Reasons why it's impossible to believe in the theory of evolution

Seriously?

Reasons why it's impossible to believe in the theory of evolution.

1. Dinosaur soft tissues, blood vessels, red blood cells, and even DNA discoveries. How could any soft tissue or organic material be preserved for millions of years? It's not possible. The half-life of DNA is 521 years which means that after 50,000 years there shouldn't be any recognizable DNA left in the sample. It has been difficult to analyze DNA from soldiers who died in WWII war, so claims that dinosaurs lived 65 million years ago are absurd. For DNA to be preserved even for over 4,000 years, it needs special conditions, such as rapid burials.
   
   

   

   T.Rex red blood cell

2. DNA doesn't dictate organismal traits or characteristics. This is easily understood by examining mechanisms that regulate cellular differentiation. For example, in a human body, there are ~300 different cell types and the same DNA can be found in all of them (there are only a couple of exceptions). This means that DNA doesn't determine cell identity, tissue type, organ shape and function, or body plan. DNA is just passive information that needs epigenetic information to be read correctly. Epigenetic mechanisms control DNA and this is why change in organisms is based on epigenetic modifications.
   
   
3. We can observe only epigenetic modifications or information loss in organisms living in the wild. There are over 2 million harmful mutations in the human genome worldwide, and every newborn brings 100-200 novel germline mutations into the human genome. The total absence of random, beneficial mutations proves that evolution is not taking place.
   
   
4. Methylated cytosines are prone to turn to thymines in deamination caused by oxidative stress (for example, induced by UV light). This inevitable phenomenon has serious consequences: 
   
   
• Gradually the GC content of the genome turns to AT content.
• The genetic diversity decreases. Low genetic diversity is the most significant reason for the loss of biodiversity.
• High AT content results in CFSs (common fragile sites), which are the main reason for chromosome fusions and a need for DNA rearrangements.
• Low GC content can be observed in pathogenic bacteria and viruses and venomous or toxic organisms.
• CpG islands, important epigenetic regulatory areas, only collapse.
  
  
5. We can observe mechanical structures functioning in the cell with accuracy and efficiency far better than in human-engineered engines. The best example is MO-1 marine bacterium which has seven ion flow motors synchronized with a 24-gear planetary gearbox.
   
   

   

   MO-1 marine bacterium and seven ion-flow motors
   synchronized with a 24-gear planetary gearbox.

6. Cellular information handling mechanisms are far more advanced than human-engineered software programming solutions. Complex DNA repair machinery, redundant biological codes, and especially histone markers functioning like a top modern database point to designed mechanisms, not random mutation-driven evolution.
   
   

   

   Histone epigenetic markers function like a top modern database regulating and guiding thousands of cellular jobs. Modifications are inheritable by using non-coding RNA molecules.

7. There is not a single scientific (observed, verified, repeated, measured) evidence for evolution. All we can observe is rapid epigenetic adaptation resulting in loss of information and a need for DNA rearrangement. The best example is Lenski's experiment (LTEE): After ~90,000 generations (just in 35 years) of bacteria we haven't seen a single evolutionary event, but the bacteria have lost ~3% of their DNA.
   

Seriously, you are free to believe in evolution even without scientific evidence, but please let people with inquiring and rational minds make conclusions that there is an intelligent Creator behind life and biodiversity. 

Remove even one element from a cell and it dies

It is not possible for the cell to have evolved step by step

1. The endoplasmic reticulum

https://byjus.com/question-answer/can-a-cell-live-without-endoplasmic-reticulum/

"Without the endoplasmic reticulum, the cell will not survive. Without rough ER the cell will not be able to synthesize new lysosomal enzymes, plasma membrane proteins, proteins for Golgi apparatus, and proteins essential for extracellular secretion."

2. Golgi apparatus

https://byjus.com/question-answer/what-would-happen-to-the-life-of-a-cell-if-there-was-no-golgi-apparatus/

"Lysosomes would not be generated in the absence of the Golgi apparatus, and the cell would eventually die as a result of the buildup of dead and damaged molecules and organelles. Materials would no longer be packaged or transported if the Golgi apparatus were absent."

