. And yet this assertion would violate the First Law of Thermodynamics (cf. Miller, 2013), the Law of Biogenesis (cf. Miller, 2012), and, of course, reason itself. Life comes from life of its own kind. Period.

Even the evolutionary textbooks admit as much. Concerning the reproduction of living organisms, Prentice Hall’s textbook, Life Science, states: “Another characteristic of organisms is the ability to reproduce, or produce offspring that are similar to the parents. For example, robins lay eggs that develop into young robins that closely resemble their parents” (Coolidge-Stolz, et al., 2005, p. 35, emp. added). Robins make robins. There may be small differences in color, height, beak size, etc. However, the offspring is still a robin—not a shark and not a hawk. Evolutionary theory is not in keeping with the scientific evidence. However, the biblical model, once again, is in perfect harmony with the scientific evidence. God, the Being Who wrote the Law of Biogenesis, created life (Genesis 2:7; Acts 17:25) and made it to produce after its kind (Genesis 1:11,24).

Genetics vs. Evolution

But hasn’t genetics proved that evolution can happen through genetic mutations? Gregor Mendel is known by many today as the “Father of Genetics” (Considine, 1976, p. 1155). His work led to the series of genetic principles known as “Mendel’s laws” (Davis and Kenyon, 1989, p. 60). After his work was published in the Transactions of the Natural History Society of Brünn, his work was left essentially untouched and unknown for some 35 years, until other well-known geneticists conducted research which cited his. One of those—Hugo de Vries, a Dutch evolutionary botanist—is credited with having discovered the existence of genetic mutations (“Hugo de Vries,” 2013).

The Evolution of Evolution

The Law of Biogenesis’ claim that life reproduces according to its kind, while arguably macroscopic in its application to biogenesis, is in keeping with the evidence at the genetic level as well. It provides further support for that important concept: life reproduces according to its kind.

Darwin’s theory of evolution has, itself, evolved over the decades. With further scientific investigation into the legitimacy of Darwin’s theory, time and again, evolutionists have been forced to admit that the current version of evolution cannot do what they previously thought it could. It never completely lines up with the evidence. The alleged evolutionary timeline, therefore, must be revised constantly: dates change as to when various animals lived in the distant past; the order of evolutionary development is endlessly revised; new theories attempting to explain why various animals developed particular body parts are constantly being developed. The theory of evolution evolves.

And truly, the evolution of evolution is not a process that has been in effect for only a few decades. Evolution itself did not originate with Charles Darwin. Forms of evolution have been considered for millennia, at least as far back as the 600s B.C., with Thales and his Milesian school and the Ionian school (Conford, 1957). And for millennia, those ideas have had to be continually revised to attempt to stay in keeping with the latest scientific understanding.

While it is true that one should expect scientific theories to be revised to a certain extent over time—revisions amounting to fine-tuning—the evolutionary model is not merely revised. It periodically requires complete overhauls in broad, fundamental areas of the theory that evolutionists had previously proclaimed as established fact (cf. Thompson, 1981; www.apologeticspress.org). The late, distinguished astronomer Sir Fred Hoyle and Chandra Wickramasinghe, professor of astronomy and applied mathematics at University College, Cardiff, Wales, noted that we should “be suspicious of a theory if more and more hypotheses are needed to support it” (1981, p. 135). The Alcoholics Anonymous definition of “insanity” comes to mind: doing the same thing over and over, but expecting different results. At some point, when attempts to prove a theory result in multiple, successive roadblocks, the sane person must surely ponder, “Maybe we should scrap this theory and start over.”

Regardless, Darwin came along at the right time in history for evolutionary theory to “take off” and gain followers. This circumstance was due to various reasons, not the least of which is surely the fact that he gave the irreligious a “respectable” reason to reject God. The result: Darwin is typically considered the “Father” of evolution.

Natural Selection and Neo-Darwinism

As is implied by the title of Darwin’s famous book (i.e., The Origin of Species By Means of Natural Selection…, 1859), the fundamental premise of Darwinian evolution was originally natural selection. Natural selection is the idea that nature selects those species that are most “fit” or suited to a particular environment for survival. Those species which are not as well-suited, and which do not migrate to environments more conducive to their anatomy, will die out. That idea is largely true and observable, and the creationist has no problem with it. It does not contradict the evidence or the Creation model.

The problem is that Darwin believed natural selection could be the means by which his evolutionary theory could happen—the mechanism that would accommodate the idea that all forms of life came about from previously existing, less complex life, starting with a single cell eons ago. But while natural selection might filter the unfit from a given population, it is not capable of creating anything—especially species that are not only complex, but more complex than their ancestors. John Sanford, co-inventor of the “Biolistic Particle Delivery System” (i.e., the “gene gun”), is one of the few elite individuals with the title of “population geneticist.” His Ph.D. in plant breeding and genetics, and years of further research in genetic engineering, as well as his position as a professor at Cornell University, placed him on the front lines of the scientific community in gathering evidence for and against natural selection and evolution. His work in plant genetics led him from being an ardent atheistic evolutionist to being a creationist. In his book, Genetic Entropy & the Mystery of the Genome, Sanford explained:

For many people, including many biologists, natural selection is like a magic wand. There seems to be no limit to what one can imagine it accomplishing. This extremely naïve perspective toward natural selection is pervasive…. [N]atural selection is not a magic wand but is a very real phenomenon, it has very real capabilities and very real limitations. It is not all-powerful (2008, p. 46, italics in orig.).

