BIOCHEMISTRY AND MOLECULAR BIOLOGY ARE INCONSISTENT WITH DARWINISM
BIOCHEMISTRY AND MOLECULAR BIOLOGY ARE INCONSISTENT WITH DARWINISM
Biochemistry and Molecular Biology are sciences of life. Biochemistry gives us catalysis, metabolism, regulation and communication. Then molecular biology takes that biochemistry and centers it on proteins, three-dimensional structure, DNA and RNA. Molecular biology explains how the 3-D structure of molecules determines the function of those molecules. Beyond structure and function, molecular biology describes how cells store, read, use and even reproduce that information.
When writing about evolution, authors frequently use words that conceal complexity. Neo-Darwinists especially glance over complex subjects. In this review of biochemistry and molecular biology I will place all complex concepts and systems in bold that I believe require more thought as we apply the life sciences to evolution. I encourage the reader to question how the natural selection of random mutations could be responsible for the creation of complex systems, concepts and information processing. The purpose of this paper is to illustrate that because the interplay of structure, function and information is so astronomically complex, Darwin’s theory of evolution by the natural selection of random mutations is not possible. I will divide this paper into two sections: the basic sciences of biochemistry and molecular biology, and examples of molecular biology in human systems.
All cells need amino acids as they are the building blocks of all proteins. There are over 300 amino acids found in nature, but the human body only uses 20. These 20 amino acids are almost completely of the left-handed type (amino acids found in nature may be either left or right-handed in shape and are usually present in a 50:50 ratio). Here is our first encounter with the specificity required for human anatomy and physiology. DNA determines each specific amino acid our bodies use.
Proteins are made of 20 different amino acids and each protein is made from a specific sequence of amino acids. Each sequence of amino acids produces a unique 3-D structure to the protein, which provides a unique function. Many proteins require over 1000 amino acids and the order must be exact—more specificity and less randomness. This takes us to the next topic—proteins.
Proteins are the most diverse class of biological molecules which make up enzymes, hormones, antibodies and muscle. Seventy percent of body weight is water and approximately 17% is protein. Cells make approximately 20,000 distinct proteins with variations of a core group of amino acids for a total of well over 100,000 different forms—specificity. Proteins fold in a manner that is dependent on their flexibility and electronegativity, into 3-D structures in ways that are not at all random. Ahern cites Cyrus Levinthal who in the 1960’s, “showed that the number of ways a small polypeptide of just 100 amino acids could fold would be in the same ballpark as the number of atoms in the universe.” Specificity has now become astronomical.
To assist in correct protein folding, cells have helper proteins called “molecular chaperones.” This adds another layer of complexity and moves the process of creation further away from random mutations. But for Darwinists it gets even worse. There are several classes of chaperones that work together to ensure proteins are properly folded. One class helps in the actual folding process. A second class works with misfolded proteins to allow them to refold correctly. A third class tags hopelessly misfolded proteins for destruction. There are two interesting chaperones that illustrate the extreme complexity and specificity of molecular biology. First, “heat shock proteins” refold partially heat-denatured proteins. Secondly, some chaperones provide a folding molecule with a temporary 3-D space where it can fold without interacting with other molecules.
These chaperones must be able to identify the 3-D shape of a molecule, “know” what the correct shape should be, then correct the shape or destroy the misfolded protein! This leads to 4 good questions. How much information does that require? How is that information achieved by Darwin’s random mutations? How many mutations did natural selection try and discard before hitting on the right ones? And lastly how much time did it take to obtain the right mutation? Remember, a misfolded protein results in non-functionality, disease or death. One example are prion diseases, which result from protein misfolding such as Creutzfeldt-Jacob disease, Kuru and “fatal familial insomnia” (and you thought you had trouble sleeping.) Darwinists have no answer except, “it takes billions of years.”
Now let’s get a little bit more specific and discuss a specific type of protein—an enzyme. Enzymes are just one type of protein without which life would be impossible.
Enzymes speed up a chemical reaction that would normally take millions of years in the absence of that enzyme! Remember, sequence and 3-D structure are all important; if you change the sequence of amino acids, you change the shape of the enzyme, which changes the function of the enzyme or the speed of the reaction.
