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.”[1] 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.[2]

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).[3] 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.[4] 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.”[5] 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.[6]

            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.)[7] 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.”[8] Cell growth is defined by gene expression patterns, and gene expression is controlled by how the DNA is packaged into chromatin.[9] 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.”[10] 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.[11] 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.[12] 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.”[13] 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.[14]


“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.[15] 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.[16] 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.”[17]

            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.[18] This requires “dramatic reprogramming of gene expression.”[19] A second major event that must occur early is embryo compaction and polarization, which occurs in the eight-cell stage.[20] 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.[21] 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.[22]

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.”[23] 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.[24] Despite everything described here, the authors conclude that, “understanding of the genes required for the first lineage specification remains elusive.”[25] 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.”[26] 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?”[27] 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].”[28] 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”[29]

            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.”[30] 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.

[1] 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.

[2] Id.

[3] Id.

[4] Id.

[5] Id.

[6] I., 3.

[7] Id.

[8] Id., 1.

[9] Id., 3.

[10] Id.

[11] Id., 6.

[12] Id., 8.

[13] Id.

[14] Id., 10.

[15] 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.

[16] Id.

[17] Id., 25.

[18] 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.

[19] Id., 33.

[20] Id.

[21] Id., 34.

[22] Id., 39.

[23] Id., 41.

[24] Id.


[26] 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.

[27] Id., 49.

[28] Bora Zivkovic, “BIO101-From Two Cells to Many: Cell Differentiation and Embryonic Development,” Scientific American, September 10, 2001. Accessed online at July 4, 2019.

[29] Id., 47.

[30] Id., 49.

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