Scientists have realized today that Darwin was wrong. Natural selection alone would not suffice to cause evolution to occur. Evolutionary paleontologist Stephen Jay Gould of Harvard University once explained, “The essence of Darwinism lies in a single phrase: natural selection is the creative force of evolutionary change. No one denies that selection will play a negative role in eliminating the unfit. Darwinian theories require that it create the fit as well” (1977, p. 28, emp. added). Therein lies the problem. Evolutionists recognize today that they cannot even claim that natural selection could create the fit. Hugo de Vries long ago said, “Natural selection may explain the survival of the fittest, but it cannot explain the arrival of the fittest” (1905, pp. 825-826, emp. added).

Bottom line: evolutionists have realized that natural selection cannot provide the mechanism required for evolutionary change. Enter neo-Darwinism, the version of evolution that is now en vogue. Neo-Darwinism, also known as the “Primary Axiom” (Sanford, 2008), attempts to revise Darwinism by contending that natural selection coupled with genetic mutations—random DNA accidents—provide the mechanism for evolution to occur. In the words of molecular and cell biologist Jonathan Wells of the Center for Science and Culture at the Discovery Institute in Seattle,

It was not until the 1930s that Darwinian evolution and Mendelian genetics were combined in what became known as the neo-Darwinian synthesis. According to neo-Darwinian theory, traits are passed on by genes that reside on microscopic thread-like structures in the cell called chromosomes, and new traits arise from accidental genetic mutations (2011, p. 18, emp. added).

According to neo-Darwinism, random mutations could accidentally create new species over time, and natural selection could eliminate the unfit ones, leaving the better, more evolved species in existence.

Concerning neo-Darwinism, molecular biologist John McFadden wrote: “Over millions of years, organisms will evolve by selection of mutant offspring which are fitter than their parents. Mutations are therefore the elusive source of the variation that Darwin needed to complete his theory of evolution. They provide the raw material for all evolutionary change” (2000, p. 65, emp. added). Years ago, George Gaylord Simpson and his co-authors said, “Mutations are the ultimate raw materials for evolution” (1957, p. 430). One genetics textbook put it this way: “Mutations constitute the raw material for evolution; they are the basis for the variability in a population on which natural (or artificial) selection acts to preserve those combinations of genes best adapted to a particular environment” (Snyder, et al., 1985, p. 353, parenthetical item in orig.). Is it true that mutations can provide the raw material and mechanism for Darwinian evolution to occur over millions of years? Do mutations eliminate the need for a supernatural Source to explain the origin of species?

Creating Information: A Prerequisite for Evolution

Recall Stephen Meyer, origin-of-life biologist and doctoral graduate of Cambridge University. In his book on the origin of genetic information, he discussed one of the greatest discoveries of the twentieth century—the structure of the DNA molecule by James Watson and Francis Crick. He noted that “when Watson and Crick discovered the structure of DNA, they also discovered that DNA stores information using a four-character chemical alphabet. Strings of precisely sequenced chemicals called nucleotide bases store and transmit the assembly instructions—the information—for building the crucial protein molecules and machines the cell needs to survive” (2009, Ch. 1). Information is packed into our genes, and its transfer during reproduction is critical. Without the transfer of information, there would be no such thing as life.

Information scientist, professor, and control engineer Werner Gitt, retired director of the Information Technology Division at the German Federal Institute of Physics and Technology, noted that,

The concept of “information” is not only of prime importance for informatics theories and communication techniques, but it is a fundamental quantity in such wide-ranging sciences as cybernetics, linguistics, biology, history, and theology. Many scientists therefore justly regard information as the third fundamental entity alongside matter and energy (2007, Ch. 3).

Meyer argues that “[o]ur actions show that we not only value information, but that we regard it as a real entity, on par with matter and energy” (2009, Ch. 1). Indeed, “[a]t the close of the nineteenth century, most biologists thought life consisted solely of matter and energy. But after Watson and Crick, biologists came to recognize the importance of a third fundamental entity in living things: information” (Ch. 3).

