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.
- NEUROSCIENCE INVALIDATES DARWIN’S THEORY OF EVOLUTION (9/11/2020)
NEUROSCIENCE INVALIDATES DARWIN’S THEORY OF EVOLUTION
Darwin’s theory of evolution by the natural selection of random mutations fails as a scientific theory. The authors of the state-of-the-art textbook, Neuroscience, 6 Ed. (Oxford, 2018), proclaim their belief in Darwinism. They state, “As the geneticist Theodosius Dobzhansky famously said, “Nothing in biology makes sense save in the light of evolution.” I disagree and claim Darwinism fails miserably as a scientific theory. I will use the evidence presented in Neuroscience, much to the authors’ dismay, to support my argument.
Let’s look closer at Dobzhansky’s statement. If nothing makes sense in biology without considering Darwinism, it would not be possible to make advances in the sciences of molecular biology, molecular genetics and medicine without demonstrating how and why Darwinism is integral. I can promise you, after 38 years as a physician treating patients in the emergency department, I never once had to consider Darwinian evolution. This is because Darwinism is not only not integral, Darwinism is not a scientific theory. Darwinism is a worldview—a metaphysic, or in some cases a religion. Dobzhansky and the authors of Neuroscience are clearly incorrect. All of medicine, anatomy and physiology makes perfect sense in the absence of Darwinism.
Darwin believed (and Neo-Darwinists today continue to believe) that humans were created by the natural selection of random mutations. But the complexity of the human body—and in this essay the central nervous system specifically—is blatantly inconsistent with Darwin’s theory. Darwin dismisses complexity, claiming the fossil record would provide the evidence to prove his theory correct. But the fossil record has not rescued his theory. In fact, as scientists learn more and more about molecular biology, genetics and other health related sciences, complexity explodes. As complexity increases, Darwin’s theory becomes more unrealistic.
Neuroscience possesses astonishing complexity, and the neuroscience of a developing brain only exaggerates this complexity. There is no better example of how Neo-Darwinists dismiss complexity than their avoidance of the role DNA plays in embryology. Remember Darwin based his theory on the proposition that, “[N]o complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications. . .” This ignores embryology and the role DNA plays in every developing organ. On that fact alone Darwin’s theory fails. Nevertheless, the complexity of embryology needs explaining. Therefore, in this essay I will clarify four very complex elements of the neuroscience of developing brains. I will provide the reader with logical questions that Neo-Darwinists should be asking but are not. In doing so we will discover patterns, or paradigms, that exist in the Neo-Darwinian worldview.
This essay is divided into four sections: A. Overview of Early Brain Development, B. Formation of the Central Nervous System, C. Formation of Major Brain Regions, and D. The Molecular Basis of Neural Induction.
A. Overview of Early Brain Development
All anatomy and physiology of the human body exists, and is dependent upon, information encoded in human DNA (which itself exists, and is dependent upon, information encoded in human DNA). Neo-Darwinists neglect the fact that the human body must be created from two cells that transform over time and proceed through various, unique stages of development: embryo, fetus, child, and adult. Each stage requires distinctive and very precise DNA instructions. Those DNA instructions for the dynamically, transforming human reside within the DNA. What are the nucleotide sequences of each piece of information in that code? How is this code activated, and how is it shut down when it is temporarily or permanently no longer needed? Neo-Darwinists do not have the answers and would like us to ignore the questions.
Nonetheless, with these questions in mind, let’s begin observing what logical questions are neglected. According to the authors of Neuroscience, who discuss embryology and development of the central nervous system, the human brain is a “product of cell-to-cell signals, genetic instructions, and their consequences. . .[T]he initial formation of the major brain regions, the generation of neurons and glial cells from undifferentiated neural stem or precursor cells and the migration of neurons. . .These processes set the stage for the subsequent differentiation of local dendrites, axons, and synapses as well as long distance axon pathways.”
That one paragraph from Neuroscience, is packed with complex information regarding operational systems and structures. Scientists do not fully understand how these operational systems work, other than they are controlled by information within DNA. And that is my point. It is insufficient to state that “it’s in the DNA,” and then imply we fully understand DNA. Where in the DNA do the instructions exist? What are the responsible nucleotide sequences? How do the responsible nucleotide sequences transform information into structure and function? These are questions that Neo-Darwinists cannot answer, and they are questions that Neo-Darwinists never ask because they know the natural selection of random mutations cannot cause this degree of complexity. But we will ask in order to illustrate how little is actually known about human anatomy and physiology. And by asking we will demonstrate how unrealistic it is to believe in Darwinism.
The cited paragraph above is an excellent example of how, throughout the literature that supports Darwinism, you will read about complex systems and structures that are merely mentioned but never explained. It seems that authors confuse readers with facts then move on quickly before anyone has a chance to ask questions that they should be asking.
Let’s see how this intellectual laziness manifests by dissecting the cited paragraph. First, cell-to-cell signaling requires knowledge of how signals are sent and received, what information is passed, and why that information is needed. Second, neurons and glial cells must “generate” neurons, and neurons must “migrate.” How does this happen? Can anything go wrong when something generates or migrates? Why do structures migrate, and from where to where? How do they know when to stop migrating? Then there is the question of “differentiation.” How do dendrites, axons, synapses and axon pathways differentiate? What do they differentiate from, and what do they become? How does that work? Remarkably, there are no answers to all these questions. In fact, rather than answers, scientists keep making more unexplained observations.
Does it make any sense that a scientist is more likely to answer these questions if he or she believes structure and function arose from random mutations; or is it more likely that a curious mind will search for specific answers if he or she believes there is a specific design that can ultimately be discovered?
In this section we saw how complex systems and structures are mentioned but not explained. Now let’s see what we can observe in the next section.
A. Formation of the Central Nervous System
As the spherical mass of embryonic cells expands, numerous complex operations (or processes) form numerous structures. One of the first complex process, gastrulation, forms the structure, the gastrula. Gastrulation is the process where the single-layered hollow sphere of embryonic cells is reorganized into a multilayered structure called the gastrula. The following is how the authors describe gastrulation, and once again it illustrates how complex systems and structures are mentioned but not explained, “Gastrulation begins as a local invagination of a subset of cells in the very early embryo… by time invagination is complete, the embryo consists of three layers of cells called the germ layers: an outer ectoderm; a middle mesoderm;… and an inner endoderm…[which] determine the position of all organ systems…”
Look at the complex operations that are not explained; “invagination of a subset of cells.” How do cells know how to “invaginate,” and which cells invaginate? How do they know when to stop invaginating? What are the nucleotide sequences that control that process? Which “subset” of cells do all this work, and why those and only those? How is the process of “determining” the position of all organ systems accomplished? The authors give us observations, not explanations. Claiming Darwinism is the mechanism that explains these astronomically complex operations is preposterous and is merely an argument from ignorance.
