This text is presenting some surprising scientific facts which provide convincing evidence against the theory of evolution and for a Creator.

Evolution, theory or fact?

A short compilation of thoughts and scientific evidence questioning Darwin’s theory of evolution

Foreword

I have studied science, mostly biology and some chemistry, with a focus on vertebrate development and physiology over the course of 10 years and wrote my PhD level dissertation about anthropogenic effects on marine wildlife. During this time (and for 10 years after that) I was fully convinced about the commonly taught theories of the creation of the universe and the earth, as well as the theory of evolution to be able to fully explain eons of cosmic history up to where we are today. After all, I had no reason not to be convinced of it since I was never confronted with any contrary view. Being enclosed in an academic system with like-minded people never opened up the discussion for something so far out of the consensus. The idea of creation by intelligent design was never mentioned at any point during my academic life. Even though I have not experienced it myself, the academic environment does not only ignore the idea of intelligent design but actively suppresses it. Multiple scientists have come to the forefront and brought to light that this suppression ranges from ridicule, to intimidation and penalisation in terms of position and funding. This attitude to react to the alternate approach of intelligent design to analyse scientific evidence is rather surprising for a self-proclaimed, evidence driven field. This displayed behaviour reminds me more of a fanatical attitude when common consensus is challenged, rather than an investigative spirit. Where does this antagonism to the idea of intelligent design come from? If science was solely focussed on the objective assessment of presented evidence, considering all potential explanatory possibilities, this antagonism would have no place in it. It therefore seems, that not only knowledge and objectively analysed evidence drive the scientific field, but a very subjective mindset. A mindset that is constrained to follow a certain world view. One thing that has always puzzled me is the title of PhD – (Philosophical doctorate, or Doctor of Philosophy), the highest level of academic achievement in the scientific field. Why do scientists get awarded a title of doctor of philosophy, rather than a doctor of sciences? After all, an equivalent title in the music and arts field is a “Doctor of arts”, an equivalent title in the field of medicine is a “Medical doctor” and an equivalent title in the educational field is a “Doctor of education”. Why does the title of the highest scientific qualification not suggest that its carrier has an achievement in the scientific field, but rather a philosophical one? Additionally, the title of "doctor" originates from the same Latin word doctor, meaning "teacher". Together, a PhD title can therefore be read as “the teacher of (a) philosophy”. Does this not indicate that what is being taught at schools and universities in the scientific field is not only knowledge and ideas, but rather a philosophy? And everything that is presented, may it be old knowledge or recent findings has to be analysed and understood under this philosophy? However, if a philosophy is taught, rather than true knowledge and the ability to critically assess evidence with an open mind, it sounds more like indoctrination than education.

What is then this philosophy that many of the most intelligent minds of this world, any new theory and evidence in the scientific field have to bow to? It is the philosophy of an universe where everything came from nothing, where mindless, undirected processes created the laws of physics, elements, planets, solar systems, galaxies, the universe and – life. The only problem is, that this philosophy, that claims to be the standard by which we have to understand all of the aforementioned is not in a position to proof any of it. Complex theories are developed, hypothesis tested and reformulated. Whereas within the scientific community it is clear that these theories are exactly this, a theory, an idea to be tested, they are often presented to people outside of the field as confirmed knowledge. However, when looking at the very core of the problem, the definitive answer to be big questions of life, the reply will always be the same. We do not know. This answer strangely does not raise concerns about the standard of evaluation but only drives the creation of more complex theories in an effort to justify or replace the previous one. However, this approach is acting against one of the very basic philosophical principles in science. The principle that when faced with two competing explanations for the same phenomenon, the simpler one is more likely to be true, as it is known under the term “Occam's razor”. This philosophical concept, attributed to William of Ockham, suggests that entities should not be multiplied beyond necessity, advocating for explanations that make the fewest assumptions. It is often paraphrased as "the simplest explanation is usually the best one" and is used as a principle to guide scientific inquiry and problem-solving.

For example, let’s have a look at what the scientific community considers as the most simple explanation for the creation of the universe:

One leading hypothesis is cosmic inflation, a period of exponential expansion that occurred a fraction of a second after the Big Bang. According to this model, the universe began as a tiny patch of space with a repulsive gravitational field, which caused it to expand rapidly. This inflationary phase may have been driven by quantum fluctuations in a vacuum state, where energy inherent in empty space caused the universe to grow exponentially. When inflation ended, the energy was converted into matter and radiation, creating the hot, dense primordial soup associated with the Big Bang. Out of this soup the stars and planets were formed.

Opposed to this is the following statement: In the beginning, God created the heaven and the earth (Genesis 1:1).

Which of these two explanations seems simpler? And not only simpler, but also does not leave room for doubt, mistakes and assumptions and provides the answers to this and many more fundamental questions?

Further, looking at this leading theory of the creation of the universe through the Big Bang, that proposes that at one point in time there was an infinitely small and infinitely dense point which then exploded into everything. It seems to me, with my very limited understanding about the physics behind it and even about the term “infinite”, that something that is infinite has no beginning and no end. Given this definition:

How can infinite energy cool down in order to be able to form matter?

How can something that is infinitely dense ever be not infinitely dense?

How can something infinite that explodes ever stop exploding?

The only explanation to me would be that the referred to point at the origin of the Big Bang was not infinitely dense or contained an infinite amount of energy. But how can something finite form an infinite universe?

Like for the creation of the universe, the current scientific understanding, still has no answers to the fundamental questions about:

1.     The incredibly rare chances of the precise properties of our solar system and the earth to be able to favour life

2.     The origin of life

3.     What life actually is

4.     The incoherence of the theory of evolution against mathematical improbabilities and actual findings

These are some thoughts to ponder on to highlight that science is far away from explaining any of the fundamental questions that it is investigating. Keeping this in mind, lets dive into the actual topic of this document, to present critical evidence against the exclusively taught theory of evolution and to open up to you, the reader, the possibility to make an informed decision about this matter.

During my early journey, peaking outside of the commonly accepted scientific philosophy, it was of importance to me to stay scientific. To not replace an evidence based approach with unfounded ideas and claims. In this document, I am listing some of the (for me) most interesting discoveries that I made along my journey. These discoveries are not my own but are rather a collection of scientific thoughts and investigations of experts in their fields. These findings have not only challenged my understanding of what I thought to be true and provided convincing evidence against the theory of evolution, but have also confirmed the biblical creation narrative to me.

What is evolution according to Darwin?

To better understand the topic that we will be dealing with, it is important to have a basic knowledge about the theory of evolution after Darwin. First of all, it is useful to highlight what this theory does not address and in fact cannot explain: The origin of life. With this clear limitation, the theory of evolution as presented by Darwin presupposes the existence of life, based on a modifiable and hereditary, information storage, which possesses enough tolerance towards alteration from external and internal stressors in the form of random, non-fatal changes (mutations) over prolonged periods of time.

This information storage is nuclear Deoxyribonucleic acid (DNA), a molecule of about 1.8 to 2 m of length and 3 billion nucleotide pairs (for the human genome) which is present in each of our cells (with few exceptions like mature red blood cells). The nucleotide pairs that create the information rich code which is contained in DNA consist of 4 different types called adenine, guanine, thymine and cytosine. It is on the succession of these building blocks of the DNA molecule that changes occur that are referred to as mutations. During mutations, one, or multiple nucleotides and thus the contained information is changed. How can a change in the nucleotide succession significantly affect an organism in a way, that, over time, it will, supposedly, evolve into a new species?