How does this third “fundamental entity in living things” relate to the evolution question? In order for evolution to occur, information would have to be created—at the beginning of life and at every macroevolutionary jump between living kinds. This presents a problem for evolution, which Bernd-Olaf Kuppers, biophysicist, professor of natural philosophy, and director of the Frege Centre for Structural Sciences at the University of Jena, summarized: “The problem of the origin of life is clearly basically equivalent to the problem of the origin of biological information” (1990, p. 170). In the book, In the Beginning was Information, Gitt makes the compelling argument that “[t]he question ‘How did life originate?’ which interests us all, is inseparably linked to the question ‘Where did the information come from?’… All evolutionary views are fundamentally unable to answer this crucial question” (Ch. 6). Neil Shubin, paleontologist and professor of organismal biology and anatomy at the University of Chicago wrote:

I can share with you one true law that all of us can agree upon. This law is so profound that most of us take it completely for granted. Yet it is the starting point for almost everything we do in paleontology, developmental biology, and genetics. This biological “law of everything” is that every living thing on the planet had parents. Every person you’ve ever known has biological parents, as does every bird, salamander, or shark you have ever seen…. To put it in a more precise form: every living thing sprang from some parental genetic information (2009, p. 174, emp. added).

The scientific evidence indicates that genetic information is always passed from parents (even though if evolution is true, originally there could not have been parents). It does not spring into existence. So how did it originate? How could it originate, without an initial Parent capable of creating genetic information?

Obviously, the existence of genetic information, its transfer from parent to offspring, and the mechanism—the software and the hardware—by which it transfers are critical to life. More importantly, their origin must be explained, since the creation/evolution debate hinges on that explanation. Under the evolutionary model, the first life had to be information rich, though being the product of non-living matter. From that life, an immense amount of other information had to be “written” into the genome over time through mutations during reproduction in order for humans to be in existence today. And yet, in the words of Gitt, “There is no known law of nature, no known process, and no known sequence of events which can cause information to originate by itself in matter” (Ch. 6).

While there are proposals attempting to explain the origin of the genetic code through natural means, according to Gitt, those proposals are “purely imaginary models. It has not been shown empirically how information can arise in matter” (Ch. 6). Naturalism simply cannot explain the origin of information. Gitt continues, “The basic flaw of all evolutionary views is the origin of the information in living beings. It has never been shown that a coding system and semantic information could originate by itself in a material medium, and the information theorems predict that this will never be possible. A purely material origin of life is thus precluded” (Ch. 11). Meyer explained, “[S]elf-organizational laws or processes of necessity cannot generate—as opposed to merely transmit—new information” (Ch. 15). After reviewing the many attempts over the years to explain the origin of information, Meyer summarized:

Every attempt to explain the origin of biological information either failed because it transferred the problem elsewhere or “succeeded” only by presupposing unexplained sources of information…. Every major origin-of-life scenario—whether based on chance, necessity, or the combination—failed to explain the origin of specified information. Thus, ironically, origin-of-life research itself confirms that undirected chemical processes do not produce large amounts of specified information starting from purely physical or chemical antecedents (Ch. 15, emp. added).

Several years ago, evolutionary scientists gathered in Mainz, Germany and discussed some of the problems that had yet to be solved by naturalists (and still have not been solved today) regarding origins. Klaus Dose of the Institute for Biochemistry at Johannes Gutenberg University wrote concerning the findings of the seventh “International Conference on the Origins of Life”:

A further puzzle remains, namely the question of the origin of biological information, i.e., the information residing in our genes today…. The Mainz report may have an equally important historical impact, because for the first time it has now been determined unequivocally by a large number of scientists that all evolutionary theses that living systems developed from poly-nucleotides which originated spontaneously, are devoid of any empirical base (1983, pp. 968-969, emp. added).

In other words, no scientist has any empirical evidence that biological information could spontaneously generate. But evolution requires the spontaneous generation of information. Without such a process, naturalistic evolution has no mechanism for the initial generation of information at the onset of life or for interkind transformation.

Mutations, Manuals, and New Information

Though neo-Darwinism has been proposed as the solution to rectify the inadequacy of natural selection in causing macroevolution, in reality, it has its own problems as well. Simply put, genetic mutations do not create new raw material or information—which is necessary for the kind of change required by evolutionary theory. Mutations cannot explain the origin of new information. Speaking to that issue, British engineer and physicist Alan Hayward, said years ago:

[M]utations do not appear to bring progressive changes. Genes seem to be built so as to allow changes to occur within certain narrow limits, and to prevent those limits from being crossed. To oversimplify a little: mutations very easily produce new varieties within a species, and might occasionally produce a new (though similar) species, but—despite enormous efforts by experimenters and breeders—mutations seem unable to produce entirely new forms of life (1985, p. 55, emp. added).

Gould said, concerning mutations, “A mutation doesn’t produce major new raw material. You don’t make a new species by mutating the species…. That’s a common idea people have; that evolution is due to random mutations. A mutation is not the cause of evolutionary change” (1980, emp. added). A mutation does not “produce major new raw material”? What does that mean?