3. A nucleus

https://byjus.com/question-answer/can-cell-survive-without-nucleus/

"So nucleus is the essential and the most important cell organelle of the body. So, a cell cannot survive without the nucleus. The cell will die in absence of a nucleus."

4. A membrane

https://byjus.com/question-answer/can-cells-survive-without-a-membrane/

"A living cell cannot survive without a membrane. Apart from acting as a barrier and attachment site, cell membranes play important roles in living cells. Membranes have carrier proteins for transport, cell membranes also contain enzymes for a certain reactions."

5. Ribosomes

https://byjus.com/question-answer/can-you-live-without-ribosomes/

"Every chemical process and damage repair in cells requires proteins. Without proteins, the cells in the body will not be able to synthesise proteins and function properly. So, without ribosomes, life will not be possible in living organisms."

6. DNA

https://sciencing.com/would-happen-cell-dna-2424.html

"Without a nucleus, the cell cannot get what it needs to survive and thrive. A cell without DNA lacks the capacity to do much of anything other than its one given task. Living organisms depend on genes in DNA to guide proteins and enzymes. Even primitive life forms have DNA or RNA."

7. DNA repair

https://news.harvard.edu/gazette/story/2017/03/harvard-scientists-pinpoint-critical-step-in-dna-repair-cellular-aging/

"DNA repair is essential for cell vitality, cell survival, and cancer prevention, yet cells' ability to patch up damaged DNA declines with age for reasons not fully understood."

8. Cytoplasm

https://lambdageeks.com/cell-without-cytoplasm/

"Cells generally do not survive without the gel-like cytoplasm as many chemical reactions necessary to support the cells occur within cytoplasm along with embedding of various cell organelles. On removing the cytoplasm, the organelles would stop functioning which would lead to the death of the cells."

Conclusions: The cell is irreducibly complex. The theory of evolution is a fairytale.

Why OBSERVED change in organisms is not evolution?

Reasons for organismal change and why it doesn't result in evolution

Most people consider the theory of evolution as fact. This is because people are not taught serious science. Instead, even small children are indoctrinated with pseudoscientific fairytales. Today, evolution is a synonym for change. Let's have a closer look at organismal change and the reasons behind it.

1. Adaptive radiation

A common definition: "Adaptive radiation refers to the adaptation (via genetic mutation) of an organism which enables it to successfully spread, or radiate, into other environments. Adaptive radiation leads to speciation and is only used to describe living organisms. Adaptive radiation can be opportunistic or forced through changes to natural habitats."

This is WRONG! Why?

Serious science: Epigenetic mechanisms and factors help organisms adapt to changing environment. This might result in changes in phenotypes that may inspire biologists to name new species. No novel information arises. The most significant mechanism behind protein diversity and speciation is alternative splicing. No evolution.

An example. Darwin's Finches.

https://bmcecolevol.biomedcentral.com/articles/10.1186/s12862-017-1025-9

"In contrast, we did find dramatic epigenetic differences between the urban and rural populations of both species, based on DNA methylation analysis."

Other examples of epigenetic-controlled adaptive radiation: Rapid adaptive radiation and speciation of Lake Malawi cichlid fishes

2. Allopatric, peripatric, sympatric and parapatric speciation. 

These are man-made definitions for phenomena occurring due to different environmental and living conditions. For example, different nutrition results in changes in sex pheromone production and this leads to so-called reproductive isolation. Mate preferences (sexual selection) are driven by changes in certain olfactory receptors. The most significant mechanism behind modifications in olfactory receptors is alternative splicing which is regulated by epigenetic mechanisms and factors. No evolution. An example:

https://www.mdpi.com/2073-4425/11/6/592

"We also found evidence of some genes showing differential expression or alternative splicing, which may be associated with odorant-sensing between sexes. Most chemosensory receptor genes showed evidence of expression in the zebrafish olfactory epithelium, with a higher expression level in males than in females. Taken together, our results provide a comprehensive catalog of the genes mediating olfactory perception and pheromone-evoked behavior in fishes."