When the DNA is read, its nucleotide code is transcribed by a protein called RNA polymerase into mRNA (which is a single string of nucleotides, where thymine found in DNA is replaced by the mRNA specific nucleotide uracil). Then, a whole machinery of proteins, called the spliceosome is maturing this mRNA by cutting out certain section of the transcribed mRNA in order to remove sections that will not be used for the next step, the translation of the nucleotide code through proteins called ribosomes. During the translation, the succession of 3 nucleotides is coding for one specific amino acid. Therefore, a change in the succession of only one nucleotide can change the amino acid that a given set of 3 nucleotides coded for. For example, the nucleotide sequence of cytosine-adenine-adenine (CAA) is coding for the amino acid Glutamine. When changing this sequence only slightly to cytosine-uracil-adenine (CUA), (substitution of the middle nucleotide adenosine (A) to uracil (U)), the resulting amino acid is Leucine. These two distinct amino acids, even though in nucleotide code very similar, have different chemical formulas and very different biochemical properties. Glutamine for example is a polar amino acid, whereas leucine has non-polar properties. These different biochemical properties have important implications for the resulting protein due to their different behaviour during two and three-dimensional folding as we will read later on. Even worse, if there is an insertion or deletion of one nucleotide, multiple amino acid sequences may change. During the translation of the nucleotide code into the amino acid code by the ribosomes, amino acids themselves, through linkage of the N and COOH terminal ends are forming chains ranging from as little as 11 amino acids (TAL protein), for the smallest known protein up to 34 000 amino acids for the largest know protein (Titin). On average amino acid chain length is of 472 in eukaryotes and 320 in procaryotes. Once these long amino acid chains have formed (primary structure), they undergo a process called folding. First a two-dimensional (secondary structure), then a three-dimensional (tertiary structure) folding. This folding is dependent on the exact sequence of amino acids which allow for defined binding of specific domains of the amino acid chain, forming features like helices and sheets (secondary structure) which determine the three dimensional folding. Here, the change of amino acids can have a major impact. It has been shown that the formation of features (loops or helices) of the secondary structure is heavily dependent on the polarity of the amino acids. If, therefore, polar amino acids (e.g. Glutamine) are replaced by non-polar amino acids (Leucine), the original loop or helices might not form. However, these secondary features are detrimental for the tertiary structure. Only once the three dimensional folding is complete, and correct, are the active sites of a protein created which gives them their physiological function to carry out defined physiological tasks. A change of amino acid has thus the potential to a change the primary, secondary, tertiary structure and thereby the active site of a protein and by this its functionality.

It is on these changes of the active sites of proteins that the proposed process of evolution through natural selection can act, as none of the previous stages have any functional purpose. Accordingly, changes of the active site of proteins are proposed to cause a decrease or an increase in the fitness of the animal through, for example, a more or less performant active site. This change in the fitness of the animal would then lead to a lower or a higher chance for survival and the passing on of its genetic information. Mutations that cause an increase in fitness would favour that the mutation is passed on. Those mutations with a negative impact on fitness would have a fitness disadvantage, leading to the eventual disappearance of the original DNA sequence. This process is called natural selection. As can be seen from the above, these mutation cannot occur in any cell, as mutation in somatic cells (any cell of a multicellular organism other than a germ cell) will not be passed on to the next generation but will only have consequences for this organism. As such, the mutations have to occur in germ cells (any cell that gives rise to the gametes of an organism that reproduces sexually) as only such mutations can be passed on to the next generation. The problems that are linked to this limitation are discussed further in the corresponding section below.

However, since such random mutations are, as the term suggest, random, and for example the human genome is about 3 billion nucleotide pairs long, the theory of evolution requires the intervention of long periods of time. We will later deal with exactly how much time is needed in order to statistically have one new, functional active site formed by random mutations. This time is needed for random mutations, to accumulate in very specific parts of the coding region of a gene which will not prevent a functional three dimensional folding of the resulting protein.

These changes in protein functions are the basis upon which the proposed process of evolution takes place, transforming the very first, singular cell in the primordial soup over billions of years to all of the complex life that we can see today.

Now that there is a general understanding of the underlying ideas of the theory of evolution, lets have a look at the problems and impossibilities that this theory faces.

The problems of the theory of evolution

Protein active sites – the basis upon which evolutionary processes act

Seeing that the theory of evolution is based on the change of the function of proteins, having a look at the implications of their changes will start to give an understanding about the complexity of the matter.

The problem of the change of active sites through random changes in the amino acid sequence is made evident when looking at the way that these active sites work. These functional areas of proteins and their targets that they interact with in order to fulfil their function work through a lock and key principle. Meaning, that only a specifically shaped active site of a protein can interact with a specifically shaped active site of another protein in order to fulfil their function. There is only very little room for change in this relationship. Therefore by substantially changing the active site of one protein, this lock and key compatibility might be destroyed, thus rendering the newly “evolved” (more of a devolution) protein incompatible. Such a mutation would lead to the decrease of the fitness of the animal as the previous physiological function of the protein would no longer be fulfilled. This shows, that the random mutation of the nucleotide code will not only have to appear in the coding region of a gene, but also change the amino acid sequence in a specific way that the active site or the resulting protein will be altered just enough that it can interact more effectively with its counterpart.

In addition to these challenges, the above described mechanism will not lead to the development of a new function, but only acts upon an already existing one. For example, a change in the proteins involved in the detection of a chemical stimuli (e.g. the smell of a rancid smell of food) may yield a higher sensitivity to this smell but will not enable the organism to perceive a new, previously undetectable smell. In order to develop a new function, the changes in the protein have to be substantial in order to create a completely new active site with new functions. But what is the use of a new key (completely changed active site of a protein) if it does no longer fit in the old lock (the partner protein it interacts with) and there is no other lock it can fit into? Hence, there would need to be a simultaneous change in the active sites of multiple proteins that together can serve a newly emerging physiological function.

The above described problem becomes even more complex when considering that many of the essential cellular processes are driven by multiprotein complexes. For examples the RNA polymerase that we mentioned earlier to be responsible to transcribe DNA into mRNA is a protein complex of 14 subunits. Fourteen different proteins that interact with each other in order to form the working RNA polymerase complex. In such proteins, essential to cellular life, beneficial mutations would be severely limited due to the interaction of the different complex subunits. For such a complex to gain a new function, multiple involved proteins would have to undergo simultaneous, interdependent mutations to allow for the formation of a new, functioning complex with a new function. To understand what this means for a process driven by random mutations becomes evident when looking at the mathematical chances that are involved in creating only one new active protein site through random processes.