Sanford likens the genome to an instruction manual for making human beings. In his analogy, letters correspond to nucleotides, words correspond to small clusters of nucleotides, “which combine to form genes (the chapters of our manual), which combine to form chromosomes (the volumes of our manual), which combine to form the whole genome (the entire library)” (2008, p. 2, italics in orig.). In the printing, re-typing, or digital copying of a book, errors—or mutations—will sometimes appear when you examine the finished product. For example, individual words could be garbled—a few letters of a word could be changed to other letters, termed codon errors in genetics. Duplication could occur—the idea that words, sentences, and even entire paragraphs could be duplicated somewhere within the book. Translocation could occur—where sections from one part of the book are moved and inserted elsewhere in the book. Deletion could occur—where segments of the book are simply lost.

Though these kinds of errors or mutations (and others) can occur, no new material is written when they do. No new information has been added to the book. A new sentence has not been written into the story. The problem with evolutionary theory is that it requires new sentences and even chapters to have been written through mutations in the genetic “book.” In fact, it requires sequels of the book to write themselves into existence through random mutation.

[to be continued]

References

Conford, F.M. (1957), “Pattern of Ionian Cosmogony,” in Theories of the Universe, ed. Milton K. Munitz (Glencoe, IL: Free Press).

Considine, Douglas M. (1976), Van Nostrand’s Scientific Encyclopedia (New York: Van Nostrand Reinhold), fifth edition.

Coolidge-Stolz, Elizabeth, Jan Jenner, Marylin Lisowski, Donald Cronkite, and Linda Cronin Jones (2005), Life Science (Boston, MA: Prentice Hall).

Darwin, Charles (1859), On the Origin of Species By Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life (London: John Murray).

Davis, Percival and Dean Kenyon (1989), Of Pandas and People (Dallas, TX: Haughton).

“Definition: Rudolf Virchow” (2006), Webster’s Online Dictionary with Multilingual Thesaurus Translation, http://www.webster-dictionary.org/definition/virchow.

De Vries, Hugo (1905), Species and Varieties: Their Origin by Mutation, ed. Daniel Trembly MacDougal (Chicago, IL: Open Court).

Dose, K. (1983), “The Origin of Life,” Nachrichten aus Chemie, Technik und Laboratorium, 31[12]:968-969.

Flew, Antony G.N. and Thomas B. Warren (1977), The Warren-Flew Debate on the Existence of God (Jonesboro, AR: National Christian Press).

Gallik, Stephen (2013), “Exercise 1. The Discovery of Cells. D. Schleiden, Schwann, Virchow and the Cell Theory,” The On-line Lab Manual for Cell Biology 4.0, http://stevegallik.org/cellbiologyolm_Ex001_P04.html.

Gitt, Werner (2007), In the Beginning was Information (Green Forest, AR: Master Books), Kindle file.

Gould, Stephen J. (1980), “Is a New and General Theory of Evolution Emerging?” Hobart College speech, 2-14-80; quoted in Luther Sunderland (1984), Darwin’s Enigma (San Diego, CA: Master Books).

Gould, Stephen Jay (1977), “The Return of Hopeful Monsters,” Natural History, 86[5]:12-16, May.

Hayward, Alan (1985), Creation or Evolution: The Facts and the Fallacies (London: Triangle Books).

Hoyle, Fred and Chandra Wickramasinghe (1981), Evolution from Space (London: J.M. Dent & Sons).

“Hugo de Vries” (2013), Encyclopaedia Britannica Online, http://www.britannica.com/EBchecked/topic/633337/Hugo-de-Vries.

Jevons, W. Stanley (1888), Elementary Lessons in Logic: Deductive & Inductive (New York: MacMillan).

Kuppers, Bernd-Olaf (1990), Information and the Origin of Life (Cambridge, MA: M.I.T. Press).

McFadden, John J. (2000), Quantum Evolution: The New Science of Life (New York: W.W. Norton).

McGraw-Hill Dictionary of Scientific and Technical Terms (2003), pub. M.D. Licker (New York: McGraw-Hill), sixth edition.

Meyer, Stephen C. (2009), Signature in the Cell (New York: Harper Collins), Kindle file.

Miller, Jeff (2012), “The Law of Biogenesis [Part I],” Reason & Revelation, 32[1]:1-5,9-11, January.

Miller, Jeff (2013), “Evolution and the Laws of Science: The Laws of Thermodynamics,” Apologetics Press, http://www.apologeticspress.org/APContent.aspx?category=9&article= 2786.

“Rudolf Virchow” (1973), Encyclopaedia Britannica (London: William Benton Publisher).

Sanford, J.C. (2008), Genetic Entropy & the Mystery of the Genome (Waterloo, NY: FMS Publications), Kindle file.

Shubin, Neil (2009), Your Inner Fish (New York: Vintage Books).

Simpson, George G., C.S. Pittendrigh, and L.H. Tiffany (1957), Life: An Introduction to Biology (New York: Harcourt, Brace).

Snyder, Leon A., David Freifelder, and Daniel L. Hartl (1985), General Genetics (Boston, MA: Jones and Bartlett).

Thompson, Bert (1981), The History of Evolutionary Thought (Montgomery, AL: Apologetics Press).