3. Chromosome fusions

The GC --> AT mutation bias results in a reduced level of GC content in all kinds of organisms. So-called Common Fragile Sites are AT-rich chromosomal regions (they contain a lot of Adenine-Thymine pairs due to harmful mutations). In meiotic recombination, DNA is rearranged by complex rules mediated by histone epigenetic markers. The cell tries to maintain a necessary level of GC content (Guanine-Cytosine pairs). In this process, chromosomes are occasionally fused. Chromosome fusions point to genetic entropy. No evolution.

Summary and conclusions:

• Speciation is a man-made word.
• Adaptive radiation means epigenetic modifications. No evolution.
• Allopatric, peripatric, sympatric, and parapatric speciation are due to epigenetic changes in pheromone production or olfactory receptors. The most significant mechanisms behind these alterations are alternative splicing and RNA editing.
• Bringing different 'species' into the same environment (such as a zoo) often breaks these reproductive barriers especially when animals are fed with similar food.
• Chromosome fusions are due to mutational load and they always result in loss of biological information.
• Speciation is like dog breeding; the more adaptation and variation, the more information loss and genetic entropy.
• There is no mechanism for evolution.

Huge differences between human/chimp lncRNAs refute the theory of Evolution

LncRNAs determine the fate of stem cells, tissue type's identity, organ function, and even body plan

https://www.frontiersin.org/articles/10.3389/fgene.2020.00277/full

Excerpt: "Pluripotent stem cells have broad applications in regenerative medicine and offer ideal models for understanding the biological process of embryonic development and specific diseases. Studies suggest that the self-renewal and multi-lineage differentiation of stem cells are regulated by a complex network consisting of transcription factors, chromatin regulators, signaling factors, and non-coding RNAs. It is of great interest to identify RNA regulatory factors that determine the fate of stem cells. Long non-coding RNA (lncRNA), a class of non-coding RNAs with more than 200 bp in length, has been shown to act as essential epigenetic regulators of stem cell pluripotency and specific lineage commitment. In this review, we focus on recent research progress related to the function and epigenetic mechanisms of lncRNA in determining the fate of stem cells, particularly pluripotency maintenance and lineage-specific differentiation."

My comment: LncRNAs regulate e.g. cellular differentiation processes.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8143134/

Excerpt: "Long non-coding RNAs (lncRNAs) are a large class of gene transcripts that do not code proteins; however, their functions are largely unknown and many new lncRNAs are yet to be discovered. Taking advantage of our previously developed, super-fast, novel lncRNA discovery pipeline, UClncR, and rich resources of GTEx RNA-seq data, we performed systematic novel lincRNA discovery for over 8000 samples across 30 tissue types. We conducted novel detection for each major tissue type first and then consolidated the novel discoveries from all tissue types. These novel lincRNAs were profiled and analyzed along with known genes to identify tissue-specific genes in 30 major human tissue types. Thirteen sub-brain regions were also analyzed in a similar manner. Our analysis revealed thousands to tens of thousands of novel lincRNAs for each tissue type. These lincRNAs could define each tissue type’s identity and demonstrated their reliability and tissue-specific expression."

My comment: LncRNAs define also different tissue type's identities.

https://www.sciencedirect.com/science/article/pii/S2589555920301117

Excerpt: "Long non-coding RNAs (lncRNAs) are important biological mediators that regulate numerous cellular processes. New experimental evidence suggests that lncRNAs play essential roles in liver development, and normal liver physiology"

My comment: LncRNAs also regulate organ development and function.

https://academic.oup.com/mbe/article/32/9/2367/1030095

Excerpt: "A high diversity of transiently expressed lncRNAs also was present during the first 24 h of metamorphosis, when the larval body plan is being resculpted into the juvenile/adult body plan. Finally, the number of expressed lncRNAs increased at the establishment of the juvenile body plan and in the adult."

My comment: LncRNAs are involved even in the regulation of body plans.