The statistical impossibility of the formation of a new active site through random mutations

The below information is a compilation of quotations from a theoretical approach as presented by Stephen C. Meyer (From his book « Signature in the Cell: DNA and the Evidence for Intelligent Design» Chapter 9) where Dr Meyer is discussing and expanding on the findings of a scientific paper published by Douglas Axe (Estimating the prevalence of protein sequences adopting functional enzyme folds 2004; DOI: 10.1016/j.jmb.2004.06.058). The compilation of quotations was taken from an article called “The Odds of a Cell Forming Randomly by Chance Alone” by Mark Goodnight published in 2018; https://cyberpenance.wordpress.com/2018/08/20/the-odds-of-a-cell-forming-randomly-by-chance-alone/ (Accessed 01.10.2025):

“The results of a paper he published in 2004 were particularly telling. Axe performed a mutagenesis experiment using his refined method on a functionally significant 150-amino-acid section of a protein called betalactamase, an enzyme that confers antibiotic resistance upon bacteria. On the basis of his experiments, Axe was able to make a careful estimate of the ratio of (a) the number of 150-amino-acid-sequences that can perform that particular function to (b) the whole set of possible amino-acid sequences of this length. Axe estimated this ratio to be a 1 to 1074. 

Since proteins can’t perform functions unless they first fold into stable structures, Axe’s measure of the frequency of folded sequences also provided a measure of the frequency of functional proteins – any functional proteins – within that space of possibilities (or “sequence space”). Indeed, by taking what he knew about protein folding into account, Axe estimated the ratio of (a) the number of 150-amino-acid sequences that produce any functional protein whatsoever to (b) the whole set of possible amino-acid sequences of that length. Axe’s estimated ratio of 1 to 1074 implied that the probability of producing any properly sequenced 150-amino-acid protein at random is also about 1 to 1074.  In other words, a random process producing amino-acid chains of this length would stumble onto a functional protein only about once in every 1074 attempts.

In nature every amino acid found in proteins…has a distinct mirror image of itself; there is one left-handed version, or L-form, and one right-handed version, or D-form…The probability of attaining, at random, only L-amino acids in a hypothetical peptide chain 150 amino acids long is…again roughly 1 chance in 1045.

Axe’s improved estimate of how rare functional proteins are within “sequence space” has now made it possible to calculate the probability that a 150-amino-acide compound assembled by random interactions in a prebiotic soup would be a functional protein. This calculation can be made by multiplying the three independent probabilities by one another: the probability of incorporating only peptide bonds (1 in 1045), the probability of incorporating only left-handed amino acids (1 in 1045), and the probability of achieving correct amino-acid sequencing (using Axe’s 1 in 1074 estimate). Making that calculation (multiplying the separate probabilities by adding their exponents: 1045+45+74) gives a dramatic answer. The odds of getting even one functional protein of modest length (150 amino acids) by chance from a prebiotic soup is no better than 1 chance in 10164.

The generally accepted age of the universe is around 13.8 billion years. When you translate that into seconds, the number of seconds that have passed in the entire history of the universe is 1017, also known as 10 to the power of 17. This is 1 followed by 17 zeroes. Or 100,000,000,000,000,000. 

Therefore, It is impossible to convey what this number represents, but let me try. We have a colloquial expression in English, “That’s like looking for a needle in a haystack.” We understand from this expression that finding a needle will be difficult because the needle – the thing we want – is mixed in with a great number of other things we don’t want. To have a realistic chance of finding the needle, we will need to search for a long, long time. Now consider that there are only 1080 protons, neutrons, and electrons in the observable universe. Thus, if the odds of finding a functional protein by chance on the first attempt had been 1 in 1080, we could have said that’s like finding a marked particle – proton, neutron, or electron (a much smaller needle) – among all the particles in the universe (a much larger haystack). Unfortunately, the problem is much worse than that. With the odds standing at 1 chance in 10164 of finding a functional protein among the possible 150-amino-acid compounds, the probability is 84 orders of magnitude (or powers of ten) smaller than the probability of finding the marked particle in the whole universe. Another way to say that is the probability of finding a functional protein by chance alone is a trillion, trillion, trillion, trillion, trillion, trillion, trillion times smaller than the odds of finding a single specified particle among all the particles in the universe.

And the problem is even worse than this for at least two reasons. First, Axe’s experiments calculated the odds of finding a relatively short protein by chance alone. More typical proteins have hundreds of amino acids, and in many cases their function requires close association with other protein chains. For example, the typical RNA polymerase – the large molecular machine the cell uses to copy genetic information during transcription… – has over 3,000 functionally specified amino acids. The probability of producing such a protein and many other necessary proteins by chance would be far smaller than the odds of producing a 150-amino-acid protein.

Second, as discussed, a minimally complex cell would require many more proteins than just one. Taking this into account only causes the improbability of generating the necessary proteins by chance – or the genetic information to produce them – to balloon beyond comprehension. In 1983 distinguished British cosmologist Sir Fred Hoyle calculated the odds of producing the proteins necessary to service a simple one-celled organism by chance at 1 in 1040000. At that time, scientists could have questioned his figure. Scientists knew how long proteins were and roughly how many protein types there were in simple cells. But since the amount of functionally specified information in each protein had not yet been measured, probability calculations like Hoyle’s required some guesswork.

If we assume that a minimally complex cell needs at least 250 proteins of, on average, 150 amino acids and that the probability of producing just one such protein is 1 in 10164 as calculated above, then the probability of producing all the necessary proteins needed to service a minimally complex cell is 1 in 10164 multiplied by itself 250 times, or 1 in 1041000.”

To summarise, the above information shows that from a statistical point of view, the whole age of the universe is by far not sufficient in order to create only one functional protein through random processes, not even considering the needed minimum of 250 functional proteins needed for a simple living cell.

For the following sections, we will have to ignore this overwhelming mathematical evidence against the power of random mutations and natural selection to be the basis for evolutionary processes, as any further discussions would be pointless.

Mutation of somatic cells vs germ cells – the difference of mutation on the organism level vs hereditary changes

As previously mentioned, mutations can occur in any cell of the body that contains DNA. However, where evolution is concerned, mutations in somatic cells is of little interest, since changes in somatic cells are only organism specific and cannot be passed on to the next generation. For a mutation to be passed on to the next generation it would have to occur in a germ cell, a cell that produces gametes (sperm and eggs) through meiosis. The logic behind this is simple, something that you do not give to your offspring cannot have any effect on it. This limitation has profound effects on the likelihood of mutations to occur (even less useful mutations), since the cell population of gametes is far lower than that of somatic cells. The human body nearly exclusively consists of somatic cells (estimated 3 trillion somatic cells), which are the building blocks of tissues and organs. In contrast, germ cells are far fewer in number and are specifically located in the gonads—testes in males and ovaries in females. Not only the low number of germinal cells makes a mutation in them less likely, but also their location. Gonads are usually well protected within the organism to protect these germinal cells from damage and environmental influences. As such, important external mutation factors like UV radiation have a much lesser influence on these cells.

Further, since the germinal cells contain the DNA for future generations, these cells and their DNA are underlying the most stringent DNA quality control and repair mechanisms. Whereas somatic cells mostly rely on a mechanism that is based on a process called non-homologues end joining (NHEJ), germinal cells mostly rely on a process called homologues repair (HR). The difference between these two repair mechanisms is that the NHEJ process is much more prone to mistakes as it directly ligates broken DNA (it finds the two broken ends of a DNA double strand break and glues them back together). In contrast, the HR is utilizing an intact sister chromatid or homologous chromosome as a template to ensure accurate repair without loss of genetic information. As a result, it is not surprising that germinal cells show mutations rates up to 10 fold lower than that of somatic cells.