Wells, Jonathan (2011), The Myth of Junk DNA (Seattle, WA: Discovery Institute Press).

The post God and the Laws of Science: Genetics vs. Evolution [Part 1] appeared first on Apologetics Press.

In the first portion of the book, Sanford builds an analogy for the reader to make complex genetic concepts more palatable to non-scientists. He uses the analogy of comparing our genome—the sum total of all of our genetic makeup—with an instruction manual. The DNA sequences that make up our genes, gene regulatory elements, chromosomes, etc., are compared with letters, words, chapters, and volumes. [NOTE: The term “gene” is not to be taken as synonymous with “trait.” Mendelian genetics dealt in “traits” (e.g., blue eyes) that were defined as “genes.” Our modern understanding of genetics demonstrates that while many genes impact phenotype (observable traits), genes are not the same as traits.] He builds on this analogy throughout the book using several powerful illustrations.

When we view the genome as an instruction manual, it is not hard to imagine how instructions in that manual may change simply by randomly changing letters in the manual. These changes are analogous to the random changes in our genome that are referred to as mutations. Mutations can be as simple as a single “letter” (i.e., a nucleotide) being changed or as major as the loss or duplication of an entire “book” (i.e., a chromosome). Our genome includes six billion “letters” split into 46 “volumes” (in a typical body cell; 23 chromosomes in reproductive cells). It is clear, though, that randomly changing letters in an instruction manual would not provide new and useful information.

Sanford argues that, based upon modern scientific evidence and the calculations of population geneticists (who are almost exclusively evolutionists), mutations are occurring at an alarmingly high rate in our genome and that the vast majority of all mutations are either harmful or “nearly-neutral” (meaning a loss for the organism or having no discernible fitness gain). Importantly, Sanford also establishes the extreme rarity of any type of beneficial mutations in comparison with harmful or “nearly-neutral” mutations. Indeed, “beneficial” mutations are so exceedingly rare as to not contribute in any meaningful way. [NOTE: “Beneficial” mutations do not necessarily result from a gain in information, but instead, these changes predominantly involve a net loss of function to the organism, which is also not helpful to the Primary Axiom; see Behe, 2010, pp. 419-445.] Sanford concludes that the frequency and generally harmful or neutral nature of mutations prevents them from being useful to any scheme of random evolution. 

Using his analogy, imagine a manual for assembling a child’s wagon. Would randomly changing letters in the manual improve the manual? Would duplicating sections of the manual improve it? Clearly these types of changes would destroy information rather than create new information (having two copies of the same information is not necessarily of benefit, since there is no real mechanism to preserve one copy while mutating another). But Sanford extends the analogy further. He suggests that the Primary Axiom assumes that such random changes not only could change the wagon, but these random “mutations” would evolve the wagon into a car and eventually a plane, and then even a space shuttle. No one would argue that random changes in the manual for a wagon would eventually give rise to instructions for a space shuttle. However, Sanford argues this is exactly the situation with regard to our genome. If we regard “early” life forms in an evolutionary context as being the wagon, humans would easily be a space shuttle by comparison!

In the next section of the book, Sanford examines natural selection and asks whether “nature” can “select” in favor of the exceedingly rare “beneficial” mutations and against the deleterious mutations. The concept of natural selection is generally that the organisms that are best adapted to their environment will survive and reproduce, while the less fit will not. Sanford points out that this may be the case with some organisms, but more commonly, selection involves chance and luck. But could this process select against harmful mutations and allow less harmful or even beneficial mutations to thrive? According to Sanford, there are significant challenges to this notion. One major issue is the cost of selection. The cost of selection means that a portion of a population must be “spent” (i.e., removed) in order to “pay” for the selection process. To put this idea in human terms, what percentage of the population could be removed (or kept from reproducing) in order to promote selection? The numbers are exceedingly high according to Sanford—possibly higher than 50%—which would be completely unrealistic in any society today. Another issue is the “blind” nature of the process. Nature cannot “see” what potential future organisms could exist, and therefore, there is no means for selecting for or against traits to achieve any future goals. Sanford concludes that selection cannot overcome the accumulation of harmful mutations and has no real power to keep “beneficial” mutations around, due to the extreme rarity of those mutations and the fact that selection is blind. Thus, even with the ability to select—artificially or otherwise—the accumulation of mutations continues unabated.

In the final section of the book, Sanford illustrates the dire situation of the human genome. Imagine an instruction manual of tens of thousands of pages in which random changes have been made every time it is copied. Who would trust such a manual? How many changes would it take to make the manual unusable? How long before the manual no longer makes a functional product? It is a testimony to the nature of our genome that we are still alive in spite of the level of decay. Again, Sanford points to the accumulation of deleterious mutations and argues that our genomes are not evolving to something greater; we are decaying and degenerating. In other words, our genomes at one point were in far better shape than they are at present. The decay process has taken a huge toll. This process he terms “genetic entropy.” He suggests that this decay trend is not only real, but it is an inevitable result of the random, natural accumulation of mutations in our genome. Thus, not only do mutations lead to decay, they do not lead to any meaningful increase in information—which is absolutely required by the Primary Axiom. In order for organisms to evolve from one form to another, new genetic information is needed in order to provide “instructions” for building the proteins and other features of the organism. Sanford clearly establishes that any expectation of getting new, useful information from these random processes is a completely blind trust in an impotent process. His book also provides an appendix with several more arguments against the Primary Axiom, along with answers to some counterarguments.