The vast majority of biomolecules found in a cell are made by reactions catalyzed by enzymes. Every cell must have thousands of enzymes to catalyze the thousands of different types of molecules within that cell. What are the chances of all these thousands of harmonious enzymatic reactions occurring by Darwin’s random mutations? Now we are getting into specificity in linked reactions that must be exact.
At any given time, cells carry out thousands of metabolic reactions, breaking down and building up molecules. These reactions must occur extremely fast. As mentioned early, millions and even trillions of times faster than a naturally occurring reaction. Each cell manages billions of reactions every second. Excessive or insufficient enzyme activity results in disease and death. To “manage” the reactions, cells must sense levels of molecules then turn on enzymes to metabolize those molecules, keep the reaction on, then sense when to turn it off. These sensing systems demonstrate even more complexity that is indicative of highly engineered systems, not the gross morphology to which Darwin limited his investigation and Neo-Darwinist choose not to discuss. Since I brought it up, how do these enzymatic systems work? We are solidly within very specific, exact, complex systems.
Cells build molecules one step at a time where the product of reaction one is the substrate for reaction two, and so on. This sequence of ordered reactions is called a pathway. As an example, the pathway for making steroid hormones has 30 reactions that must occur in the correct order, and must be tightly regulated. Control of enzyme activity depends on; 1) being able to sense levels of different molecules, then 2) being able to increase or decrease enzyme activity in response to those levels. What to me is interesting from a philosophical perspective is that the instructions controlling DNA enzyme activity is provided by the DNA, which is being created by the enzyme controlled activity that DNA is creating. This is self-promoting and self-creating.
Another interesting example of systems-complexity are zymogens. Zymogens are enzymes that are inactive until needed. Blood clotting uses zymogens. The body makes all the proteins necessary for clot formation, but clotting remains inactive until needed. If the signals that activate this complex pathway are sensed incorrectly, death occurs from clotting or bleeding—pick your poison.
BASIC SCIENCE—MOLECULAR BIOLOGY
DNA AND RNA BASICS
We’ve learned that a human body is structured as an assembly of finely tuned, interacting 3-D molecules that function as nanomachines. Now with the advent of DNA and RNA, structure adds information to function. Specificity and complexity just took a quantum leap. A major function of the information in DNA is to provide instructions for making proteins. Amazingly, DNA also contains information that controls when and how proteins are made.
If DNA were stretched out it would be approximately 7 feet in length. But it gets stuffed into the nucleus of a cell that cannot be seen with the unaided eye. This is accomplished by dividing itself into 46 pieces—chromosomes. With an eye towards randomness versus complexity let’s examine DNA and RNA.
DNA in our cells constitutes our genome. Almost every cell in our body has the exact DNA copied very faithfully from the original instructions in the fertilized egg. Between fertilization and birth the number of cells grows to over 30 trillion.
While DNA stores information, RNA does the work of making the protein. DNA makes RNA, which then make proteins. DNA making RNA is called transcription and RNA coding for and making proteins is called translation, terms we all learned in high school. But what we didn’t learn is the extreme complexity of transcription and translation. Unlike DNA, RNA can fold into 3-D structures which allows it to carry out functions beyond encoding information.
There are three types of RNA: messenger RNA (mRNA), transfer RNA (tRNA) and ribosomal RNA (rRNA). Messenger RNA carries codon information for making protein from DNA to ribosomes, which are the site of synthesis of proteins. Transfer RNA carries amino acids to ribosomes and provides a decoder of the codons (codon is a sequence of three amino acids) called anti-codons. Ribosomal RNA provides a scaffolding where ribosomal proteins bind and form structures. Ultimately, RNA has three functions, catalysis, carrying information and protein synthesis. We will talk more about these three functions later, but first let’s look into an amazingly complex subject I have briefly touched upon when I mentioned copying DNA faithfully—DNA replication.