As such, the statistical improbability of the above section “The statistical impossibility of the formation of a new active site through random mutations” is even further complicated through the three above described limitations:

1.     The cell population in which a hereditary functional mutation occurs is very low

2.     The location of the germinal cells protects them from exogenous factors

3.     Germinal cells have sophisticated DNA repair mechanisms which makes the integration of a mutation into the genome very unlikely

In addition to these further limitations, also the location of the mutation within the germline genome has to be correct. Not any gene has to be mutated in order to lead to the evolution of new species. In order to evolve new body plans and substantial changes of an animals phenotype very specific and highly regulated genes have to be affected. These genes, called Homeobox genes, are the only possibility for the proposed evolutionary processes to generate substantial change and the appearance of new life forms. Let’s have a closer look at the problems that the mutation of these genes would entail.

Hox genes, the bodies’ structural blueprint

For new functions to appear, significant changes have to take place within the animal. Especially when considering evolutionary milestones like the development of exo- and endoskeletons, lungs from gills, the development of flight, or the development of whales from dog-like animals. All these major evolutionary steps, needed a complete remodeling of the previous body structure. It is evident, that such changes and their implications in the fetal development are massive. Faced with this problem, evolutionists thought to have found the answer when scientists discovered the existence and role of so called homeobox genes.

Homeobox (Hox) genes are master control switches that control the realisation of the body plan from the genotype (the information on the contained in the code of the DNA) to the phenotype (how this information is expressed on physical characteristics). These genes are active during embryonic development and are of crucial importance for the formation of a well-functioning organism. Specific Hox genes may control where the head forms, where limbs form, a tail or wings. These master switches work like circuit breakers and either turn on or turn off an array of other genes. During experimentation with the fruit fly, Drosophila melanogaster, researchers caused Hox genes to be expressed in abnormal locations and either prevent development of structures or promote their development. For example Pax-6 (a Hox gene) expression controls the development of eyes. A fly with abnormal expression could form an eye on a leg, the antenna or abdomen. It is for this reason that evolutionists have regarded these genes as the genetic answer to their long asked questions how mutations can generate significant alterations in the body plan. Thereby, for example, explaining how crabs evolved into spiders and dinosaurs into birds.

The problem with this theory is, however, as fundamental as the importance of the Hox genes themselves. Changes in the expression of the Hox genes and thereby in the orderly embryonic development never result in the creation of a new body plan. Even slight mutations in these genes will lead to catastrophic developmental changes which will inevitably lead to a non-viable, or severely deformed embryo. This critical role of the Hox genes and the fact that only slight changes to their orderly expression leads to deformed and non-viable offspring has been repeatedly shown: A study on the experimentation on the alteration of the ALX1 gene (the class of Hox genes that determines facio cranial development) in chickens showed, using targeted gene expression (gain- and loss-of-function), that all of the resulting embryos had severe craniofacial malformations (reduced expression) or abnormal, nonfunctional morphologies (increased or misexpression) (Fritz, J. A., et al. (2019). "Shared developmental program strongly constrains beak shape diversity in birds." Science 366(6464): 1339–1343.)

However, since Hox genes are the master switches that regulate the body plan, they are the only possible explanation for major changes to account for the development of the diverse life of today, originating from one single ancestor cell. If therefore, even the slight manipulation of their orderly expression leads to deformed and on-viable offspring, these genes cannot have played a role in the proposed evolutionary development.

Useless evolutionary leftovers or essential structures?

When looking at modern man, evolutionists have long argued about apparent useless leftovers of evolutionary processes that can still be found in the human body. One of these supposed evolutionary leftovers is the appendix. This structure is often regarded as useless and will simply be removed if inflamed. However, modern research has found that this tiny structure has important functions during embryonic development, as well as throughout a persons life.

The following extract was taken from “The Appendix: A Thorn in Evolution's Side? » by  BRIAN THOMAS, PH.D (published in 2013 ; https://www.icr.org/article/7304 Accessed 01.10.2025):

« The appendix is a worm-shaped organ attached to the entrance of many mammal's colons. It contains lymphatic tissue, which integrates with the body's circulatory and immune systems. Researchers recently discovered that it harbors a cache of beneficial bacteria that can recolonize the gut after alimentary trauma. In contrast, Darwin imagined that it was a useless leftover from a distant evolutionary past. Darwinists today expect the appendix to appear in animals that supposedly share evolutionary ancestors. But details from a new study on the appendix refute both Darwin and Darwinists.

Publishing in Comptes Rendus Palevol, an international team mapped the distribution of mammalian appendixes onto a preconceived picture commonly called a "tree of life." These diagrams depict which animals are supposedly most closely related to others, and they assume that all the represented creatures share a common ancestor.

The tree of life should reflect evolutionary origins if the appendix showed up along lines of evolutionary ancestry. But, as is typical when constructing these imaginary trees, the data did not fit any evolutionary pattern.

The study authors found the appendix in 50 different mammal forms, most of which they believe to have evolved along separate lines of ancestry. For example, some primates, some rodents, and certain carnivores harbor an appendix, but it doesn't appear in all members of any one of those categories.

Science Now said about the study, "They found that the 50 species are scattered so widely across the tree [of 361 mammals] that the structure [the appendix] must have evolved independently at least 32 times, and perhaps as many as 38 times." «

Very interesting that an appendix developed 32 times in mammals in which this structure is postulated to be a useless remain of evolutionary processes.

Actually, the appendix plays a significant role during embryonic development, particularly in the establishment of the immune system within the gastrointestinal tract and is developed as early as the 6th week of pregnancy. This early development suggests that the appendix functions as a site for primary antigen stimulation, potentially initiating immune responses before birth, which aligns with the theory that the development of gut microbiota begins in utero (Single-cell sequencing of the vermiform appendix during development identifies transcriptional relationships with appendicitis in preschool children Lingdu Meng et al 2024 (https://doi.org/10.1186/s12916-024-03611-9)).

Furthermore, the appendix's strategic position and complex histological structure, including its rich blood supply and specialized tissues, indicate it is not a vestigial organ but a specialized structure with important developmental functions. Its development coincides with critical periods of gut organization and immune system maturation, suggesting its importance extends beyond its adult function (A review of the function and evolution of the cecal appendix Heather F. Smith 2022 (https://doi.org/10.1002/ar.24917).

Besides of the appendix, there are also other structures like wisdom teeth and tonsils which have been shown to be not mere evolutionary leftovers.

The problem of slow gradual change over long periods of time

The evolutionary philosophy also encounters serious problems when long periods of time with slow gradual changes are faced with the existence of highly complex cellular machines and structures. The complexity of such cellular features has been described as irreducible. This means that they can only work if all of the components and building blocks of this machine/structure are there at the same time, arranged in a very specific manner. When only a few components are removed from these complex structures, they cease to function. But what would the driving force of evolutionary processes be to preserve a whole array of different proteins that do not fulfil any function until the very last needed protein has evolved that fits perfectly with the previously evolved components to then form a functioning complex? One of the most striking examples for such a molecular machine is the flagella, a complex molecular engine which is used for locomotion of unicellular life forms. The complexity of this machine becomes evident when looking at it in a little more detail:

“The bacterial flagellum is an irreducibly complex process. An irreducibly complex system is one that requires several interlacing parts to be present at the same time, where the removal of one or more parts causes the whole system to malfunction. Destroy one part and the whole system falls apart. Like an electrical motor, the flagellum contains a rod (drive shaft), a hook (universal joint), L- and P-rings (bushings/bearings), S- and M-rings (rotor), and a C-ring and stud (stator). The flagellar filament (propeller) is attached to the flagellar motor via the hook. To function completely, the flagellum requires over 40 different proteins. The electrical power driving the motor is supplied by the voltage difference developed across the cell membrane. This motor is one of the nature’s best molecular machines! Some scientists have called bacterial flagella the “most efficient machine in the universe” with its self assembly and repair, water-cooled rotary engine, proton motive-force drive system, forward and reverse gears, operating speeds of 6,000 to 17,000 rpm, direction-reversing capability, and hard-wired signal-transduction system with short-term memory. » (Bacterial Flagella—Icon of the Intelligent Design Movement by Dr. Alan L. Gillen published in 2015 (https://answersingenesis.org/intelligent-design/bacterial-flagella-icon-of-the-intelligent-design-movement/ (Accessed 01.10.2025)).

