The Antarctic Icefish: Intelligently Designed
The biochemist Michael Behe distinguishes between evolution, the idea that organisms derive from their ancestors, and the process by which evolution occurs. There is almost universal agreement that evolution does happen. The debate is whether changes develop by random mutation, as in Darwinian evolution, or by the addition of designed units, as in the theory of intelligent design.
It is becoming clear that a mutation can cause only limited changes, such as those Darwin saw in Galápagos finches. Intelligent design is the only mechanism powerful enough to cause complexity. Only intelligent design explains the origin of the Antarctic icefish, which outcompetes supposedly stronger fish in water colder than zero degrees centigrade. If the idea of an abstract designer is difficult to accept, imagine that the designer is from an alien civilization millions of years older than humanity.
Darwin specified the criterion for rejecting Darwinian evolution
Charles Darwin was a thoughtful scientist and acknowledged the problems with his concept of evolution. He admitted that the problem posed by the eye gave him a cold shudder. “To suppose that the eye with all its inimitable contrivances … could have been formed by natural selection, seems, I freely confess, absurd in the highest degree. Yet reason tells me, that if numerous gradations from a perfect and complex eye to one very imperfect and simple, each grade being useful to its possessor, can be shown to exist; … then the difficulty of believing that a perfect and complex eye could be formed by natural selection, though insuperable by our imagination, can hardly be considered real.”
Identification of the predicted transitional forms has been elusive. According to the Wikipedia, a transitional form “has not been found, nor is it expected to be found. Fossilization rarely preserves soft tissues, and even if it did, … as the remains desiccated, or as sediment overburden forced the layers together, … the fossilized eye [would] resemble the previous layout.”
In other words, the evidence to disprove Darwin’s prediction is missing. Blaming the incompleteness of the fossil record strikes me just as hearing “the dog ate my homework” must strike students who actually did their homework. The inability to test a scientific theory makes it “nonfasifiable.” To some scientists, nonfalsifiablility is the hallmark of pseudoscience, a criticism often inaccurately levied at intelligent design. As we shall see, the key elements of intelligent design, irreducible complexity and fine-tuning, have been tested numerous times.
According to Darwinists, beneficial mutations give an animal a competitive edge, increasing the chance it will pass its genes to another generation. One problem for Darwinian evolution is that the chances a mutation will be beneficial decrease as the complexity of the animal increases. Which outcome is likelier: that a random change in the software code of a jet airliner will make it fly better or that it will cause it to crash?
The credibility of Darwinian evolution depends on how much statistical improbability one is willing to accept. When the odds of a random mutation explaining an observation get too long, Darwinists may need a god to pray to. We’ll say they pray to Fortuna, the Roman goddess of chance.
Irreducible complexity
In the 19th century, when Darwin lived, scientists had no idea that life was driven by chemical reactions that capture energy from food and synthesize building blocks for infrastructure. It was not until the 20th century that biochemists opened what Behe calls “Darwin’s Black Box” in his excellent book by that name, revealing the complexity of life on a molecular level.
In his book, Behe advances the idea of irreducible complexity to describe the property of functioning only when all the components of an entity are present and operating. Without one part, the entity ceases working. A mousetrap is an example of irreducible complexity. Further, the individual components are otherwise useless and would tend to be eliminated in a competitive environment.
Because competitiveness is improved by a beneficial trait, not a potential trait, irreducible systems present as a functional unit, not one part at a time. According to intelligent design, major evolutionary advances arise by the addition of irreducibly complex units to an organism. The possibility of irreducible complexity arising by chance decreases as the number and complexity of components increase. Thus, irreducible complexity is much likelier to be the result of design.
Glycolysis, the Calvin cycle, citric acid cycle, urea cycle, pentose phosphate shunt, and electron transport chain are examples of multistep biochemical pathways. Such pathways have been described as “nano-engineering that surpass[es] anything human engineers have created.” Many antibiotics, chemotherapeutic agents, and poisons interrupt these pathways, killing bacteria, cancer cells, insect pests, and weeds.
These pathways can be thought of as assembly lines in which a raw material is transformed in multiple steps to produce a finished product and, often, waste material. Each step in the assembly line is really a different chemical reaction, and the work at each step is performed by a protein.
Proteins are molecular machines composed of chains of smaller molecules that fold in very specific ways to generate a three-dimensional structure.
Bacteria have hundreds to thousands of different proteins, and humans have approximately 20,000. Proteins are so complex it has been argued that they cannot evolve via random mutation. One reason is that it would be impossible for a random process to test the functionality of more than a fraction of possible protein sequences. An average size protein can be made from 10^390 different chains. That is 1 followed by 390 zeros. It is estimated that a random process would “stumble onto a functional protein only about one in every 10^50 to 10^74 attempts.” For comparison, the universe is only 4.4 x10^17 seconds old.