Each time a cell divides its DNA is copied: this is called replication. To replicate, cells need enzymes, primers, numerous proteins and a replisome. Two enzymes required for replication are helicase and topoisomerases. Helicase breaks hydrogen bonds in DNA and unwinds the helix at 6000 rpm. Topoisomerases relieve torsional stress of the unwinding DNA. SSB’s (single-strand binding proteins) keep the unwound strands of DNA separated. Without these proteins and enzymes working together, the unwinding strands of DNA would curl up and break apart just like the wood shavings that curl off a lathe and end up as broken pieces on the floor.
Replication requires dozens molecular structures with interesting names; clamp loader, replication fork enzyme, sliding clamps, RNA primer, primase, DNA ligase and telomerase to name a few. As you can imagine, with all of this complex machinery working at 6000 rpm, mistakes are going to happen. But the error rate in DNA replication is only 1 nucleotide in 10 million.
DNA replication comes equipped with numerous repair mechanisms. With 6 billion base pairs and an error rate of 1 in 10 million nucleotides copied, there could be 600 uncorrected mistakes per round of replication in each cell, even with proofreading. When coupled with the fact that the trillions of cells in the body that are dividing at any given time, the number of mistakes could be staggering.
One repair mechanism uses DNA polymerase, which adds a new nucleotide and double checks it to make sure it’s right in a process called proofreading. James Watson describes 7 other repair mechanisms in his textbook: 1) mismatch repair system, 2) recombinational repair, 3) double-strand break repair, 4) translesion synthesis, 5) base excision repair, 6) nucleotide excision repair, 7) nonhomologous end joining. As you can imagine just by the names, none of these repair mechanisms are simple one-trick ponies. They are all elaborate and highly complex mechanisms. For repair to occur the repair system must be able to; 1) scan the DNA, 2) identify the nucleotide, 3) remove the nucleotide and then 4) correctly fill the gap. This increasing complexity makes Darwin’s natural selection of random mutations embarrassingly inadequate. How does a repair mechanism gradually appear over time when we know a quarter, or a half of a repair mechanism is nonfunctional? Adding to the complexity of DNA replication, we turn from repair mechanisms to the phases of replication.
Cell replication becomes more complex with the addition of several phases occurring only when conditions are appropriate. This requires regulation, proofreading DNA, signaling and various mechanisms called check points that allow advancing from one phase to the next only after establishing that everything is in order. A human cell must replicate 6 billion base-pairs of DNA to divide. If the rate of replication was one nucleotide per second, it would take 190 years. To avoid this, DNA has 30,000 to 50,000 origins of replication. And to ensure that each origin of replication only fires once, a “licensing factor protein” is used then destroyed, otherwise runaway replication would occur. When DNA is replicated, every nucleotide is copied, however transcription (reading DNA sequences to make RNA) only copies selected regions of DNA. Let’s delve into transcription.
DNA TRANSCRIPTION INTO RNA
Regions of DNA that get transcribed into RNA are called genes. Human cells shuffle their genes to make 100,000 different proteins using fewer than 30,000 coding sequences. To do this, RNA polymerases must know where to start copying and where to stop. Since there are over 6 billion base-pairs of DNA and the average size of a gene is between 10,000 to 15,000 base pairs the challenge is immense. That is like finding a 5-foot stretch of road on a 60- mile trip. It takes promoters and terminators and lots of engineering.
Making matters even more complex, protein synthesis is energetically expensive. Proteins are made when needed, and in the amounts needed, and cells need different amounts at different times. Obviously, the complex transcription process becomes even more complex by the systems of regulation required. Here we see Darwin’s greatest error. Darwin narrowly focused his theory on gross shapes and structure of organs. Although that structure is more complex than he realized, what is astronomically more complex, and that which he avoided or did not comprehend are the associated communication and regulatory information systems. Neo-Darwinists cannot describe how random mutations gave rise to transcription, nor can they describe how our next topic came to be—translation.
TRANSLATING RNA INTO PROTEINS
Cells must read the information in mRNA and use it to direct protein synthesis. This occurs in three phases: initiation, elongation and termination. Each phase is once again very complex and requires numerous very specific 3-D biomolecules. Translation occurs at the rate of 15-20 amino acids per second or 45-60 nucleotides per second. Transcription must occur at a specific rate otherwise as translation occurs the two biomolecular systems will run into each other. Speed is not just interesting it is a well-controlled aspect of the entire system. Translation must put amino acids together in the right sequence. Next that sequence must fold into the correct 3-D structure. Then that 3-D structure must be transported to the right spot in the cell where it performs a specific function. Yes, it is a new concept, getting a biomolecule to the right place at the right time. And yes, it is even another layer of complexity. And no, the Neo-Darwinists cannot tell us how this system arose by the natural selection of random mutations.