Looking at such complex systems, evolutionary processes cannot account for their development since the supposed non-functioning pre-cursors, the incomplete assembly parts of the whole machine, would not have been selected for by natural selection.

The glomerulus, friend or foe?

The glomerulus is a specialised tissue in the kidney. It can be described as the ultra-filtration center of the body in which the blood is purified from toxins and excess levels of minerals to be excreted with the urine. As such, the glomerulus is playing a critical part in the bodies survival as it would otherwise intoxicate itself through metabolic waste products.

In addition to the purifying function of the glomerulus, it also plays a crucial role by preserving the water balance within the body. Excess water is rejected through an increased filtering activity, whereas the filtering activity is reduced and the urine concentrated in order to preserve the available resources.

Considering this function, the glomerulus can work in two ways. Let’s take the example of a fish. For a fish that lives in fresh water conditions like lakes and rivers, where the osmotic pressure of their environment is lower then the physiological osmotic pressure (the salt concentration of the environment is lower than the salt concentration of the inside of the animal), the glomerulus has to actively eliminate large volumes of water. This is because the higher salt concentration within the animal is drawing water from the less salty water in an effort to equilibrise the osmotic pressures. Without the continued work of the glomerulus, the fish would swell up with water and eventually explode.

On the other hand, for fish that live in salt water conditions like the ocean, the osmotic pressure is inversed. Here the environmental salt concentration is much higher than the physiological salt concentration. As a result, the salty environment is constantly pulling water out of the organism. Here the glomerulus, if it was working at full potential, would lead to an aggravation of the problem by eliminating additional fresh water from the animal. As a result, the glomerulus in salt water living fish has been found to be turned off completely.

Keeping the above in mind, following the proposed phylogenetic tree, all life is supposed to have originated in the oceans. Land animals are supposed to have developed from a species of fish called lobe-finned fish. The particularity of this fish species is that it possesses fleshy fins which support their weight which is taken by evolutionists as a basis upon which this fish was able to venture for short periods of time onto land. Then, over millions of years those fish evolved into tetrapods—four-limbed vertebrates from which evolved amphibians, reptiles, birds, and mammals. The oceans during the time period when this transition from ocean based life to land based life took place are thought to have had the same salinity (salt concentration) as the oceans today. Given these environmental conditions, the same osmotic pressure acted upon the lobed finned fish as described above. Fresh water was constantly drawn out of the fish’s tissue following the osmotic pressure. It is therefore more than surprising that early lobe-finned fish have glomeruli. Why would an exclusively salt water living fish evolve a glomerulus, a structure that not only has no positive but a negative effect on its fitness and survival unless it is turned off. Why would this fish have a structure that eliminates fresh water from its body in an environment that is already draining its from this vital resource? As such, the glomerulus stands in direct opposition to the fundamental requirements of evolutionary processes where mutations are only preserved through natural selection if they infer a fitness advantage.

Evolutionists claim that the glomerulus was evolved by marine fish as a useful and needed structure in order to eliminate divalent ions like magnesium, calcium, and sulfate as part of their osmoregulation. However, why would the lobed finned fish (and all teleost) need to evolve such a highly complex structure which as a side effect of eliminating these ions also eliminates valuable fresh water, if a much more advantageous process did already exist? Lobe finned fish, like all teleost are capable to excrete excess ions through their gills, a process that does not include the elimination of “fresh water”. The glomerulus of lobed finned fish has been shown to, even though evolved in a marine environment, be adapted to the demands of freshwater life, where the primary challenge is excreting excess water.

This contradictory picture changes completely if we look at the apparent incoherence of the presence of a glomerulus in a salt-water fish from a different angle. If we consider that these fish did not undergo evolutionary processes in a salty ocean but were created for a fresh water environment which then changed during the global flood during Noah’s time solves the mystery of the glomerulus.

Intelligent design/creation advocates postulate, that the addition of salt to the world’s oceans happened during the global flood as described in Genesis. Here, the "fountains of the great deep" (Genesis 7) were opened and released vast amounts of salty, subterranean brine into the oceans. Additionally, the Flood caused massive erosion of landmasses, volcanic activity, and the weathering of volcanic ash and basalt, all of which contributed large quantities of sodium and other salts to the oceans. The intense post-Flood climate, which was hotter and wetter, is believed to have further accelerated the weathering of rocks and the release of salts into the sea. As evidence for this process, the presence of massive, pure salt deposits composed of halite (NaCl), in the geologic record beneath the Mediterranean seafloor are given. These indicate the catastrophic salt deposition during the flood. These deposits could not have formed gradually through the evaporation of seawater during the proposed Messinian and Lago Mare event which are supposed to have taken place 5.97 and 5.33 million years ago when the Mediterranean became largely isolated from the Atlantic Ocean. As can be seen from modern processes driven by evaporation, such long-term processes are producing impure salt deposits that contain organic matter. As such, the pure salt beds found in the geological record were formed by the rapid precipitation of super-heated, supersaturated salt brines extruded from deep within the Earth during the Flood, which then cooled and precipitated out in pure form.

The Cambrian explosion

Have you ever heard about the Cambrian explosion? The Cambrian explosion is a period of time believed to have accrued around  541 million and approximately 530 million years ago at the beginning of the Cambrian Period. In rock layers that are attributed to these times of earth’s history, a sudden (therefore the term explosion) appearance of fossils occur that present all of the know body plans of modern animals. Whereas the previous, older rock layers do not show a record of transitional forms that might have led, through evolution, to the appearance of such diversity. These early Cambrian rock layers show that forty phyla of complex animals suddenly appear in the fossil record, no forerunners, no transitional forms leading to them. This topic is dealt in detail with in the book “Darwin’s doubt - The Explosive Origin of Animal Life and the Case for Intelligent Design” by Stephen C Meyers and clearly elaborates the difficulties that this sudden appearance of such a diversity of body plans poses for the theory of evolution. In his book Meyer argues that during the Cambrian period (~540 million years ago), many major animal phyla appear abruptly in the fossil record, over a “geologically short interval,” with complex body plans, organs, etc., and without obvious precursors in earlier (Precambrian) strata. He holds that the fossil record’s lack of transitional forms (ancestors with intermediate features) for many of these animal types is not simply due to preservation or scarcity of fossils, because many Precambrian rock layers are good for fossilization and do preserve soft-bodied organisms, but still don’t yield the expected precursors. Furthermore, this sudden appearance of large quantities of fossils that exhibit a previously unprecedented diversity and complexity of life and body plans can be seen on a global scale.