The number of DIFFERENT lncRNAs in a human body according to NONCODEv5 is 172,216. However, the number of different lncRNAs in a chimp body is only 18,604. LncRNAs play a very significant role in cellular differentiation, tissue type regulation, organ function, and even body plan. We should also remember that the number of different lncRNAs in a human body is almost 9 times higher than the number of protein-coding genes. Studies have also revealed that human/chimp lncRNAs are very different (non-conserved). Evolution believers claim that lncRNAs have evolved through mutations (HAR = human accelerated regions). However, medical science is aware that lncRNAs don't tolerate mutations:

https://www.qmul.ac.uk/blizard/about/news/items/long-noncoding-rnas-in-neurological-diseases.html

Excerpt: "Because of their important role in gene expression regulation, it should not be surprising to assume that any malfunction of lncRNAs, for example due to mutations, could have even serious consequences on the normal development of body organs. In fact, this is exactly what has been found by comparing the sequences of these RNAs in normal people versus diseased individuals.
In the field of neurology, mutations in lncRNAs have been associated with abnormalities of neurological development or neurodegenerative diseases such as Alzheimer’s, Parkinson’s, Huntington’s and ASD (Autism spectrum disorder). Given the high personal and social impact of these diseases, it is very important to understand how these RNAs carry out their activity and what goes wrong following disease-causing mutations."

Summary and conclusions:

• LncRNAs have a crucial epigenetic role in several cellular processes such as stem cell differentiation, tissue type regulation, organ function, and body plan.
• DNA doesn't determine stem cell fate, tissue type, organ function, or body plan. DNA is passive information used in a sophisticated way for the cell to construct active RNA molecules.
• The number of different lncRNAs in a human body is almost 9-fold compared to that of chimps.
• It's ridiculous to claim that this huge difference in the number of human lncRNAs could have arisen after a chromosome fusion because biological information is always reduced during chromosome fusions.
• LncRNAs don't tolerate mutations. It's impossible for lncRNAs to evolve through mutations. Science is not aware of positive mutations in these regulatory lncRNAs.
• We are not related to chimps.

Horizontal Gene Transfer doesn't lead to evolution

A rapid decline in Bacterial genome size after intense adaptation

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6986707/

Recombination and gene loss occur simultaneously during bacterial horizontal gene transfer

Excerpt: "Bacteria can acquire new genes by incorporating environmental DNA into their genomes, yet genome sizes stay relatively constant. In nature, gene acquisition is a rare event so it is difficult to observe. However, the Caulobacter crescentus CB2A genome contains 114 insertions of genetic material from the closely related NA1000 strain, providing a unique opportunity to analyze the horizontal transfer of genetic material. Analyses of these insertions led to a new model that involves preferential recombination at non-homologous regions that are flanked by regions of homology and does not involve any mutational processes. The net result is the replacement of segments of the recipient genome instead of the simple addition of genetic material during horizontal gene transfer. Analyses of the genomes of closely related strains of other bacterial and archaea genera, suggested that horizontal gene transfer occurs preferentially in non-homologous regions in these organisms as well. Thus, it appears to be a general phenomenon that prokaryotic horizontal gene transfer occurs preferentially at sites where the incoming DNA contains a non-homologous region that is flanked by regions of homology. Therefore, gene replacement is a common phenomenon during horizontal gene transfer.

My comment: There seems to be a genus-specific maximum limit for genome size in bacteria. In some cases, bacteria are able to partially restore their genome contents by plasmid transfer.

Horizontal gene transfer in the human genome has never been observed.

A rapid decline in Bacterial genome size doesn't support evolution

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4988878/

Excerpt: "After 50,000 generations, average genome length declined by 63 kbp (~1.4%) relative to the ancestor"

My comment: 'Horizontal Gene Transfer' has been one of the favorite 'proofs of evolution' for evolution believers. Now this outdated theory has been debunked. Instead, we can observe rapid loss of biological information during adaptive processes within all kinds of organisms. Lenski's famous LTEE proves this fact; after 50,000 generations of bacteria (~25 years) there's a significant loss of information in bacterial genomes. Today, after ~90,000 generations the loss of information is very likely more than 3% because after mutations hit DNA repair mechanisms, the effect of hypermutability arises very rapidly resulting in the extinction of bacterial strains. Evolution never happened.