Let’s proceed. The notochord is a cylinder of mesodermal cells that defines the long axis of the body. It is a temporary structure that disappears once early development is complete. The notochord sends inductive signals to the overlying ectoderm that cause a subset of cells to differentiate in a process called neurulation. The neuroectoderm lying above the notochord gives rise to the entire nervous system.
This process of neurulation is filled with complex structures: neuroectodermal precursor cells, neural plate, neural tube, floorplate and neural stem cells. It is the neural stem cells that give rise to the entire brain, spinal cord and most of the peripheral nervous system including all the cell types.
Look at the complex operation of the notochord, which is merely a temporary structure. The notochord “sends inductive signals.” Sending signals is not a simple singular function! Signals are created because they are needed. Signals must have the correct information and receiving cells must know what to do with the signals. This is a tremendously complex operation and no Neo-Darwinist can describe which nucleotides mutated from what to what, over what period of time, in order to produce the specific desired outcome of signaling. The outcome of signaling must be desired and specific because the developing brain cannot tolerate ambiguous information.
The authors conclude the section on early brain development with this illustrative, albeit long and complex sentence, “The past decades have witnessed an explosion of molecular biological knowledge about the inductive signaling events and their consequences for gene expression and differentiation that transform neuroectodermal precursors and neural stem cells into the diverse cell and tissue types of the nervous system, including the neural crest.”
Once again, observations without explanations. The complexity of the sentence above is so great it is difficult to follow even as a mere observation. The explanations of these complex systems, operations and structures would fill books. This complexity demonstrates that Darwin’s theory of evolution could only have been proposed in the 1800’s or earlier, before significant scientific knowledge was discovered.
B. Formation of Major Brain Regions
The authors go into significant detail in this section, but I will merely mention operations and structures to illustrate our developing paradigms. The authors state, “Soon after the neural tube forms, the forerunners of the major brain regions become apparent as a result of morphogenetic movements that bend, fold, and constrict the tube. . .Once the primitive brain regions are established, they undergo at least two more rounds of partitioning. . .”
Any inquisitive person would likely ask, how do the cells know when and where to bend, fold and constrict? Which cells do this, and which cells do not? How do they know when to stop bending, folding and constricting? If these morphogenic movements are not done precisely in this early stage of development, the results will be disastrous.
The following is a partial list of structures, mentioned by the authors, that are involved in the developing brain: cephalic flexure, prosencephalon, mesencephalon, rhombencephalon, telencephalon, ganglionic eminences, diencephalon, optic vesicles, metencephalon, myelencephalon. These structures, like all structures, are created from encoded information in DNA. There is no randomness in the structure of a developing brain. It is irrational to think a random process creates non-random structures.
C. The Molecular Basis of Neural Induction
The molecular biology of the developing brain is overwhelmingly complex. As the brain develops, there are changes that occur within the spatial relationships of structures over time. But this is merely an inevitable consequence of change. Neo-Darwinists surreptitiously imply that the position of cells in relation to their neighbors is actually the mechanism that explains development. They claim that spatial relationships over time have some kind of causative power. The cause of the developing embryo is DNA, not positions in time. As an example, the authors state, “Neural stem cells in the early neural plate and tube, and subsequently in each nascent brain region, must acquire instructions that establish their capacity to make nerve cells specific to each region.” This is clever, but wrong. The neural cells don’t serendipitously acquire instructions; DNA provides the instructions which are utilized when and where the design indicates.
The authors continue to press their Neo-Darwinist worldview, “Cells that are moved either acquire the identity of the new region in which they are placed (thus receiving instructions based on their new location), or they retain an identity that reflects their original position (and thus possess immutable instructions from their original location).” But wait, does this not prove my point? If some cells change according to signals received based solely on location, and others do not, does that not indicate a more highly engineered set of instructions that supersedes spatial relationships? Spatial relationships are pseudo-mechanisms.
Neo-Darwinists would like us to ignore the fact that embryonic cellular and structural changes in space and time are merely observations without power. They would like us to believe that time and position are causal agents. DNA is the only causal agent.
In this very superficial overview of neuroscience it is obvious that Neo-Darwinists do in fact subscribe to Darwin’s 1800’s theory of evolution by the natural selection of random mutations. However, their support incorporates flawed paradigms:
1.Neo-Darwinists ignore the existence and complexity regarding the role DNA plays in a dynamically developing embryo, fetus, child and finally an adult.
2.Neo-Darwinists create pseudo-mechanisms such as giving causal power to spatial and temporal cellular relationships, whereas only DNA has causal power.
3.Neo-Darwinists neglect the fact that operating systems and structures are controlled by and created by the same DNA.
4.Neo-Darwinists confuse observations with explanations, and imply they are synonymous.
5.Neo-Darwinists fail to understand that DNA exhibits specific, non-random information and do not address the question, “Can a random process create a non-random structure or operating system?”
6.Neo-Darwinists use the logical fallacy of argument from ignorance, or what I like to call “Darwin of the gaps.”
7.Neo-Darwinists ignore the fact that design, not randomness, generates scientific curiosity and leads to discovery.
1. Dale Purves, George J. Augustine, et. al., editors, Neuroscience, 6 ed. (Oxford: University Press 2018), 767.
2. Id., 491.
4. Id., 492.
6. Id., 494.
7. Id., 495.
8. Id., 498.
- BIOCHEMISTRY AND MOLECULAR BIOLOGY ARE INCONSISTENT WITH DARWINISM (4/4/2020)
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.
- Changes in Circulation at Birth (11/16/2019)
Fetal circulation demonstrates an engineering complexity that requires advanced planning. Astonishingly, the fetus survives in a fluid-filled environment (the amnion) and is busy developing a respiratory system designed for breathing air! Therefore, there must be a temporary mechanism or system that converts a non-air-breather into an air-breather at birth. This temporary, “in between,” system functions in the presence of: 1) three shunts, 2) unique fetal hemoglobin and 3) a blood supply that travels to and from a proxy lung—the placenta.
At the moment of conception, DNA contains not only the information required in the form of Watson’s blueprint, but also; 1) the capability to obtain the physical elements, 2) that manufacture the nanotechnology, 3) which produces the molecules, 4) that create the structures, 5) which interact with other structures in a rapidly changing physical environment.
The engineering of fetal circulation must anticipate a high-pressure, non-functioning pulmonary system that will change in one instant to a low-pressure and now instantly functioning respiratory system. Furthermore, the maternal-fetal system must include a mechanism to expel the now unnecessary placenta, because a retained placenta causes maternal death. Fetal circulation is not compatible with adult life, and adult circulation is not compatible with fetal life.