In conclusion, Sanford’s book builds a strong case against the Primary Axiom using modern scientific information combined with powerful, yet simple, logic. His arguments are solid but written on a level that can be understood by students and non-scientists. He clarifies several misconceptions about mutations, natural selection, and the overall decay of the genome. He accurately describes the concept and reality of genetic entropy, and he concludes from that principle our dependence upon the One who designed everything. Rather than viewing life as a purposeless by-product of the Primary Axiom, Sanford argues that genetic entropy points us to our need for and reliance upon God as the Creator. Perhaps this system of genetic decay is simply one more way God reminds us of the Fall (Genesis 3) and of our complete dependence upon Him.

REFERENCES

Behe, M. J. (2010), “Experimental Evolution, Loss-of-Function Mutations, and ‘the First Rule of Adaptive Evolution,’” Quarterly Review of Biology, 85[4]:419-445.

Sanford, J.C. (2008), Genetic Entropy & the Mystery of the Genome (Waterloo, NY: FMS Publications).

The post A Book Review and Summary of John C. Sanford’s Genetic Entropy and the Mystery of the Genome appeared first on Apologetics Press.

Next Generation Science Standards (NGSS) is currently developing the science standard for some 26 states. Now is the time to take action and speak out against the indoctrination of young minds with the bad science of evolutionary theory. If the science standards pass as they are written now, Darwinian evolution will be a required topic in your child’s science education, if you live in one of the states that adopts this standard. The NGSS is currently accepting input from the public over the next few days (until January 29, 2013) on the second draft of their proposed science standards in the form of a survey on their website (www.nextgenscience.org). We strongly recommend that you take five minutes and speak out for God and the biblical view of origins. Now may be the only time for many years (or ever) to let your voice be heard in a direct, effective way on this matter.

The Villa Rica church of Christ in Georgia is taking a lead in this effort, and has developed a website to help you in this process. If you need help getting straight to the critical issues in the science standard, click here (http://www.unity-in-christ.org/Articles/christians4science_is_an_apologe.html). At the top of that Web page are two red rectangular links that will be helpful to you in sifting through the information on the NGSS website.

Please let your voice be heard. There is absolutely no doubt that the promulgation of evolutionary theory in America’s school system is one of the most effective ways that Satan has “taken advantage of us” (2 Corinthians 2:11) over the last 50 years, turning Americans and the world away from the God of the Bible. But we are not “ignorant of his devices” (2 Corinthians 2:11). Remember the famous words of exhortation credited to Edmund Burke, a British statesman from the 1700s: “All that is necessary for the triumph of evil is that good men do nothing.” Take up the sword of truth, and fight with us.

The post Affecting the Next Generation Science Standards for the Lord (Update) appeared first on Apologetics Press.

[EDITOR’S NOTE: A.P. auxillary staff scientist Dr. Deweese holds a Ph.D. from  Vanderbilt University in Biochemistry.]

With the rapid advancement of genome sequencing technology, researchers have dramatically increased the number of genomes that have been completely sequenced in the last few years. This genomic information has vastly increased our knowledge of living organisms. Recently, researchers reported the complete genome sequence of gorillas (Scally, et al., 2012).

Evolutionists consider gorillas to be one of our “closest” living evolutionary relatives, second only to chimpanzees (Scally, et al.). One of the goals of genome sequencing is to examine whether the sequence supports the proposed evolutionary relationships. Comparisons of the nucleotide sequences have been used to generate hypothetical relationship trees (sometimes called “trees of life”). [NOTE: Comparing nucleotide sequences is similar to comparing letters between two books; more letters in the same order leads to the sequences being considered “more similar”—which evolutionists interpret as a reflection of evolutionary relationship. It should be noted that sequences that are only present in one of the “books” and not the other are ignored—thus, these are often not included in calculations of “similarity.” This and other technical details can result in a misunderstanding of the true amount of differences between organisms (cf. Cohen, 2007).]

What did they learn from this work? By comparing the already available human and chimpanzee sequences, the researchers concluded that 70% of the human and chimp genomes are more similar to each other than to the gorilla (Scally, et al.). However, 15% of the gorilla sequence was more similar to the human sequence than the chimpanzee sequence, and the remaining 15% of the gorilla sequence was closer to the chimpanzee sequence than the human sequence (Flatow, 2012; Smith, 2012).