The first assumed life form would have had to build several complex protein machines, otherwise life would not have continued

Life without DNA repair mechanisms is not possible

Many environmental factors, such as solar UV radiation, background radiation, and carcinogens, are highly harmful to the cell's DNA, leading to various types of damage. Some of these damages, if left unrepaired, can be fatally harmful, and even smaller errors, when accumulated, can cause severe diseases after just a few cell divisions. According to the theory of evolution, the first cells developed in a primordial soup, an environment where they would have been exposed to several harmful environmental factors. Without efficient DNA repair systems, the theorized first cell would not have been able to survive for long. To produce repair enzymes, mere DNA or RNA is not enough; it requires a precisely functioning machinery of protein production, guided and regulated by epigenetic mechanisms and factors. The hypothetical evolution would have halted at the point when the cell and its contained DNA needed to be duplicated. To achieve this, the first cell would have had to build complex replication machinery within its short lifetime. For instance, the active lifespan of bacteria is typically only a few days, so in a relatively short time, the first cell would have had to obtain a complex replication mechanism both for the cell and DNA to sustain life.

Science has also not yet determined how proteins that detect DNA errors can recognize grammatical errors in DNA. How can proteins recognize informative code? According to research, DNA's grammar is more complex than that of any known language.

DNA repair mechanisms are controlled by epigenetic mechanisms.

Life without DNA repair mechanisms ends quickly

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC34173/

"Mice lacking a precise DNA repair activity have been generated, and these mutants show various combinations of defective embryogenesis, tissue-specific dysfunction, hypersensitivity to DNA-damaging agents, premature senescence, genetic instability, and elevated cancer rates. That repair-deficient animals display such abnormalities underscores the fundamental importance of DNA repair in protecting against the mutagenic and cytotoxic effects of DNA damage."

A question for evolution believers:

"How did the first presumed life form develop the cell's copying machinery and DNA repair systems during its own lifetime?"

The more speciation, the more information loss

C>T mutation bias leading to inevitable genetic entropy now explained

Epigenetic modifications elevate the risk of cytosine-to-thymine mutations. Methylated cytosines (5mC) are prone to turn to thymines in deamination caused by i.e. oxidative stress. After my previous articles, atheists have attacked them claiming that I don't understand these mechanisms or that I'm lying. So, now it's better to explain fundamentally, why these C>T mutations happen and why they result in inevitable genetic entropy.

Most C>T mutations are associated with epigenetic modifications

https://onlinelibrary.wiley.com/doi/full/10.1111/brv.12453

Excerpt: "Links between epigenetic marks and mutation rates are best documented for DNA methylation patterns, which were first demonstrated to be mutagenic in E. coli in 1978 (Coulondre et al., 1978; Duncan & Miller, 1980). Overall at the molecular level, as the rate of deamination of 5-methylcytosine into thymine is about 3.5 times higher than that of unmethylated cytosine into uracil (Jones et al., 1992), and as mismatched uracils are excised up to 6000 times more efficiently than mismatched thymines (Schmutte et al., 1995), the mutation rate of 5-methylcytosine appears about 20000 times higher than that of unmethylated cytosines (Gorelick, 2003). As a consequence, methylated cytosines are suspected to cause 30–40% of germline point mutations in humans (Jones et al., 1992). This very large difference in genomic stability results from the cumulative effects of natural cytosine and 5-methylcytosine deamination, plus the differential efficiency of mismatch repair and maintenance methylation, plus natural tautomeric shift processes (Gorelick, 2003). It has also been suggested that this difference in mutability may result from the joint action of various types of covarying epigenetic marks or their interactions (review in Makova & Hardison, 2015)."