Proteins have built in addresses, which is a portion of the amino acid sequence called a signal sequence—an address label. The now addressed amino acid sequence is ready to be transported and is helped to the right place by what are called carrier proteins. Now that we have DNA transcribed to RNA and RNA translated into proteins, it’s time to investigate protein synthesis and controls.
PROTEIN SYNTHESIS CONTROLS AND EPIGENETICS
Division of a fertilized egg produces over a trillion cells by the time a baby is born. Gene expression allows all these cells to be so different despite the fact that they all have identical DNA. Each different cell type uses a different subset of the genes in the DNA to synthesize a distinctive set of RNA’s and proteins. Cells can respond to change by increasing or decreasing the activity of a particular protein. And they alter which proteins are made at all.  They do this by regulating gene expression. So, we have just added another layer of regulation of proteins beyond the control of their activities. Now the question is what controls which genes will be expressed at a given time, where in the body, and to what extent? This regulation occurs via proteins called repressors, activators, inducers, promoters, enhancers and silencers. We are now in the realm of truly complex systems called epigenetic control—the overall control of what cells do which act over and above the information in DNA sequence. So what happens if this control is lost? Disease, disability and death happen when control is adversely affected. We call loss of genetic control a genetic disease.
Gene disorders affect 1 in 100 people worldwide. Ten thousand human diseases are caused by a single gene. Humans have 20,000 genes with over 10,000 gene-specific disorders. Rather than dwelling on grim statistics, let’s consider some interesting anatomy and physiology from a molecular biology perspective.
EXAMPLES OF MOLECULAR BIOLOGY IN HUMAN SYSTEMS: HEMOGLOBIN, HORMONES AND HEARING
The mechanism by which hemoglobin binds oxygen is interesting and an excellent example of how structure determines function. Hemoglobin changes its shape in the presence of oxygen in the lungs to accept as much oxygen as it can. Then, in the low oxygen content of tissues, hemoglobin releases oxygen. Hemoglobin loads and unloads oxygen because of complicated 3-D structural molecular cooperativity between structure and function. When a single oxygen molecule tugs an iron molecule a fraction of a nanometer the entire hemoglobin becomes loaded with oxygen before it exits the lungs. The opposite occurs in low oxygen content of the peripheral tissues.
But hemoglobin has other tricks as well. It binds carbon dioxide and protons, which affect the pH of blood. If the blood is too acidic or alkaline death occurs. Just to make matters more complicated, there is a difference in hemoglobin used by a fetus. Unique fetal hemoglobin is required because the fetus is taking oxygen directly from the placenta not the lungs. Remember, the structure of fetal hemoglobin is coded in our DNA and production must be shut off after birth—more complexity.
Communication systems are constantly active in our bodies, relaying information about internal and external conditions of our cells. Humans have over 200 types of cells in our bodies. Communication and coordination between these cell types occurs by hormones. Endocrine glands release hormones only inside the blood stream (pineal gland, pituitary gland, thyroid gland, parathyroid, thymus, adrenals, pancreas and ovaries or testes).
Cellular communications depend on biomolecular messages and biomolecular receivers, which trigger information transmission that results in cellular changes. Errors in communication result in disease or death. Cellular communication involves sensing and signaling, and hormones are communication molecules of which there are two types. First, are those hormones that act within minutes through binding receptors on the surface of cell membranes. Second, steroid hormones act slowly and bind to receptors inside cells. As you can imagine, signaling occurs in a variety of complex ways adding to the Darwinist’s dilemma.