In fetal development, the heart is being formed to function as an adult. However, we know that the fetal and adult circulation systems are incompatible with each other, therefore, this incompatibility must be taken into account. The system engineered to overcome this incompatibility includes three shunts and specific physiologic changes. But how does this all come about by Darwin’s required “numerous, successive, slight modifications?”
No Darwinist can explain how nature purports to select mutations that possess immediate beneficial effects, which also provide intricately engineered physiologic mechanisms that are required for future developing and interacting organ systems within incompatible physiologic environments.
- BAD NEWS FOR DARWIN-DNA MUST CODE FOR EMBRYOGENESIS (11/16/2019)
BAD NEW FOR NEO-DARWINISTS—DNA MUST CODE FOR EMBRYOGENESIS
CHROMATIN REGULATION OF EARLY EMBRYONIC LINEAGE SPECIFICATION
Darwin’s theory of evolution—the creation of human beings by the natural selection of random mutations—is a wholly inadequate scientific theory to explain the astronomically complex anatomy and physiology of human beings. Darwin based his theory of evolution on the morphology (shape) of different species. He knew nothing of genetics, embryology and molecular biology. Without incorporating these (and other) sciences, Darwin’s theory necessarily fails as a mechanism for the creation of humans.
Unfortunately, Neo-Darwinists who are aware of these sciences have no excuse for their acceptance of such an unsophisticated worldview of creation. If Neo-Darwinists expect us to believe that the current human genome is an accumulation of random mutations, they first need to explain how DNA codes for the constantly changing anatomy and physiology of an embryo, fetus, child and finally an adult. Naturally, no Neo-Darwinist has yet attempted this.
Most unfortunate for Neo-Darwinists, every adult must begin as an embryo and very little is known about the function of DNA in embryology. Recently, elegant research has been done in this area and the complexity is awe-inspiring.
Knott and Latham provide a collection of current research in Advances in Anatomy, Embryology and Cell Biology: Chromatin Regulation of Early Embryonic Lineage Specification (Springer, 2018), which addresses the topic of how DNA effects embryologic development. It is my goal to provide a simple and very brief description of the research presented in order to illustrate the failure of Darwinism. This book consists of five research papers. I will present a short glossary of terms used by the authors, then a synopsis of four papers, and finally conclude with some thoughts on what that means for Darwinism. If the reader is expecting support for Darwinism, he or she may be disappointed—or hopefully, enlightened.
Before getting started, I would like to present a very brief embryology lesson so that the authors’ findings will be more accessible. The journey from fertilization to an adult is extremely complex and is controlled at every step and every moment by countless genes. The authors illustrate this complexity when they state, “Every cell in an organism contains the same genome, and yet there are multiple distinct cell types, all of which exhibit different dynamic gene expression profiles. Therefore, when we consider cell fate choices, we are witnessing the rewiring of these gene regulatory networks (GRN) to create new stable cell types.” The authors further elucidate the complexity involved. A cell’s identity is defined by the genes it expresses and those it represses, therefore, to understand cell fate decisions we must understand how gene expression and gene repression are controlled.
Within the first five days of development, a single-celled zygote grows by a very well-ordered series of cleavage divisions and successive differentiation events to create three lineages: trophectoderm (TE), epiblast and primitive endoderm (PrE). But how do cells “know” how to respond appropriately to stimuli and ensure the correct expression of specific genes? The solution to this problem are the chromatin modifiers and remodelers. Chromatin modifiers and remodelers facilitate . . . the genes required in the new cell state and prevent aberrant expression of those that are undesirable. An important question is implicit, how are the signals decoded by the cells at the chromatin level? “Whether a gene is transcribed or silent is largely dependent upon its chromatin environment.” Thus we see the importance of chromatin in embryologic development. The following articles will expand upon other important molecular structures. But first:
Chromatin—a complex of DNA, RNA and proteins from which chromosomes condense during cell division.
Epigenetic—changes in an organism caused by modification of gene expression rather than alteration of the genetic code.
Inner Cell Mass—the mass of cells in an embryo, which eventually become the fetus.
Primitive endoderm—the layer of cells, which develop into the digestive tract.
Trophectoderm—the membrane of cells that forms the wall of the early embryo, which provides nutrients to the embryo and later becomes the placenta.
“Chromatin Remodelling Proteins and Cell Fate Decisions in Mammalian Preimplantation Development,” Anzy Miller and Brian Hendrich.
The authors begin with a good review of the embryologic process. The very first cell divisions produce a ball of cells, each cell having the potential to form any cell in the developing embryo or placenta. As more and more cells are produced, some are located on the outside of the embryo and some are completely surrounded by other cells. It is here that cells undergo the very first lineage commitment event. The outer cells form the trophectoderm (TE) and lose the potential to form embryonic lineages. The inner cells form the Inner Cell Mass (ICM), which retain embryonic potential.
The second cell-fate commitment occurs as the ICM transforms into extraembryonic primitive endoderm (PrE) and what is called a pluripotent epiblast (where pluripotent means each cell has the potential to become many different cell types; and epiblast is the ball of rapidly growing cells.) This enlarging embryo goes through several identifiable stages including preimplantation, implantation, placentation and gastrulation (the gastrula is the stage where the embryo consists of three layers—ectoderm, mesoderm and endoderm). Growth from one stage to the next is controlled by many different factors which, “modulate embryonic chromatin structure, impose cellular polarity and direct distinct gene expression programs in the first cell lineages.” Cell growth is defined by gene expression patterns, and gene expression is controlled by how the DNA is packaged into chromatin. And here lies an unavoidable reality; all of the information and programming needed for the embryo to grow into an adult is present at the beginning of first cell division. No further information is gained. A second fact with which Neo-Darwinists must deal is that a simple one-to-one relationship of DNA-to-morphology as Darwin’s theory implies, cannot exist. (For a medical example involving vision see my book The Collapse of Darwinism, chapter 9 Genetics, p. 184.)
From the beginning of cell division we are already dealing with complex “gene expression patterns,” “gene expression programs,” and “molecular mechanisms through which chromatin remodelers facilitate the successful completion of the first cell fate decisions.” We are also dealing with vague and poorly understood processes naively referred to as “controlled,” “impose” and “direct.” All of these patterns, programs and molecular mechanisms along with their control, imposition and direction must be encoded within DNA and ready to go at fertilization. Darwinists are incapable of describing the accumulation of random mutations that led to this arrangement and function of DNA.