Based upon the prevailing view of the evolutionary “tree,” the 15% higher similarity between humans and gorillas would not be predicted since humans would have more recently broken off from our supposed chimpanzee relatives. Thus, the DNA sequence would reasonably be expected to reflect this relationship. In order to explain the anomalies among chimp, gorilla, and human DNA, the concept of “incomplete lineage sorting” has been employed (Scally, et al.). According to this concept, interbreeding between early chimps, gorillas, and humans continued to occur for some time after the initial “split.” The interpretation is that different regions of the genomes reflect varying degrees of relatedness to the evolutionary “relatives” resulting from the interbreeding. This finding is not an isolated incident. A 2007 study found that 23% of the human genome shares “no immediate genetic ancestry with our closest living relative, the chimpanzee” (Ebersberger, Galgoczy, et al., 2007).

To boil these results down, researchers have found that some DNA sequences in humans, chimps, and gorillas are very similar, while other regions are not. In essence, some of the DNA could be interpreted to suggest relationship, while other parts do not support—and even contradict—these alleged relationships. A much simpler interpretation of DNA sequence similarities between various living organisms would be that humans, gorillas, and chimps are not evolutionarily related at all, and that common sequences represent common design features that were implemented by God for various creatures that share common biological processes, environments, and anatomy. Sequence similarities across species, then, reflect the preservation of key regions of DNA over time because of the essential functions encoded by these regions rather than evolutionary relationship. In fact, this concept can be used to identify potential functions for unexplored or poorly understood regions of various genomes by comparison with regions of known function in other organisms [NOTE: for a review of recently identified DNA functions, see Shapiro and von Sternberg, 2005 and Wells, 2011].  In this discussion, it is essential to recognize the difference between the facts and the interpretations placed on those facts.

Interestingly, there has been a slowly growing discontent regarding the concept of a universal tree of life, which is used to catalog evolutionary relationships. While still firmly holding to evolution, some scientists have suggested what would amount to a major overhaul of the concept, including some evolutionists who hold that there was not a single common ancestor of all life (Bapteste, Susko, et al., 2005; Doolittle, 2009; McInerney, Pisani, et al., 2011). While evolutionists continue to debate their interpretations of the facts, it will be interesting to watch for the next genomic breakthrough as God’s Word continues to be upheld by the evidence.

REFERENCES

Bapteste, E., E. Susko, et al. (2005), “Do Orthologous Gene Phylogenies Really Support Tree-Thinking?” BMCEvolutionary Biology, 5:33.

Cohen, J. (2007), “Evolutionary Biology. Relative Differences: The Myth of 1%,” Science, 316[5833]:1836.

Doolittle, W.F. (2009), “The Practice of Classification and the Theory of Evolution, and What the Demise of Charles Darwin’s Tree of Life Hypothesis Means for Both of Them,” Philosophical Transactions of the Royal Society B: Biological Sciences, 364[1527]:2221-2228.

Ebersberger, I., P. Galgoczy, et al. (2007), “Mapping Human Genetic Ancestry,” Molecular Biology and Evolution, 24[10]:2266-2276.

Flatow, I. (2012), “Gorilla Genome Sheds Light On Human Evolution,” Science Friday, http://www.npr.org/2012/03/09/148306985/gorilla-genome-sheds-light-on-human-evolution.

McInerney, J.O., D. Pisani, et al. (2011), “The Public Goods Hypothesis for the Evolution of Life on Earth,” Biology Direct, 6:41.

Scally, A., J.Y. Dutheil, et al. (2012), “Insights into Hominid Evolution from the Gorilla Genome Sequence,” Nature, 483[7388]:169-175.

Shapiro, J.A. and R. von Sternberg (2005), “Why Repetitive DNA is Essential to Genome Function,” Biological Reviews of the Cambridge Philosophical Society, 80[2]:227-250.

Smith, K. (2012), “Gorilla Joins the Genome Club,” Nature News, http://www.nature.com/news/gorilla-joins-the-genome-club-1.10185.

Wells, J. (2011), The Myth of Junk DNA (Seattle, WA: Discovery Institute Press).

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I have heard someone argue that changing even a few nucleotides in DNA could kill an organism. Is this a good argument to use against evolution since most theories of evolution involve genetic changes (mutations)?

A:

It is possible for a single amino acid change in a protein (which results from changing one to three nucleotides), or the deletion of a single nucleotide from DNA, to be fatal to an organism. In the scientific literature, this is called heterozygous lethal and instances can be identified by a search of literature databases (e.g., Burkitt-Wright, et al., 2012; Tsurusaki, et al., 2012). Heterozygous lethal means one of the two copies of a given gene in an organism are defective due to mutation (heterozygous) leading to the death of the organism (lethal). Normally, humans have two functional copies (homozygous) of all genes (except those on the X and Y chromosome in males). In some cases, mutations in one copy of the gene do not lead to a major problem (this is called “haplosufficiency”). When a gene is “haploinsufficient,” the loss of one copy of that gene can lead to major problems (like cancer) and sometimes death (as in heterozygous lethal).