HEARING (AND OTHER SENSES)
Receptors for sight, sound, taste, smell and feel offer distinct inputs that we must assemble, interpret and then respond to. These interacting systems demonstrate the extreme complexity of human anatomy and physiology. But let’s begin with sound. It seems I can’t move past Darwin flippantly dismissing hearing as if it was just another thing you could pick up at Walmart, “How a nerve comes to be sensitive to light, hardly concerns us more than how life itself first originated: but I may remark that several facts make me suspect that any sensitive nerve may be rendered sensitive to light, and likewise to those coarser vibrations of the air which produce sound.” The sensitivity of the hearing mechanism is such that movements as small as half the diameter of an atom can be detected.
Interestingly, sound is processed at a rate of tens of microseconds while vision is slower. This means that when an event occurs, such as snapping your fingers, the brain must patch the two stimuli of vision and hearing together and present it to your consciousness as one event. The consequence of delaying information processing and patching signals together means that we all live just a little bit in the past. Before concluding this paper, I’d like to throw in just a couple more examples—taste and vision.
Taste is comprised of salty, sour, sweet, umami and bitter. Salty and sour produce signals via sodium and calcium channels which lead to an electric potential that sends a message to the brain. Sweet, umami and bitter use three distinct G-protein-coupled receptors which then activate another G-protein (Gustducin) again ultimately activating ion channels. Bitter is the most complex taste and requires 43 genes. Oddly, taste receptors are found in places other than our mouths. Sweet receptors are found in the intestines and probably help with glucose metabolism control. Bitter receptors are found in the lungs.
Darwin was concerned with the optics of vision, how the eye focuses light and how aberrations are corrected. He was admittedly not interested in how the brain interprets optical information as we have seen. Darwin literally dismisses the most complex part of vision, which involves amazing anatomy, physiology and molecular biology. He disregards the complex signal processing and information handling of vision. But unlike Darwin, how a nerve is sensitive to light (and sound) is of great concern to anyone who is serious about science.
Without belaboring the point (which may be impossible to do when the point is astronomically complex) I will just mention areas of research involving the neuroscience of vision. In a textbook edited by Chalupa and Werner, the authors provide over 1,700 pages of visual neuroscience, anatomy, physiology and molecular biology. Here is a partial list of the sections—remember each concept is a manifestation of molecular biology:
- Developmental Processes—the authors discuss the development of the retina, visual function, the numbers and types of cells, cortical connectivity, spatial selectivity, response timing and plasticity.
- Retinal Mechanisms and Processes—topics include transduction, retinal circuitry, synapses, neurotransmitters, molecules of visual signaling, physiology of several types of cells, and spatial regularity.
- Organization of Visual Pathways—including visual areas in the cortex, the communications between cortical areas, and discussion of ventral and dorsal cortical processing systems.
- Subcortical Processing—visual relays and functions of different structures involved in vision as well as discussion of feedback systems.
- Detection and Sampling—the authors investigate the formation and acquisition of retinal image, how signal noise is handled, and rod-cone interactions.
- Brightness and Color—including brightness, lightness, color, molecular genetics, retinal circuitry.
- Attention and Cognition—authors investigate human visual attention and the role attention plays in the cerebral cortex.
- Theoretical and Computational Perspectives—authors discuss boundaries, surfaces, motion and the neural basis of visual consciousness.
As mentioned earlier this list is incomplete, nevertheless, the complexity of vision seems overwhelming. Although Darwin seemed to be totally disinterested in how a nerve becomes sensitive to light (or sound), I think even he would have been fascinated by some amazing molecular biology of vision. There are approximately 130 million photoreceptors in the retina which absorb light then transmit signals to the brain. The bandwidth of the human retina is approximately 9 megabits per second, which is about the same bandwidth as a standard DVD. Much video posted on the web is less than 1 megabit per second.
I could go on sharing amazing examples of molecular biology of human anatomy and physiology. Many books have been written on the subject; but I believe I have presented enough information to demonstrate that the human body is complex beyond our understanding. Furthermore, one cannot help but conclude that believing we were created by Darwin’s natural selection of random mutations is intellectually embarrassing.