Now the authors delve into the complex genetics, which I have very briefly and superficially summarized. Briefly, Chromatin remodelling complexes are divided into four classes (SWI/SNF, ISWI, IN080 and CHD families). Each chromatin remodeler controls distinct aspects of chromatin biology. The complexity of chromatin remodelling is impressive. There are many complexes that belong to each family some of which contain as least 15 different subunits. And loss of subunits is incompatible with successful development. The authors suggest this when they state, “This work highlights two important points: that the essential targets of a chromatin remodeler may vary depending on the tissue and/or developmental stage and that, while the developing embryo is fairly robust, only small changes in gene expression can be enough to culminate in developmental failure.” Here we see that not only is chromatin complex, it is delicate. And this is merely the tip of the iceberg.
In summary, chromatin remodelling proteins ensure that cell fate decisions occur correctly throughout development, and importantly, very specific proteins are necessary for these cell fate decisions.
“CHDI Controls Cell Lineage Specification through Zygotic Genome Activation,” Shinnosuke Suzuki and Naojiro Minami.
In this article the authors focus on cell lineage specification (the process of cell division and differentiation). Cell lineage specification is dependent on epigenetic factors (factors that regulate gene expression) and chromatin remodeling factor CHD1. Together, epigenetic factors and CHD1 are involved in gene expression networks. Immediately after fertilization, the zygote becomes a totipotent cell (a cell that can differentiate into every type of cell needed). This totipotent cell initiates a developmental program that eventually results in the production of a new organism, which consists of a myriad of differentiated cells after extensive reconfiguration. This reconfiguration process is dependent on transcripts and proteins that remodel maternal and paternal genomes.
The authors go into great detail describing the chemical structure, function and interdependency of numerous transcription factors involved in cell lineage specification. And of course these are only the factors about which we know anything. Although the authors go into excruciating detail discussing how some factors operate, and illuminate the incredible complexity of fetal development, they make it clear that this is merely the tip of the iceberg, “However, it is still far from clear how the gene expression required for each developmental stage is controlled.”
For our purposes—applying embryology to Darwin’s theory—this article clearly demonstrates the astronomically complex state of DNA controlled fetal development. This development requires highly controlled genetic networks that interact and are interdependent on poorly understood epigenetic factors and proteins. The likelihood of these dynamically functioning genetic networks having been created by Darwin’s numerous successive slight modifications becomes increasingly remote with the discovery of every new molecule.
“Transcriptional Regulation and Genes Involved in First Lineage Specification During Preimplantation Development,” Wei Cui and Jesse Mager.
The authors investigate how successful development from a single-cell zygote into a complex multicellular organism requires precise coordination of various cell-fate decisions. They note that multiple transcription factors are enriched and others are upregulated. This article reviews transcriptional control mechanisms and the genes responsible for the distinct differences in first cell lineage specification, which are categorized into three separate major events.
The first major event to occur is the maternal-to-zygotic transition (MZT), which includes degradation of maternal mRNA’s and replacement with zygotic transcripts. This requires “dramatic reprogramming of gene expression.” A second major event that must occur early is embryo compaction and polarization, which occurs in the eight-cell stage. Compaction must occur in a precise manner so that cell polarization and thus cell division-dependent repositioning may occur properly. A third critical event that must occur is blastomere allocation into two distinct types of cell divisions during the 8-16-cell transition, which requires “appropriate regulation and mutually exclusive localization” of transcription factors. The authors go on to explain in great detail how these transcription factors and genes interact and what can go wrong when any one of 53 genes do not interact appropriately.
To illustrate the astronomically complex nature of early implantation the authors state, “Our screen selected genes to target based solely on expression during preimplantation and resulted in 7.4% of genes (53/712) with phenotypes. If there are ~11,000 genes expressed during preimplantation (Stanton and Green 2001), our results suggest that ~800 genes are required for lineage development and/or specification during preimplantation-the majority of which have yet to be discovered.” The authors conclude that first cell lineage decision is determined by many distinct mechanisms some of which act in parallel and some that act in networks. Despite everything described here, the authors conclude that, “understanding of the genes required for the first lineage specification remains elusive.” It seems quite unbelievable that Darwin’s random mutations could produce such incredibly complex networks of genetic interaction. The sheer number of genes alone (not to mention the complexity of information) is pushing the likelihood of Darwin’s mechanism to the point of infinity.
“ROCK and RHO Playlist for Preimplantation Development: Streaming to HIPPO Pathway and Apicobasal Polarity in the First Cell Differentiation” Vernadeth Alarcon and Yusuke Marikawa.
The authors begin by describing a mere embryologic observation that is misused by Neo-Darwinists as a mechanism, “In placental mammalian development, the first cell differentiation produces two distinct lineages that emerge according to their position within the embryo: the trophectoderm (TE, placenta precursor) differentiates in the surface while the inner cell mass (ICM, fetal body precursor) forms inside.” They ask the question, “What kinds of mechanisms would allow each cell to interpret its position within the embryo and to execute specific differentiation programs?” When reading Neo-Darwinists explanation of embryology, one will all too frequently encounter statements that claim organs develop as a result of the three dimensional position cells take in a growing embryo (topography). A quick internet search provides numerous examples of this oversimplification including this from Scientific American, “Thus the position (location) of a cell in the early embryo largely determines what cell type it will become in the end of the process of the embryonic development [bold not mine].” This feeble attempt to simplify embryology is also an attempt to avoid the extreme complexity inherent within embryology and antithetical to Darwin’s theory. The authors state, “Activities of RHO/ROCK are required to promote TE differentiation and to concomitantly suppress ICM formation. RHO/ROCK operate through the HIPPO signaling pathway, whose cell position-specific modulation is central to establishing unique gene expression profiles that confer cell fate”
When discussing the regulation of lineage-specific gene expressions, signaling both upstream and downstream, the authors state, “The genome content is equivalent among most cell types in the embryo, so that cell differentiation mainly occurs through differential gene expressions by transcriptional regulations of distinct sets of genes in a lineage-specific manner.” The important concepts here are the phrases “differential gene expression” by “distinct sets of genes.” There is no simple position-to-cell-type relationship as Neo-Darwinists would have it. There is in reality a massively complex set of interacting genetic programs. The authors describe over 30 genes and other genetic factors involved in just this study of preimplantation development during first cell division.
This book presents complex information that is ignored by Neo-Darwinists. The creation of species through the natural selection of random mutations must occur in the DNA, and that DNA must direct development of an embryo, fetus, infant, child and finally an adult. As an example healthy, disease free vision requires input from every chromosome demonstrating there is no simple one-to-one relationship of DNA to functioning anatomy and physiology; and no computer model exists that can demonstrate which nucleotides mutated to what nucleotides to produce any organ, system or network in the human being. No Nobel Laureate, professor or politician can prove this last statement wrong, and by Darwin’s own words his theory absolutely breaks down.
 Anzy Miller and Brian Hendrich, “Chromation Remodelling Proteins and Cell Fate Decisions in Mammalian Preimplantation Development,” Chromatin Regulatioin of Early Embryonic Lineage Specificaiton (Cham: Springer, 2018), 4.