All, the explosive appearance of a large number of fossils, the global distribution of such fossils and their presence, are indications for a global, catastrophic flood that caused the death of large numbers of animals where the waters covered the whole earth. The absence of missing transitional forms is easily explained by the fact that all animals were created rather than appeared and changed over millions of years of evolution.

Epigenetics – Change through inbuilt adaptability rather than mutation

We have previously established that the proposed process of evolution can only work on the changes of active sites of proteins and that these proteins are coded for in the nucleotide sequence of the DNA.

However, scientists have discovered that significant changes within an organism can take place within an animals lifetime and that these changes can even be preserved over multiple generations even though not based on the change of the DNA nucleotide sequence. It is therefore fitting that these processes were called epi-genetics (epi=above). Epigenetic processes involve non-permanent changes to the DNA where epigenetic factors bind to it and the proteins (histones) that organise the DNA. Through such a binding, the DNA sequences, and therefore the genes that are found on them, are rendered accessible or inaccessible for transcription by the RNA polymerase. The effects are important, as a gene that cannot be accessed, cannot be transcribed and will not be translated into a protein. The lack of a specific protein can affected whole physiological processes and cause them to be dormant. Also the reverse can be the case where the binding of an epigenetic factor leads to an increased accessibility of the DNA, therefore more copies of the genes that are located on this region and more proteins, thereby boosting the affected physiological process.

A very prominent example for this is the synthesis of melanin. When exposed to sun, we produce pigments, called melanin, which are deposited in the upper layers of our skin in order to protect the underlying cells from harmful UV-rays. During winter, when there is little sun, few of these pigments are produced, since the metabolic costs for producing them does not justify the little protection they give against the weak winter sun. In summer, however, when we are exposed to prolonged periods of more intense sunlight, larger amounts of this pigment are expressed. We can therefore see, that significant short-term changes in our skin can occur, without the need of mutations. This is, however, only possible if the information for the synthesis, transport and degradation of melanin is already present in the genome. It is only a matter of rendering it accessible. Besides of this example, epigenetic regulation has been found to be responsible for many other characteristics like hair colour, height, obesity, immune function, behaviour like the stress response and environmental adaptation.

Another striking example for the short-term change due to epigenetic processes are salmon. Especially, where male salmon are concerned, their appearance changes completely when transitioning from their ocean phase to the fresh water phase in preparation to mating. During their ocean phase, these salmon are relatively unremarkable with a grey, silvery and fish typical, streamlined shape (See Figure 1 below) but when transitioning to their fresh water phase, the change in salinity is bringing about massive changes in their appearance (See Figure 2 below). This changes appearance is marked by a bright red colour, the formation of hook shaped mouth and a dorsal hump. This change only takes days to several weeks. Seeing the important difference in their appearance, one could think that these are different species of fish. However, only the change of environmental parameters is bringing about this massive change within a very short period of time. Besides of these outward changes, the salmon also undergoes significant physiological changes due to its transition from salt to fresh water. One of those is the activation of their glomerulus, which we discussed in the section above, that enables them to eliminate excess water from their bodies.

Concluding therefore about the appearance of new species based on their appearance is in no way a sign for evolution. Darwin used the finches (also known as Darwin’s finches) as an example to show evolution by comparing their beak form and size with the environment that they were living in. According to his conclusion a variation in the beak characteristics was proof that evolutionary processes were at work that lead to adaptation of the bird’s beak to the food source that was present. Finks that needed stronger beaks to eat hard to crack foods like seeds and nuts developed larger, stronger beaks, whereas finches that were scavenging insects needed smaller, more precise beaks. However, the beaks were still beaks. Their general structure did not change, their position on the bird did not change and their function did not change. The observed changes are therefore only due to a modification of the already existing, not due to the appearance of something new. It is therefore plausible that these changes were due to epigenetic processes rather than mutations. Evolution focussed studies suggest that this change was brought about through the mutation of ALX1 which is a homeobox gene responsible for cranio-facial development (Lamichhaney S, Berglund J, Almén MS, Maqbool K, Grabherr M, Martinez-Barrio A, Promerová M, Rubin CJ, Wang C, Zamani N, Grant BR, Grant PR, Webster MT, Andersson L. Evolution of Darwin's finches and their beaks revealed by genome sequencing. Nature. 2015 Feb 19;518(7539):371-5. doi: 10.1038/nature14181. Epub 2015 Feb 11. PMID: 25686609.) However, the study did not show that an actual mutation of the ALX1 gene was responsible for the observed changes in the beak size and shape of Darwin’s finches. It was simply assumed that the ALX1 gene was affected after determining that a 240 kb haplotype was found to differ among different finches of different beak morphologies and that this haplotype comprised the location of the ALX1 gene. Remembering the serious consequences of the mutation of Hox genes, as presented in the earlier corresponding section, as well as the speed of the diversification of the beak sizes, it is unlikely that the postulated change in craniofacial features of Darwin’s finches is actually due to gene mutation but more likely due to epigenetic factors. For memory, experimentation on the alteration of the ALX1 gene in chickens showed, using targeted gene expression (gain- and loss-of-function), that all of the resulting embryos had severe craniofacial malformations (reduced expression) or abnormal, nonfunctional morphologies (increased or misexpression) (Fritz, J. A., et al. (2019). "Shared developmental program strongly constrains beak shape diversity in birds." Science 366(6464): 1339–1343.) This, therefore shows, that as discussed in the HOX gene section, that alterations of the highly conserved homeobox genes will result in catastrophic morphological changes.

Additionally, it has been shown for many animals that epigenetic changes are hereditary and can be passed on for multiple generations (mostly by the mother, since the spermatozoid is carrying very little epigenetic information when compared to the oocyte). Unfortunately, very little information is available for humans but some epigenetic based changes have already been shown to be passed on in humans. For example, epigenetic changes that are linked to maternal smoking have been shown to be passed on to children and even grandchildren.

Interestingly, in Exodus 34:7, God says to Moses that: “Keeping mercy for thousands, forgiving iniquity and transgression and sin, and that will by no means clear the guilty; visiting the iniquity of the fathers upon the children, unto the third and fourth generation.”

Whereas this passage seems to say that God will hold the following generations responsible for the sin that their father committed, this is clarified by Ezekiel 18:20: “The soul that sinneth it shall die. The son shall not bear the iniquity of the father, neither shall the father bear the iniquity of the son: the righteousness of the righteous shall be upon him, and the wickedness of the wicked shall be upon him.”

It therefore clearly stated that each and everyone is responsible for their sin and sin will not be passed on to the following generation. However, what does Exodus 34:7 then suggest? A potential answer might be found in epigenetics. As described above, epigenetic changes are hereditary. Such epigenetic changes are created through the environment (e.g. sun exposure), as well as through the lifestyle of a person (smoking, alcohol, etc.). We have also seen, that epigenetic changes have an influence on behaviour (Learning and memory, stress response, addiction, neurodevelopmental disorders). It is therefore possible that epigenetic changes caused by sinful behaviour are passed down to the children and grandchildren that inherit a propensity towards the sinful behaviour of their parents and grandparents, up to the third and fourth generation. These generations will be visited by the iniquity of their fathers through the epigenetic changes. Why then does the Bible state the iniquity of the fathers will be visited unto the children, since we read above that epigenetic changes are mostly passed on from the mother rather than from the father? The reason that the father is given in the Bible could simply be due to the sociological and cultural system that prevailed at the time when the books of the Bible were written. During these times, the father was the one from whom the children inherited wealth, title and blessings. For example, in the new testament, the genealogy of Jesus Christ is given. Here, the genealogy of Joseph and not Marie is given, even though Joseph was not Jesus’ actual father (since Jesus was conceived by Marie through the Holy Spirit and not through intercourse with her husband Joseph which was well known to the writer of the book). This highlights the social structure and how it influenced the writers of the Bible to highlight the importance of the role of the father on the following generations.