Human anatomy and physiology demonstrate engineering complexity that is nothing less than astounding. Biochemistry and molecular biology demonstrate how that astonishing complexity is conveyed to the molecular level. In this paper we discussed six complex concepts that are active throughout the human body. Neo-Darwinists never discuss how the natural selection of random mutations overcomes:
- Specificity—specificity is ubiquitous in human anatomy and physiology. Specificity occurs in 3-D shape and function, as well as complex chemical reactions and pathways.
- Speed—speed is not normally thought of as a complex system, however, we saw how speed is not only important but absolutely crucial to life.
- Transportation—the transportation of molecular structures is highly complex and highly regulated.
- Molecular folding—how molecules fold into unique 3-D structures creates a dilemma for Neo-Darwinists. To suggest that folding into a unique 3-D shape, with a unique function can occur by the natural selection of random mutations is paramount to believing that your car’s engine was created when all the different parts randomly appeared one molecule at a time and fell together over billions of years to produce a functional engine.
- Epigenetic control—epigenetic control produces a remarkable level of information control above mere sequence of nucleotides. Neo-Darwinists seem to suggest a nearly one to one relationship with a gene and a protein. But the reality is much more complex as we have seen. Every cell uses different pieces of the DNA at different times and at different rates. This kind of genetic regulation and expression is not well understood and rather miraculous.
- Information and the language of DNA—molecular biology demonstrates that human anatomy and physiology is not just dependent upon information—human anatomy and physiology is This leads us to the question, which came first the language of DNA (codons) or the information required for the language? Did humans learn to talk then develop something to talk about, or were they dealing with information and having thoughts that required a language to express? DNA is a profound enigma that could not have occurred by the natural selection of random mutations.
Darwin himself gave us the reason why his theory fails, “If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down.” As we noted previously, Darwin was only interested in the gross shape of singular organs. He completely ignored (and Neo-Darwinists of today continue to ignore) the development of complex systems. Biochemistry and molecular biology provide structure and function that could not possibly have been created by numerous, successive, slight modifications and thus Darwin’s theory absolutely breaks down.
 Kevin Ahern, “Biochemistry and Molecular Biology: How Life Works,” Vols I and II. In The Great Courses (Chantilly: The Teaching Company, 2019), Vol II. p. 133.
 Ahern, Vol I. p. 66.
 Id., 65.
 Id., 98
 Id., 68.
 Id., 113.
 Id., 117.
 Id, 117.
 Id., 117.
 Id., 118.
 Id., 121.
 Id., 23.
 Id., 24.
 Id., 158.
 Id., 179.
 Id., 180.
 Id., 180.
 Id., 183.
 Id., 154.
 Id., 170.
 Id., 156.
 Id., 172.
 Id., 173.
 James Watson, Molecular Biology of the Gene, 6th edition (San Francisco: Cold Spring Harbor Laboratory Press, 2008), p. 217.
 Ahern, Vol II. p. 213.
 Id., p. 178.
 Watson, p. 260.
 Id., 269.
 Id., 278.
 Id., 270.
 Id., 276.
 Id., 217.
 Ahern, Vol II. p. 192.
 Id., 193.
 Id., 194.
 Id., 260.
 Id., 263.
 Id., 265.
 Id., 289.
 Id., 290.
 Id., 291.
 Id., 291.
 Id., 291.
 Id., 306.
 Id., 306.
 Id., 306.
 Id., 308.
 Id., 311.
 Id., 313.
 Id., 330.
 Id., 331.
 Ahern, Vol I. p. 139.
 Id., p. 141.
 Id., p. 144.
 Ahern, Vol II. p. 59.
 Id., p. 60.
 Id., p. 62.
 Id., p. 60.
 Charles Darwin, On the Origin of Species: The Illustrated Edition, David Quammen (New York: Sterling Publishing, 2011), 189.
 Ahern, Vol II. p. 110.
 Id., 104.
 Id., 105.
 Leo Chalupa and John Werner, The Visual Neurosciences Vol. 1 and 2 (Cambridge: MIT Press, 2004), Vol. 1, 31.
 Chalupa, Vol. 1, 213.
 Id., 479.
 Id., 563.
 Id., 793.
 Id., 879.
 Chalupa, Vol. 2, 1499.
 Id., 1561.
 Ahern, Vol. II. p. 107.
 Darwin, p. 191.
Leave a Reply