 I., 3.
 Id., 1.
 Id., 3.
 Id., 6.
 Id., 8.
 Id., 10.
 Shinnosuke Suzuki and Naojiro Minami, “CHD1 Controls Cell Lineage Specification Through Zygotic Genome Activation,” Chromatin Regulation of Early Embryonic Lineage Specification (Cham: Springer, 2018), 15.
 Id., 25.
 Wei Cui and Jesse Mager, “Transcriptional Regulation and Genes Involved in First Lineage Specification During Preimplantation Development,” Chromatin Regulation of Early Embryonic Lineage Specification (Cham: Springer, 2018), 31.
 Id., 33.
 Id., 34.
 Id., 39.
 Id., 41.
 Vernadeth Alarcon and Yusuke Marikawa, “ROCK and RHO Playlist for Preimplantation Development: Streaming to HIPPO Pathway and Apicobasal Polarity in the First Cell Differentiation,” Chromatin Regulation of Early Embryonic Lineage Specification (Cham: Springer, 2018), 47.
 Id., 49.
 Bora Zivkovic, “BIO101-From Two Cells to Many: Cell Differentiation and Embryonic Development,” Scientific American, September 10, 2001. Accessed online at blogs.scientificamerican.com July 4, 2019.
 Id., 47.
 Id., 49.
- Bioinformatics-Understanding DNA (11/16/2019)
Lessons from Bioinformatics and Functional Genomics, 3rd ed. Johnathan Pevsner (Wiley, 2015)
CharlesDarwin knew nothing of information science, nothing of cellular biology, nothing of molecular genetics and molecular biology, and nothing of the physics and chemistry required to understand biochemistry. Darwin’s knowledge of anatomy and physiology is suspect since he was a medical school dropout. Yet Darwin presented a theory for the creation of life based on the shape, or morphology, of species. What Darwin did not know, and could not know, is that biology is DNA, and DNA is information. That sounds simple enough, yet DNA is so historically complex that even an elementary understanding of the amount and nature of information stored in DNA requires the use of computer databases and the new sciences of bioinformatics and genomics. This article is divided into four sections: I Definitions and Introduction of Bioinformatics and Genomics, II Brief Synopsis of Molecular Genetics, III Nature of Mutations, and IV Conclusion.
I Definitions and Introduction of Bioinformatics and Genomics
Defining bioinformatics and genomics is not a simple task. (Simplistically, bioinformatics is the sequencing of DNA nucleotide by nucleotide, and genomics refers to ultimate gene function.) The experts, of course, have more precise and useful definitions. There are three useful definitions of bioinformatics. First, according to the National Institutes of Health, bioinformatics is “research, development, or application of computational tools and approaches for expanding the use of biological, medical, behavioral, or health data, including those to acquire, store, organize, analyze, or visualize such data.”Second, computational bioinformatics is defined as, “the development and application of data-analytical and theoretical methods, mathematical modeling, and computational simulation techniques to the study of biological, behavioral and social systems.”And third from the National Human Genome Research Institute, “Bioinformatics is the branch of biology that is concerned with the acquisition storage, display, and analysis of the information found in nucleic acid and protein sequence data.”
Similarly, genomics is a complex science. A genome is the collection of DNA that comprises an organism. According to Pevsner, “Functional genomics is the genome-wide study of the function of DNA (including genes and nongenic elements) as well as the nucleic acid and protein products encoded by DNA.”These definitions illustrate the informational nature of biology that manifests as anatomy and physiology.
In 1958 Francis Crick formulated the central dogma of molecular biology that states biological information travels in one direction—DNA is transcribed into RNA then translated into protein. Information cannot travel backwards from protein to RNA to DNA.Genomics has been characterized in several ways but the most important of these is from a functional perspective in which, “the most challenging and fundamental problem in modern biology is to understand the relationship between genotype and phenotype.”(Genotype is the genetic constitution of an organism, and phenotype is an organism’s physical appearance, i.e. anatomy and physiology.)And it is here that Darwin’s theory of evolution by the natural selection of random mutations fails. Remember, Darwin based his theory on nothing more than the morphology—shape—of species.
II Brief Synopsis of Molecular Genetics
Knowing the sequence of a genome is incredibly complex but that is not enough. Understanding what information, the genome possesses is what we know as biology. Transferring information from genotype to phenotype occurs through the creation of amino acids which are linearly sequenced in a physicochemical manner that produces specific three-dimensional structures. This three-dimensional structure determines a proteins capacity to function. Countless proteins are the molecular machines that create the anatomy and function as the physiology of the human body.
Protein structure is defined at several levels. Primary structure is the linear sequence of amino acids that produce a polypeptide chain. Secondary structure is the arrangement of primary amino acids into motifs such as helices, sheets, coils or loops. Tertiary structure is the three-dimensional arrangement created by packing secondary structure elements into globular domains. And lastly, quaternary structure is the arrangement of tertiary structures into more functionally complex molecular machinery.But complexity creates its own problem and possesses an inherent disadvantage. One question that relates to DNA’s extreme complexity is, how much mutation can the extraordinarily complex DNA tolerate and not lose function or cause disease? Kimura notes that, “the rate of amino acid substitution averages approximately one change per 28 X 106 years for proteins of 100 residues,”and that “most observed DNA substitutions must be neutral or nearly neutral.”
Another problem for Darwinists, besides mutation tolerance, is the availability of time. The numbers provided by Kimura do not support the time available for one species to mutate into another, or improve a species as highly complex as a human.
III Nature of Mutations
Evolutionary biologists try their best to apply Darwin’s simplistic theory, created well before any knowledge of molecular biology or DNA existed, to the structure of DNA. But their attempts fail. Evolutionary biologists inappropriately use homology, or similarity, as a cause and effect. Pevsner quotes Margaret Dayhoff who applies current knowledge of biology to Darwinism, “An accepted point mutation in a protein is a replacement of one amino acid by another; accepted by natural selection. . . To be accepted, the new amino acid usually must function in a way similar to the old one . . .”Dayhoff is correct in locating the site of random mutations to amino acids or nucleotides which produce amino acids. Interestingly she requires that the new amino acid must function in a way similar to the amino acid which is being replaced. But the more similar amino acids are, the less change occurs in the organism and the longer it takes for organisms to evolve. (For a discussion of how little time actually exists for evolution of human beings to occur, please see my discussion of the Mitochondrial Eve Unit found in The Collapse of Darwinism, page 29.) Knowing that changes are slowed due to the requirement of mutated amino acids functioning similarly to the replaced amino acids, makes a mutation rate of 2.8 X 107 years for proteins of 100 residues wholly incompatible with Darwin’s theory.