The first living cell – a brief look into the impossible

Since the process of evolution can only act upon a living organism, the question rises on how the first living cell came into being. A question that has kept origin of life scientists busy for centuries, without finding an answer to it.

Looking at the proposed conditions of the earth when the first living cell was supposed to have auto assembled, we are faced with what is called a primordial soup (interesting how evolution keeps referring back to the term “soup” when events are described for which there is no explanation since after the big bang at the beginning of time there was a  “cosmic soup” and no at the beginning of life there is again a “primordial soup”). A large body of (most likely) fresh water, rich in inorganic elements. How did the first nucleic basis, organic molecules, form from this inorganic soup? Evolutionary scientists propose that long periods of time and spontaneous formation of the building blocks of life, carbohydrates, nucleic acids, lipids, and proteins occurred. However, even with advanced laboratory techniques, researchers cannot reliably produce the necessary molecules under prebiotic conditions, as these experiments require highly controlled, interventionist protocols that are not reflective of early Earth environments. For instance, the synthesis of amino acids in the Miller-Urey experiment, while demonstrating the formation of some organic compounds, is insufficient to explain life's origin because it produces a mixture of unnatural amino acids toxic to life and fails to address the challenges of forming biologically relevant macromolecules.

Tour emphasizes that the synthesis of life’s building blocks (carbohydrates, nucleic acids, lipids, and proteins) faces immense hurdles. Even if these molecules were present in the correct proportions, the process of linking them into functional macromolecules like proteins and RNA requires precise, step-by-step chemical interventions, including protecting groups and selective catalysts, none of which would have been available on the early Earth. Furthermore, achieving homochirality—where only one enantiomer (e.g., left-handed amino acids) is present—is essential for biological function, yet natural processes do not reliably produce such purity, and any imbalance would rapidly degrade.

Additionally, the stability of these molecules is a major issue. A recent study co-authored by James Tour and colleagues demonstrates that proteins and RNA degrade too quickly under natural conditions to accumulate in sufficient quantities for life to emerge, with degradation rates far exceeding the time required for their formation. For example, the discovery time for a functional protein in one litre of water would be on the order of 10,000 years—far longer than its half-life—making spontaneous formation implausible.

Just assuming that this process actually took place and an information rich, nucleic acid based molecule (DNA or RNA) was formed by chance, the prescribed environment is highly unfavourable for its stability. As a result, any formed nucleic acid molecule would degrade within a few minutes. To protect it, like all cells do, a cell membrane is needed in order to create a controlled, protective internal environment. The cell membrane, made up of a phospholipid bilayer (another organic molecule for which chance must be made responsible) thus has to spontaneously have formed and/or closed around the just formed fragile  nucleic acid molecule. Great, we have the first cell! Do we? No. We simply have a nucleic acid molecule encapsulated in a phospholipid bilayer. What is missing to make it a cell? Pretty much everything. Can this cell be considered living? No. In order to be living there would need to be cellular respiration with the exchange of nutrients and respiratory waste products between the extracellular and intracellular space. There would need to be the production of energy. Is this enclosed nucleic acid molecule able to replicate itself in order to be considered to be at the very root of the tree of life? If this nucleic acid molecule was DNA the answer is no. There is no complex cellular replication system in place with all of its needed proteins and cellular architecture to facilitate this process. But is this not all coded on the enclosed nucleic acid molecule? Maybe, but what is the use of the information on the nucleic acid molecule if no one can read it. Above, we have briefly described the process needed to transcribe and translate the information of the DNA and RNA into proteins. Where do therefore the specialised, highly complex protein complexes come from that can fulfill this task? Remember, we are talking here about the first DNA or RNA, enclosed in a phospholipid bilayer. If the very basis to read and translate the code of the just formed DNA or RNA are lacking, the nucleic acid molecule and its contained information is worth nothing. The only solution is that all of the needed, precise and highly specialised, interactive proteins must also all have formed by chance and then had all to be the right place at the right time to be enveloped into the phospholipid cover. Let’s assume that the nucleic acid molecule, as well as the highly specialised protein complexes came all into being by chance at the same time and were then spontaneously enveloped. Where does then the cellular energy come from that is needed to carry out these processes performed by the protein complexes? The RNA polymerase complex needs cellular energy to function, as do the ribosomes that translate mRNA into the needed amino acids. Without this energy, there will be no transcription of DNA or translation of RNA. Here, the formation of cellular energy carriers by chance can hardly be used as an explanation. The reason is that since the cell is now an enclosed environment, the limited quantity of cellular energy that was enveloped when the phospholipid bilayer closed would have been used up in a very short period of time. As such, not only the energy but also the energy yielding structures and metabolism must have been developed by chance and be at the right time at the right place to be incorporated at the time of the formation of the phospholipid bilayer around the DNA. If there is a metabolism that is producing energy, there has to be cellular respiration (exchange of needed raw materials and waste products). However, the phospholipid bilayer acts as a barrier to separate the external from the internal environment. The only solution would be to have specialised channels within the just formed phospholipid layer that allow the regulated exchange of molecules between the two sides. Where do those suddenly come from? Not only this, but the production of cellular energy cannot take place simply within the cellular space (cytoplasm) since chemical gradients have to be formed in order to yield energy rich molecules. This means that we now need a cell within a cell. A specialised compartment (cell organelle) that has its own phospholipid layer with specialised proteins therein to exchange raw materials and waste products with the cytoplasm. This cannot have formed in the cell, since the cell just came into being. Therefore it must have formed, by chance, in the primordial soup. Lets just assume that all of the above happened by chance and we have a living, functioning cell. How is it possible, that this cell, the very first one that just came into existence has all of the complex cellular architecture and precise molecular protocol to create a daughter cell? This cell would need to have all of the architecture and molecular processes to undergo cell division including the exact and complete copy of the whole nucleic acid molecule, the exact and equal separation of the copies and the original into opposite parts of the cell, cell elongation, the formation of a dividing wall at the cell’s midpoint and finally cell division into identical daughter cells. This brief explanation does not even begin to describe all of the complex molecular mechanisms and the needed cell architecture that is needed to perform a cell division.

A selection of 10 questions that evolutionists cannot answer

Below is a selection of 10 questions as they were formulated by Prof. Walter Veith and presented at the Creation or Evolution Summit in 2025 (source: https://www.youtube.com/watch?v=-xZRjqnlr3Y&t=3621s)

Question 1: If the evolution of life started with low diversity and diversity increased over time, why does the fossil record show higher diversity in the past and lower diversity as time progressed?

Question 2: If evolution of necessity should progress from small creatures to large creatures over time, why does the fossil record show the reverse?

Question 3: Natural selection works by eliminating the weaker variants, so how does a mechanism that works by subtraction create more diversity?