DNA repair enzymes will not repair methylated-cytosine-to-thymine mutations

https://www.atdbio.com/content/56/Epigenetics#Role-of-base-flipping-in-DNA-methylation

"When cytosine is mutated to uracil by spontaneous deamination, the DNA glycosylase enzyme UDG (uracil DNA glycosylase) reverses the damage, in a base excision repair mechanism. When the equivalent deamination reaction occurs on 5-methylcytosine (5mC), however, the product, thymine, is not repaired by DNA repair enzymes."

My comment: As we see, there is no specific repair mechanism for 5mC > T mutations.

https://academic.oup.com/mbe/article/22/3/650/1075932

Excerpt: "Deamination of unmethylated cytosine produces uracil (U), which can be removed by uracil glycosylase (Lindahl 1974; Lindahl, Karran, and Wood 1997), but 5mC deamination generates thymine (T), which cannot be processed by this enzyme. The consequence in humans is that the mutation rate from 5mC to T is 10-fold to 50-fold higher than other transitions (Duncan and Miller 1980; Bulmer 1986; Britten et al. 1988; Sved and Bird 1990). More than one-third of the germline point mutations that cause human genetic diseases (Cooper and Youssoufian 1988; Cooper and Krawczak 1993), and many of the somatic mutations leading to cancer (Jones et al. 1992; Hollstein et al. 1994) are caused by CpG hypermutability. The evolutionary consequence in humans is that the CpG dinucleotide is statistically underrepresented (Bird 1980) throughout almost the entire human genome (Lander et al. 2001). The extent of CpG underrepresentation is inversely correlated with GC content (Adams and Eason 1984; Bernardi et al. 1985; Bernardi 1995)."

5mC > T mutations can be observed as G-T mismatch pairs in the genome

G-T pair is a mismatched pair in regards to DNA grammar. When DNA replicates, the so-called DNA mismatch repair mechanism (MMR) often recognizes most of these mismatched pairs. However, a significant proportion of them are escaped from the repair mechanism:

https://news.osu.edu/study-reveals-how-the-most-common-dna-mutation-happens/

Excerpt: "In fact, the G-T mutation is the single most common mutation in human DNA. It occurs about once in every 10,000 to 100,000 base pairs—which doesn’t sound like a lot, until you consider that the human genome contains 3 billion base pairs.


The mutation’s survival is a real feat, since it has to overcome a good bit of basic physics. Bases pair in a certain way because of how the protons and electrons in their atoms are arranged. Base pairing requires some amount of energy, and the easiest, most energy-efficient pairs to form are the “right” ones—A-T and C-G.

In effect, the G-T pair has to overcome an energy barrier to form and maintain itself. It turns out that when the G and T bases change shape, they make themselves more energy efficient—still less efficient than a normal base pair, but efficient enough."

https://biobeat.nigms.nih.gov/2017/04/six-things-to-know-about-dna-and-dna-repair/

"Although scientists have not yet determined the full details of the human mismatch repair system, they estimate the process catches all but one out of every 1,000 or so mismatch errors."

https://www.sciencedirect.com/science/article/abs/pii/S1383574299000654

Excerpt: "The likely intermediate in the conversion of a 5-methylcytosine (5meC)⋅G bp to T:A is a 5meC⋅A or a T⋅G mismatch. The former mismatch could be produced through misreplication of 5meC, but there is no support for the possibility that DNA polymerases copy a cytosine incorrectly when it is methylated [15]. In contrast, a process called hydrolytic deamination is known to convert 5meC to T 16, 17 and is analogous to the deamination process that converts C to U [18]. For this reason, a T⋅G mismatch is the expected intermediate in the conversion of 5meC⋅G to T⋅A."

My comment: One out of every 1,000 G-T mismatch pairs are left without a repair. In DNA replication, these mismatched pairs are turned into A-T pairs due to energy-efficiency reasons. This is why C>T mutation bias is a biological fact. This is why GC content gradually turns into AT content. GC content is often elevated during meiotic recombination but the price will be loss of genes, loss of transcripts, loss of CpG islands, loss of mRNAs, and loss of non-coding RNAs.