Further complicating the situation forDarwinists is the inconvenient reality that mutations are either negative, neutral or beneficial. In his final chapter, Pevsner describes DNA variation and disease, “Mutations affect all parts of the human genome. There are limitless opportunities for maladaptive mutations to occur, and there are many mechanisms by which mutations can cause disease.”Pevsner discusses several data bases for bioinformatics and genomics that relate mutations to disease. The Human Genome Mutation Database (HGMD) project lists approximately 115,000 mutation entries for public release and 164,000 entries for commercial release. (Search of the database as of 11/15/2018 reveals the numbers have increased to 157,114 and 240,269 respectively.)The OMIM database contains entries for over 22,000 human diseases and relevant genes.What is not stated, and is profoundly significant, is the fact that there is no database with even one entry containing a mutation that leads to a beneficial change in phenotype. Pevsner provides even more evidence that defeats Darwin’s theory, “While the genetic basis of over a thousand single-gene disorders has been found, it is far more difficult to identify the genetic causes of common human diseases that involve multiple genes. Part of the challenge is that a large number of genes may each make only small contribution to the disease risk.”
In summary, the concept that the astronomically complex anatomy and physiology of human beings is created by the natural selection of random mutations defies logic and requires the reader to suspend reason. The fact that Darwin knew nothing of DNA, molecular biology, biochemistry and information science relegates his 1800’s theory of evolution to the dust bin of archaic scientific theories along with spontaneous generation and the geocentric theory of our solar system.
Kimura tells us that amino acid substitutions averages one change every 2.8 million years for proteins of 100 residues. However, we know that the Cambrian explosion occurred 540 million years ago. Applying simple math tells us that only 192.8 amino acid substitutions may have occurred from the time aquatic creatures swam in the earth’s ancient oceans until humans began to walk on land. Logic tells us that amino acid substitutions cannot be a mechanism for Darwinian evolution.
The human genome contains approximately 3 billion base pairs. It is amazing that this huge human genome has been sequenced. But knowing the sequence is not the same as knowing how every base pair functions. Pevsner makes us aware of the numerous databases and research that are attempting to discover how DNA produces three-dimensional proteins which function as machines. He makes it very clear there is much work to be done. Pevsner describes the many databases of hundreds-of-thousands of mutations, and thousands of diseases that result from mutations. It is enlightening that no author, scientist, professor or Nobel Laureate can identify one nucleotide mutation that caused an improved phenotype manifesting as improved anatomy and physiology.
Bioinformatics and functional genomics demonstrate that DNA is astronomically complex and mutations are neutral or harmful. To date, the scientific evidence proves that evolution by the natural selection of random mutations cannot be the mechanism by which humans were created.
Jonathan Pevsner, Bioinformatics andFunctional Genomics, 3rd ed. (Sussex: Wiley, 2015), 3.
 Id., 635.
 Id., 433.
 Id., 636.
 Id., 1087.
 Id., 591.
 Id., 258.
 Id., 69. Pevsner quoting Margaret Dayhoff (1978, p. 345).
 Id., 1012.
 Id., 1036.
 Id., 1047.
- Bill Nye Gets It Wrong (11/16/2019)
This paper is a review of a popular book that presents purported scientific evidence that is used to support Darwinian evolution. But I contend that this supporting evidence consists of fallacious reasoning, misinterpretation and misunderstanding of human anatomy, physiology, embryology, physics and chemistry.
Bill Nye the engineer, comedian and host of the Discovery Channel show Bill Nye the Science Guy, is a devout Darwinist. He lays out what he believes is proof of evolution in his book: “Undeniable: Evolution and the Science of Creation” (St. Martin, 2015). Nye explains what motivated him to write this book—his debate with creationist Ken Ham. Ham, is an evangelical leader and founder of Answers in Genesis who claims the earth is only 6,000 years old. Nye chose to debate Ham, “to raise awareness of the creationist movement and its inherently deleterious effects on our society, as it dulls our resolve to tackle big scientific challenges like producing energy for the burgeoning human population . . . [and] climate change.” (1)
Out of the starting blocks, Nye uses the logical fallacy of a straw man argument instead of contending with the actual argument (how evolution actually works), Nye attacks the equivalent of a lifeless bundle of straw in the form of creationists’ young Earth theory, which the vast majority of Christians never intend upon defending anyway. It is the exceedingly rare Christian who believes the earth is only 6,000 years old.
Nye also uses, circular reasoning and ad hominem attacks (a personal attack, which is commonly used with the straw man argument). We will unfortunately see other examples of illogic.
I will divide this paper into 4 sections; 1) inaccurate statements, 2) a discussion of entropy, 3) Nye’s concept of the human body being designed just “good enough” and lastly, 4) Jay Gould’s theory called punctuated equilibrium. We will see throughout this paper that Nye, like all Darwinists including Darwin himself, never touch on how or where evolution actually occurs—DNA.
1) “We are all aware that evolution happens, because we all have parents. Many of us have, or will have, children.” (2) Here Nye confuses reproduction and heredity with evolution.
2) We experience evolution every day in our culture as well.” (3) First, culture is not where a scientist can expect to find evolution (it occurs in DNA). Second, if one believes Darwin, evolution occurs imperceptibly over especially long geological times. No one can witness evolution happening.
3) “We are all so much alike, because we are all human. But it goes deeper than that. Every species you’ll encounter on Earth is, near as we can tell, chemically the same inside. We are all descended from a common ancestor. We are shaped by the same forces and factors that influence every other living thing, and yet we emerged as something unique.” (4) Darwinists make the mistake of confusing commonality with evolution. Sharing the same laws of physics and chemistry is a requirement to be a part of this universe. Creatures exhibiting different chemistry and laws of physics don’t occur because they cannot exist.Commonality is not proof of evolution, it is proof of adherence to physical laws fundamental to this universe.
4) “Many people who are troubled by evolution . . . try to push it aside or dilute it by casting doubt on the established science that supports it.” (5) This is the logical fallacy of an argument from authority. Just because many people accept it does not make it true. It is my contention, and the contention of many others who are not discouraged by the complexity of reality, that evolution is an outdated, 1800’s philosophy that was disproven once DNA was discovered. The reality is that evolution is not a science at all, it is merely the fortuitous accumulation of mutations according to Darwin’s own definitions.