We know now that cells can contain hundreds of chemical pathways, each of which may be irreducibly complex, powered by millions of nanomachines so complex that Darwinian evolution may not explain their presence.
Inherited metabolic diseases disprove that biochemical complexity arose via Darwinian evolution
Darwinists maintain that these pathways could have evolved one step at a time if an organism can live without the complete pathway and if the intermediate products are nontoxic. This is disproven by more than one thousand diseases known as inborn errors of metabolism. These diseases develop because a pathway is interrupted by a mutation. They demonstrate that an incomplete pathway can’t maintain health. In some, it is because an incomplete pathway allows the accumulation of a product that damages the cell.
Tay-Sachs disease is one example. In this disease, cells are unable to eliminate one kind of fatty molecule. Instead, these molecules accumulate, damaging the brain and spinal cord. When an infant is completely unable to eliminate these molecules, death occurs by age 3 to 5. If they cannot be eliminated, these molecules are useless. This makes the multistep pathway to synthesize, utilize, and eliminate these molecules irreducibly complex.
Scientists purposely knock out proteins in experimental animals to determine the protein’s effect on health. Analogously, these diseases knock out proteins, and the outcome demonstrates that the affected proteins are essential. These diseases conclusively show that as a rule, metabolic pathways could not have evolved one step at a time regardless of how long life has existed. This is because, generally speaking, normal functioning of these pathways is necessary to support life long enough to allow reproduction. Interrupting these pathways is harmful to all life that has them, including bacteria. Disease is the predictable outcome when even a small change is made in an irreducibly complex system.
Darwin conceded that if a complex system was found that could not have developed by numerous successive slight modifications, his theory would “break down.” Behe notes that “as the number of unexplained, irreducibly complex biological systems increases, our confidence that Darwin’s criterion of failure has been met skyrockets toward the maximum science allows.”
To save Darwinian evolution, Darwinists argue, without evidence, that irreducible complexity is just an appearance caused by pre-existing proteins that mutated to cooperate in a metabolic pathway. This explanation has the pat feel of one of Rudyard Kipling’s Just So Stories, such as “How the Elephant Got His Trunk”: the trunk stretched when a crocodile tried to pull an elephant into a river by its nose.
The Darwinist rebuttal to irreducible complexity is as speculative as biology gets. There are few data to suggest how many beneficial random mutations are necessary for their conjecture. The number of inborn errors of metabolism, roughly 1000, can yield a rough estimate of the number of metabolic pathways. This estimate may be low because mutation may knock out some pathways that are necessary for survival to birth, meaning that the error would not be recognized as a disease. I estimate that each pathway utilizes an average of 10 proteins. Thus, approximately 10,000 proteins are involved in metabolic pathways.
There are no data about the number of mutations necessary for two proteins to co-evolve and cooperate in a pathway. I very conservatively estimate that three mutations per protein are necessary. Thus, at a minimum, 30,000 beneficial mutations placed with surgical precision may suffice for Darwinian evolution to produce the irreducible complexity in a cell. Is this even possible? All experts agree that beneficial mutations are rare. One estimate is that only 1 in 1000 mutations is beneficial. Further, harmful mutations can destroy the function previously gained through a beneficial mutation. This is another of the arguments against Darwinian evolution of proteins.
An irreducibly complex system didn’t develop in 10^13 E. coli bacteria observed for 25 years, 10^20 human immunodeficiency viruses studied over decades, or the 10^20 malarial microbes that arise every year. During that time, many random mutations have been observed, such as those which create drug resistance. These are baby steps in evolution, called “microevolution.” However, an increase in complexity, or “macroevolution,” has not been seen despite 10^53 chances. It is not surprising that an assessment in 2020 concluded that “there are presently no detailed Darwinian accounts of the evolution of [irreducible complexity], ‘only a variety of wishful speculations.’”
This might be a good time for Darwinists to pray for the intercession of Fortuna: “O Fortuna, once more unto the breach of plausibility to save Darwinian evolution!”
Life is the ultimate example of irreducible complexity. Cells require energy to make proteins. However, energy production requires several of the multistep pathways mentioned above, all of which involve multiple proteins. The sequence of molecules in the chain of a protein is specified by DNA. This information is translated into protein by RNA. Both DNA and RNA require energy and proteins to synthesize them. These are just some of the chicken-and-egg problems that make life irreducibly complex.
Computer modeling and statistics also can be used to assess which process, random mutation or design, is more likely to result in cellular complexity. Computer models have not been able to re-create irreducible complexity, and irreducible complexity has been modeled that cannot develop by evolution. Also, a process called fine-tuning is being studied statistically. Fine-tuning describes the development of a process that functions only when all parts fit with each other perfectly. Extremely tight tolerances are unlikely to arise randomly. Like irreducible complexity, fine-tuning is evidence of design. The publication that introduced fine-tuning to biology in 2020 concluded that “fine-tuning is a clear feature of biological systems. Indeed, fine-tuning is even more extreme in biological systems than in inorganic systems.” Fortuna to intensive care, stat!