While it is true that relatively “small” mutations can cause major problems and conversely, some “larger” mutations do not result in immediate lethality (for example, the extra copy of chromosome 21 in Down’s Syndrome), this argument may be missing a more relevant point. It is clear that mutations cause many problems, including cancer (Hanahan and Weinberg, 2011), and that documented mutations in long-term evolution experiments do not show major evidence for macroevolutionary change (Behe, 2010). Perhaps the more important point has to do with the types of changes that can be expected. As one geneticist argued in a recent book, mutations cause the decay of the “message” of the genome rather than the formation of new information (Sanford, 2008). A summary of long-term evolution experiments also suggests that even mutations considered “beneficial” (for the organism) in these studies generally involved the loss of genetic information (Behe, 2010).

In order for organisms to progressively evolve from one form to the next, new genetic information is needed. However, there is no known mechanism or natural process for generating new information (Gitt, 2005; Sanford, 2008; Meyer, 2009). Some theorize that naturally occurring mutation processes like duplication could account for increases in genetic information. But duplication does not explain the origin of the gene being duplicated, much less explain how position-specific nucleotide changes could develop a new feature or function (Sanford, 2008). The random mutations occurring naturally have no direction and do not have a “plan” for developing a particular function (Sanford, 2008). The expectation that random changes will develop new information does not fit the available evidence, nor is it statistically likely to occur (Sanford, 2008; Meyer, 2009; Behe, 2010). [NOTE: This topic gets very complex very quickly, and care should be taken any time this is discussed to be sure that the underlying science is very well understood. Misunderstanding can lead to misrepresentation, which can harm the cause and discredit those responsible.]

In summary, some very small, but very harmful, genetic changes have been documented, and their occurrence supports the concept that the genome is decaying over time (Sanford, 2008). A larger challenge for the macroevolutionary approach is to explain how new information can develop by random, undirected means in order to facilitate the development of new features and ultimately new organisms. A better explanation? We are here by design (Romans 1:20).

REFERENCES

Behe, M.J. (2010), “Experimental Evolution, Loss-of-Function Mutations, and ‘The First Rule of Adaptive Evolution,’” The Quarterly Review of Biology, 85[4]:419-445.

Burkitt-Wright, E.M., L. Bradley, et al. (2012), “Neonatal Lethal Costello Syndrome and Unusual Dinucleotide Deletion/Insertion Mutations in HRAS Predicting P. Gly 12Val,” American Journal of Medical Genetics Part A, 158A[5]:1102-1110.

Gitt, W. (2005), In the Beginning was Information: A Scientist Explains the Incredible Design in Nature (Green Forest, AR: Master Books).

Hanahan, D. and R.A. Weinberg (2011), “Hallmarks of Cancer: the Next Generation,” Cell, 144[5]:646-674.

Meyer, S.C. (2009), Signature in the Cell: DNA and the Evidence for Intelligent Design (New York: HarperOne).

Sanford, J.C. (2008), Genetic Entropy and the Mystery of the Genome (Waterloo, NY: FMS Publications).

Tsurusaki, Y., T. Kosho, et al. (2012), “Exome Sequencing in a Family with an X-Linked Lethal Malformation Syndrome: Clinical Consequences of Hemizygous Truncating OFD1 Mutations in Male Patients,” Clinical Genetics,  http://dx.doi.org/10.1111/j.1399-0004.2012.01885.x.

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Next Generation Science Standards (NGSS) is currently developing the science standard for some 26 states. Now is the time to take action and speak out against the indoctrination of young minds with the bad science of evolutionary theory. If the science standards pass as they are written now, Darwinian evolution will be a required topic in your child’s science education if you live in one of the states that adopts this standard. The NGSS is currently accepting input from the public over the next few days (until June 1) on their proposed science standards in the form of a survey on their website (www.nextgenscience.org/next-generation-science-standards). We strongly recommend that you take five minutes and speak out for God and the biblical view of origins. Now may be the only time for many years (or ever) to let your voice be heard in an effective way on this matter.

The Villa Rica church of Christ in Georgia is taking a lead in this effort, and have developed a website to help you in this process. If you need help getting straight to the critical issues in the science standard, click here (http://www.unity-in-christ.org/Articles/christians4science_is_an_apologe.html). At the top of that Web page are two red rectangle links that will be helpful to you in sifting through the information on the NGSS website.

Please let your voice be heard. There is absolutely no doubt that the promulgation of evolutionary theory in America’s school system is one of the most effective ways that Satan has “taken advantage of us” (2 Corinthians 2:11) over the last 50 years, turning Americans and the world away from the God of the Bible. But we are not “ignorant of his devices” (2 Corinthians 2:11). Remember the famous words of exhortation credited to Edmund Burke, a British statesman from the 1700s: “All that is necessary for the triumph of evil is that good men do nothing.” Take up the sword of truth, and fight with us.

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