5) “Like any useful scientific theory, evolution enables us to make predictions about what we observe in nature.” (6) Unfortunately for Nye, evolution can make no predictions other than change happens. But change happening is a characteristic of life or entropy, not evolution. Evolution can predict nothing because evolution occurs by the natural selection of random mutations. By definition the predictive value of a random process is non-existent. But Darwinists are loathe to accept randomness despite the fact that Darwin requires it, “Evolution is also not random it’s the opposite of random. One of Darwin’s most important insights is that natural selection is a means by which small changes can add complexity to an organism.” (7) But like it or not, any system that possesses at least one random component is an overall random system. If I told you to create something out of items picked randomly from a junkyard, you would create something. If I told you to make something from any item you choose in the junkyard, you would no doubt create something far different and better. Randomness as a component produces an overall random system, which does not mean nothing can be created. As an engineer Nye should know better.
I could go on but for the sake of at least some brevity, let’s move on to a subject I touched upon, entropy.
In an attempt to remove entropy (disorder or randomness) from biological system, Nye just like other Darwinists, misinterprets entropy. I will use Nye’s own words to describe entropy, “To be sure, the Second Law of Thermodynamics really does contribute to a general winding down of the world around us. It explains why no one can build a perpetual motion machine. Somewhere, someplace in any machine you’re going to lose some energy to heat. . .The Law that entropy always increases—the Second Law of Thermodynamics—holds, I think, the supreme position among the Laws of Nature. . .The key idea is that the Second Law of Thermodynamics mathematically describes any system’s loss of energy to its surroundings. It is fundamental to the way the natural world works.” (8) Then in a self-defeating and ironic argument, Nye claims that entropy doesn’t apply to evolution (even though it is a part of our world) because, “The Second Law applies only to closed systems, like a cylinder in a car engine, and Earth is not even remotely a closed system.” (9) So which is it? Nye has just turned 180 degrees. Nye (and other Darwinian apologists) argue that the Earth is receiving energy from the sun and therefore it is an open system to which entropy does not apply. Because the sun shines, entropy cannot apply to evolution. But in this rather humorous mental gyration Nye has contradicted himself and must claim that entropy does not apply to the rest of the world, which in his own words was “winding down.”
I agree that the Earth is an open system, but entropy applies to open systems as well as closed systems unless that open system is receiving “directed” energy. Nye’s example of a closed system, the cylinder in a car, is anything but closed. The cylinder gives off significant heat to the surrounding engine block and environment as any driver (let alone engineer) knows. In reality, there is no such thing as a closed system. As just one example of our open universe, neutrinos zip through the universe and Earth rarely but occasionally interacting. A truly closed system does not exist. The closed system is merely a thought experiment used to help understand entropy.
Amazingly, Nye does yet another 180 degree turn around as he admits the Second Law occurs in open systems, “But the Second Law comes into play everywhere in your life.” (10) How can this be if it only occurs in closed systems? Nye and other Darwinians cannot have it both ways.
Nye is incorrect about entropy. He is also incorrect about his concept that the human body has been created by a process of evolution that creates systems, which are merely “good enough.” In the next section I will correct Nye’s misunderstanding of human embryology, anatomy and physiology.
HUMAN BODIES ARE GOOD ENOUGH In chapter 21 titled “Human Bodies are Walking, Talking, and Good-Enough.” Nye claims proof of evolution exists because an all-powerful God would have designed a perfect body, but the human body is merely “good-enough.” Nye claims, “You and I will wear out. You might already have aches, pains, eyeglasses, and dental fillings. But your generation, no matter which one it is, was good enough to make it this far. This is another consequence of being shaped by natural selection. In our evolutionary world, good enough is a good as it gets.” (11) Nye gives examples of what he believes are human design flaws that a conscious creator would not have made, and therefore these design flaws are proof of Darwinian evolution.
I will cite one of Nye’s examples which will demonstrate his fallacious logic and his limited understanding of embryology, anatomy and physiology. Nye claims, “One of the most obvious human design puzzles is that our waste disposal plumbing is immediately adjacent to our reproductive and pleasure producing plumbing . . .Your anus is right next to either your penis or your vagina. Would you have put the urethra right there in the middle of the whole business? If you were in charge, wouldn’t you have separated those a bit? How hard could that be? . . .Seems like a simple problem to correct.” (12) Nye completely ignores, or cannot comprehend, the fact that the urogenital system is created from a single cell. The creation occurs by cell division, differentiation and migration. It seems strange that I have to say this but each organ system is created together and simultaneously, not assembled separately then combined in a factory. What follows is a very brief summary of how the urogenital system is created.
Sexual differentiation is the epitome of complexity in DNA programming. As the fetus develops, undifferentiated embryonic organs differentiate into respective male and female organs. Below is a very incomplete list of embryonic structures that become male and female analogues:
1) Gonad testis Ovary
2) Paramesonephric duct Appendix testis Vagina, uterus
3) Mesonephric tubules Rete testis Rete ovarii
4) Urogenital sinus Bladder, urethra Bladder, urethra
5) Labioscrotal folds Scrotum Labia majora
6) Urogenital folds Spongy urethra Labia minora
7) Genital tubercle Penis Clitoris Larsen, an embryologist, summarizes our current state of knowledge regarding urogenital system development and the singular event of testicular descent. He states, “The hormonal control of testicular descent is not completely understood. Androgens and pituitary hormones are important, but other unknown testicular factors or hormones apparently play a role, as does neural input via the genitofermoral nerve.” (13) Every aspect if urogenital system development is similarly poorly understood.
One last repudiation of Nye’s uninformed claim that the human body is just good enough comes from research of the retina. Williams and Moody did not mince words in their investigation of the retina. They note that there are more than twenty thousand genes that involve the retina and that “even more genes are likely to be expressed throughout development.” (14) And in their section titled, “The Paradox of High Variation,” they state, “The apparent paradox is resolved if we come back to the point that the visual system is over-engineered and that there is much functional and developmental redundancy built into the retina of most individuals.” (15) By definition, systems that are redundant and over-engineered are anything but “good enough.”
In the final section I will give a brief repudiation of Nye’s suggestion that Jay Gould’s theory of punctuated equilibrium is further evidence to support Darwinian evolution. As we will see, it is quite the opposite.
Jay Gould’s attempt to resuscitate Darwinian evolution with his theory of punctuated equilibrium accomplishes the opposite effect. Punctuated equilibrium proves Darwin’s theory of evolution by the natural selection of random mutations is not viable. The imperceptible advancement of evolution, which Darwin required, is not demonstrated in the fossil record. This bothered Darwin but does not seem to bother Nye. Nye notes, “Darwin called the missing fossils, ‘. . . the most obvious and gravest objection which can be urged against my theory.’” (16) Nye summarizes Gould and attempts to explain away the inadequate fossil record.