Question 4: Why do the great phyla of the biome all appear simultaneously in the fossil record, in the oldest fossil records, namely in the Cambrian explosion, when they are supposed to have evolved sequentially?

Question 5: Why do we have to postulate punctuated equilibrium to explain away the lack of intermediary fossils when gradualism used to be the only plausible explanation for the evolutionary fossil record?

Question 6: If natural selection works at the level of the phenotype and not on the level of the genotype then how did genes, mitosis and meiosis with their intricate and highly accurate mechanisms of gene transfer evolve?

Question 7: The process of crossing over during meiosis is an extremely sophisticated mechanism that requires absolute precision; how could natural selection bring this about if it can only operate at the level of the Phenotype?

Question 8: How can we explain the evolution of two sexes with compatible anatomical differences when only the result of the union (increased diversity in the offspring) is subject to selection but not the cause?

Question 9: How can the evolution of the molecules of life that all require totally different environmental conditions to come into existence without enzymes when not even the perfect conditions, artificially created can bring forth some of these molecules?

Question 10: How do we explain irreducible complexity?

What does evolution do to God’s character?

Let’s have a look beyond the above, science based arguments against evolution. Because there are those that say that they believe in God, but also in evolution and an earth that is millions of years old. What do millions of years and multiple mass extinction events suggest about the character of God and why is it a problem to believe in both, an old earth in which evolution brought forth what we see today?

Looking at it from a more theological angle, the theory of evolution is distorting the character of God in multiple ways to a point that God as the loving Father, that created a perfect world in order to share His glory with it, becomes an arbitrary tyrant that created a world full of destruction and evil, seemingly without a plan, while humans, created in His image, are a mere byproduct of evolution.

Why would an omnipotent and all-knowing God need millions of years and innumerable intermediary, imperfect lifeforms in order to bring about humans, the sole creature on earth that God gave His only begotten Son for in order to save them? Why would a God that loves His creation, make an earth filled with suffering and death? In fact, evolution can only work where there is death, as otherwise there would not be any selection. Evolution therefore suggests, that God, knowingly and willfully, created or guided evolutionary processes that brought about imperfect beings, destined to die and vanish from the surface of the earth forever. Does this sound like a loving Father to His creation?

The same applies to the multiple mass extinction events during which the majority of the then living creatures are supposed to have died. Did God not create and is able to control the elements? These mass extinction events therefore suggest once again, that God knowingly and willfully brought about these events of unimaginable scale to wipe out what he had created. Counterarguments can mention Noah’s flood during which God had to destroy the earth by water in order to preserve the last living hope for the line that would bring forth the Saviour Jesus Christ. Without this last-minute and long-announced judgement there would have been no Saviour to be able to reconcile us humans to God. We see, that the reasons why God had to destroy the earth with a flood were not arbitrary, neither taken lightly, but were the last resort for Him in order to save humanity.

Which God do you prefer to believe in, to trust and to serve? A God which created a perfect world. A world without suffering, pain, want and death. A world in which all creatures lived in harmony with each other and with God, in which God provided every need to every of His creatures. A God that loves His creation so much that He gave His only begotten Son to save it. A God that has a plan and this plan is to be reunited with you in eternal peace.

Or do you prefer to believe in a God which created a world that, from the start, was based on the survival of the fittest. Where the stronger rule and the weaker suffer. In which death is a necessary means. Where suffering, pain and hunger are the outcome of a purposely imperfect creation. A God who allows for arbitrary suffering. In short a God of fear, a tyrant that remained distant from His creation as a type of video game in which he intervenes but will never share in its suffering.

Closing remarks

As we can see throughout this document, the theory of evolution is facing insurmountable difficulties at the very basis of the proposed processes. Just the formation of a new protein active site (one!) by chance alone is statistically implausible, not even considering the hundreds and thousands of such changes that are needed to create new physiological processes that can cater for new functions and body plans.

Even though this document is only a very simple exposition that does not go into detail of the involved processes it helps to draw the big picture around the theory of evolution and the difficulties it faces.

The origin of life and what life actually is will always remain a mystery to those that try and search for the answers within the common consensus of the limited philosophy of modern sciences.

For further studies into the origin of life and compelling evidence for a creation based genesis, it is recommended to have a look at the YouTube video and series from “Is Genesis History” - https://www.youtube.com/@IsGenesisHistory

For those that prefer reading over videos, the books of Stephen C Meyers are strongly recommended:
1. Signature in the Cell – DNA and the evidence for intelligent design

2. Darwin’s Doubt – The explosive of animal life and the case for intelligent design

3. The Return of the God Hypothesis – Three scientific discoveries that reveal the mind behind the universe

For the books of Stephen C Meyer, is has to be pointed out that, even though the scientific evidence speaks for itself, Mr Meyers view of the age of the universe and the earth are not in line with the biblical narrative.

Sources and References

A) The Bible

B) Peer-reviewed primary scientific research

1. Axe DD. Estimating the prevalence of protein sequences adopting functional enzyme folds. J Mol Biol. 2004;341(5):1295–1315. doi:10.1016/j.jmb.2004.06.058.

2. Fritz JA, Brancale J, Tokita M, Burns KJ, Hawkins MB, Abzhanov A, et al. Shared developmental programme strongly constrains beak shape diversity in songbirds. Nat Commun. 2014;5:3700. doi:10.1038/ncomms4700.

3. Lamichhaney S, Berglund J, Almén MS, Maqbool K, Grabherr M, Martinez-Barrio A, et al. Evolution of Darwin's finches and their beaks revealed by genome sequencing. Nature. 2015;518(7539):371–375. doi:10.1038/nature14181. PMID:25686609.

4. Meng L, Yang Y, He S, Chen H, Zhan Y, Yang R, et al. Single-cell sequencing of the vermiform appendix during development identifies transcriptional relationships with appendicitis in preschool children. BMC Med. 2024;22:383. doi:10.1186/s12916-024-03611-9.

C) Peer-reviewed scientific review

5. Smith HF. A review of the function and evolution of the cecal appendix. Anat Rec (Hoboken). 2023;306(5):972–982. doi:10.1002/ar.24917. Epub 2022 Apr 1.

D) Scholarly books

6. Meyer SC. Signature in the Cell: DNA and the Evidence for Intelligent Design. New York, NY: HarperOne; 2009.

7. Meyer SC. Darwin's Doubt: The Explosive Origin of Animal Life and the Case for Intelligent Design. New York, NY: HarperOne; 2013.

E) Non-peer-reviewed institutional / expert publications

8. Thomas B. The appendix: A thorn in evolution's side? Institute for Creation Research. Published March 6, 2013. Accessed October 1, 2025.

9. Gillen AL. Bacterial flagella—Icon of the intelligent design movement. Answers in Genesis. Published June 19, 2015. Accessed October 1, 2025.

F) Non-peer-reviewed web source

10. Goodnight M. The odds of a cell forming randomly by chance alone. Cyber Penance. Published August 20, 2018. Accessed October 1, 2025.

G) Conference presentation / recorded lecture

11. Veith W. Ten Questions Regarding Evolution. Creation or Evolution Summit; March 28, 2025. Conference presentation/video. Accessed October 1, 2025.

For more great scientific facts about how science is providing more and more strong arguments against evolution and for a Creator follow the below link:

View or download by clicking on the document below.

Explore more contents