Antarctic icefish
Antarctic icefish are one of the few species of fish that thrive in Antarctic waters. They are an example of fine-tuning and irreducible complexity involving an entire animal, not just chemical pathways.
Survival in Antarctic waters requires multiple modifications, including decreased blood viscosity. Viscosity describes the thickness of a fluid. Honey is more viscous than water, for example. Viscosity increases with decreasing temperature, creating a potential problem in Antarctic waters. At the temperature of Antarctic waters, human blood would be too thick to sustain life, like an automobile engine that “freezes” in cold weather because the crankcase oil is too thick.
The concentration of red blood cells is the strongest determinant of blood viscosity. Red blood cells contain hemoglobin, the protein that carries oxygen. Icefish have solved the viscosity problem by eliminating hemoglobin and red blood cells, making icefish “white-blooded.” They are unique among vertebrates in this regard. The loss of hemoglobin is possible because more oxygen dissolves in seawater and blood as their temperatures drop.
Nevertheless, icefish blood still carries less oxygen than red blood, so its heart pumps more blood than do the hearts of comparable red-blooded fish. This requires blood vessels that offer less resistance. Icefish have three times as many capillaries as red-blooded fish. This not only decreases resistance, but also increases contact between oxygen and tissue.
Icefish are fine-tuned and irreducibly complex
The result is a circulatory system that allows the icefish to thrive where red-blooded fish can’t. The icefish’s white blood is perfectly matched to its heart, which is perfectly matched to its blood vessels. Exchange any of these components with one from a red-blooded fish, and the icefish will die. These changes also had to occur at the same time, not in steps, making the icefish’s cardiovascular system irreducibly complex.
In addition to their highly customized circulatory system, icefish need antifreeze and other changes to live in Antarctic water. If these changes were accomplished with a single mutation in a red-blooded fish, I will congratulate Darwin and Fortuna. If not, I will congratulate the designer for very fine work.
The success of icefish confounds Darwinists, who cannot accept that the loss of hemoglobin could be anything but a handicap that icefish managed to overcome. This is seen in the title of a peer-reviewed article, “When bad things happen to good fish: the loss of hemoglobin and myoglobin expression in Antarctic icefishes,” and this statement from Scientific American: “[D]espite an evolutionary blunder that would be lethal to most fish, the icefishes’ grit — as well as a little ecological serendipity — rescued them from their own bad blood.”
In the view of these authors, Antarctic waters are a refuge for anemic mutants, an “isle of misfit toys.” Obviously, icefish don’t have grit or pluck. Not one molecule of either. Those willing to argue that icefish survive in spite of, not because of, losing hemoglobin must resort to anthropomorphizing the icefish into a scrappy underdog to justify violating the Darwinist principle of survival of the fittest.
A personal note
From the perspective of a physician, Darwinists do not place enough emphasis on health, if they consider it at all. An automotive engineer considers the optimal viscosity of motor oil more than Darwinists consider optimal blood viscosity when theorizing about icefish. Elevated blood viscosity kills humans with leukemias, in which blood viscosity is too high because too many white blood cells are present, and polycythemia vera, in which blood viscosity is fatally elevated because too many red blood cells are present. An engineer would never consider removing a steel girder from a bridge design as blithely as Darwinists propose removing a protein from a metabolic pathway.
The belief that cells are the result of random mutations necessitates ignoring, underestimating, or downplaying their undeniable complexity. The Darwinist mindset is perhaps not surprising given that they consider health to be the outcome of good luck, not good design. If Darwinists were forced to consider health, their musing would be strongly constrained.
In a lecture to my medical school class, the noted ophthalmologist Marguerite McDonald, M.D., described the impact of a sudden insight as “touching the sun.” When I learned of intelligent design after the publication of Darwin’s Black Box, I felt as though I had touched the sun. Finally, science was acknowledging the shortcomings of Darwinian evolution.
The superiority of intelligent design to Darwinism is clear. Random mutations can account for changes in only one trait, not for the wholesale complexity present in every cell of every organism.
Paradigm shifts take longer than necessary because scientists are no better than anyone else at keeping an open mind and admitting when they are wrong. The shift from Darwinism to intelligent design will be even more turbulent because of the resistance in some of accepting the existence of a higher power. The media compound the difficulty by conflating intelligent design and Creationism. Hopefully, one day humanity will accept the scientific evidence of God. It doesn’t take a microscope to look at the night sky and see the work of a power greater than ours.