Paraphrasing Gould, Nye states, “Darwin had pictured one whole species giving way to another. . . Once you let go of that old uniformitarian way of looking at things the situation becomes a whole lot clearer. When a small group of organisms gets isolated . . . some individuals are more prone to form new species In a small group, any mutation is a much bigger part of the mix, and a successful mutation is immediately a much bigger deal.” (17) He goes on, “populations get isolated. That’s when things can happen fast.” (18) This is the short and sweet of how rapid changes occur according to Nye and Gould. However, the problem is that Gould does not explain how the DNA changes occur or what the DNA changes are. The problem is not how fast mutations occur but rather which nucleotides mutate. Gould cannot explain the mechanism of evolution any better than Darwin, but Gould unwittingly demonstrates that evolution cannot work as Darwin requires. (For a more in-depth evaluation of Gould’s punctuated equilibrium please read my article devoted to punctuated equilibrium.)
1 William Nye, “Undeniable: Evolution and the Science of Creation” (New York: St. Martin Press, 2015), 11.
2 Id., 2.
4. Id., 3.
6. Id., 5.
7. Id., 23.
8. Id., 20.
9. Id., 21.
11. Id., 165.
12. Id., 167.
13. William Larsen, “Human Embryology, 3rd edition (Philadelphia: Churchill Livingston, 2001), 379.
14. Robert Williams and Sally Moody, Leo Chalupa and John Werner, eds., Chapter 5: Development and Genetic Control of Cell Number in Retina, “The Visual Neurosciences 1,” (Cambridge: MIT Press, 2004), 71.
16. Nye, 118.
17. Id., 121.
18. Id., 125.
Why Darwinism is Dangerous?
Why devote time, energy and money to illuminate the true nature of Darwinism? Because, simply put, Darwinism is a threat to society as it is:
- a metaphysical ideology
- used for censorship
- used to alter behavior of citizens and organizations
Scientific theories are rarely dangerous unless they are used to create weapons or are misused for political purposes. Darwinism falls into the latter category. Darwinism is defined as the theory of evolution by the natural selection of random mutations. Darwinism, because of its metaphysical nature, is well suited for political mischief. Historically, nearly all of the Nazi elite were devout social Darwinists and their social Darwinism had a great impact on the Nazi agenda. A partial list of infamous Nazis, besides Adolph Hitler, who were faithful social Darwinists includes: Martin Bormann, Dr. Joseph Goebbels, Heinrich Himmler, Hermann Goring, Reinhard Heydrich, Dr. Alfred Rosenberg, Julius Stretcher and Dr. Josef Mengele, MD, PhD. Darwin supporters will of course howl when confronted with social Darwinism, but the painful truth is that no other “scientific theory” has ever been used to create an ideology that was nearly responsible for the destruction of western civilization. [Where are the “social Einsteinists,” the “social Newtonians,” the “social Heisenbergists,” or the “social (place your favorite scientist/scientific theory here-ists”)]? Darwinism is used as a political ideology because it can be used in that manner, unlike any other “scientific” theory.
Today we are no longer faced with the specter of social Darwinists militarily conquering the world. The danger now lies in censorship and the suppression of any person, business or organization that dare question Darwinism. Darwinism has become wedded to the judge-made doctrine of separation of church and state. This was institutionalized in our United States Federal Court system in the case of Kitzmiller v. Dover Area School District. In this case the modus operandi were stablished—any theory that disputes Darwinism (such as Intelligent Design) is ascribed a religious connotation and because any religious teaching is verboten in the United States of America, the Darwin-opposing theory will be found unconstitutional since it will then violate the separation of church and state. This censorship is possible because Thomas Jefferson’s metaphor—a wall of separation between church and state—has been misinterpreted. Jefferson wrote his letter to the Danbury Baptists who feared that a central federal government would suppress their religion. Jefferson’s metaphor was intended to ensure the Danbury Baptists that their religious beliefs and practices would be protected from the State. After Justice Hugo Black perverted Jefferson’s metaphor and intent, now Americans live in an environment where the State is protected from religion. Any theory that threatens Darwinism will be censored by the Federal Government and this censorship will be enforced by the police arm of the State.
Why would the State be threatened by those who cannot subscribe to Darwinism? Briefly stated, Darwinism obviates the need for a supernatural creator and thus enables the State to hold ultimate power in controlling all of its citizens’ (or subjects’) behavior including all ethics, morals and day to day activities. Professors in universities and teachers in high schools will be ostracized and/or lose their jobs if they do not submit to the State’s requirement to accept Darwinism. The media will ostracize and attack political candidates if they do not tow the line of Darwinism. Your church will be slapped down by the State if you dare express your belief in a supernatural creator in a way that is too public. For now, you may believe in God if you keep your beliefs confined to your church building or home. However, if you dare take your message too far into the public sphere you will face the wrath of the United States Federal Government because you are a threat, just as Socrates and St. Paul were threats to Athens and Rome respectively.
DNA & INFORMATION
Now that it is well known all organs, structures and molecules of every animal are created by DNA, Darwin’s quote must of necessity be changed to include DNA. It may sound more cumbersome, however the addition of DNA will free us from the naive biology of the 1800’s. Darwin’s quote will be accurate if stated, “If it could be demonstrated that the DNA code writing for any complex organ existed, which could not possibly have been formed by numerous, successive, slight, modifications, my theory would absolutely break down.”
As simple as it sounds, those additional five words are a portent of exceedingly complex molecular biology, molecular genetics and information science, none of which were known in the 1800’s and each of which requires a PhD to fully understand. In the 21st century, biology is synonymous with information and it is well known that DNA is the language by which that information is delivered.
Biological information is not easily understood. Requisite for a proper and useful understanding is an unambiguous definition, of which there may be several depending on which branch of science one is interested. In our case, the term “Universal Information” is provided by Gitt, Compton and Fernandez who require biological information to provide: 1) code (a set of abstract symbols serving as an alphabet) plus syntax (rules that govern the use of code symbols), 2) meaning, 3) expected action and 4) intended purpose.
Once biological information is obtained, then and only then can we apply that information to form a logical argument either for or against Darwin’s theory of evolution. According to Kreeft, a logically sound argument must include: 1) significant terms that must be unambiguous, 2) premises which must be true, and 3) a conclusion which must logically follow from the premises, i.e. logically valid. As we will see in future blogs and podcasts, Darwinists routinely use very ambiguous terms and their premises are actually a series of dependent conjectures, from which conclusions cannot logically follow and are therefore not logically valid.
Furthermore, as Gitt et al. summarize, “While there is indeed a correlation between he material media and format that carries the information, the dictum ‘correlation does not imply causation’ certainly applies here. The material carrier cannot be and is not the cause of the information.” As we will see in future writings, Darwinists would like DNA to be the cause of the information and proceed as if that impossible dictum was in fact true.
[Werner Gitt, Robert Compton and Jorge Fernandez, “Biological Information—What is It?” pp. 11-25, in Marks et al., Ed. Biological Information: New Perspectives (Singapore: World Scientific, 2013), pp. 13-16.]