The broken laws of the theory of evolution

The broken laws of the theory of evolution

The evolutionary theory has been associated with several laws over the past 150 years. The purpose of these laws has been to consolidate the position of the evolutionary theory in the human worldview and to make the theory appear more convincing than it really is. The observations of serious science will override every law attached to the evolutionary theory. So what would we do with a theory that is not correct? Here's hard, peer-reviewed science:

1. Mendelian inheritance


Summary: Serious research cannot replicate Mendel's rules of inheritance. Students are given false information. Textbooks provide false information. The theory of dominant and recessive inheritance is not correct.

Keywords: mendelian inheritance failure, mendel was wrong

2. Weismann barrier

According to the theory developed by August Weismann, hereditary traits are transmitted to the next generation only through germ cells into the somatic cells of the organism. This theory, which has proved to be pseudoscience, has been refuted several times:


Serious science has, several years ago, found that traits of an organism are inherited, for example via RNA molecules carried by extracellular vesicles. This is called  transgenerational epigenetic inheritance, the most important mechanism by which  epigenetic information is mediated by non coding RNA molecules to establish a histone database in the cells of the organism.

Keywords: epigenetic inheritance non coding rna

3. The doctrines of population genetics:

a. DNA determines body plan, that is, the appearance and structure of organisms. DNA is a recipe for building an organism. DNA is a 'blueprint' or a kind of recipe for an organism.

None of this is true. According to serious science, DNA is a passive database, a collection of tools packaged in an optimum information-maintaining molecule from which the cell can use elements for various purposes as needed. DNA does not dictate traits or characteristics and does not control cellular events. DNA is a passive repository of information.

b. DNA is your destiny

This pseudoscientific theory is, in particular, a philosophical delusion based on the 'selfish gene' ideology invented by leading atheist Richard Dawkins. According to his theory selfish genes control the biology and inheritance of organisms. Serious science has found that DNA does not control the organism, but the organism controls the DNA.


Keywords: It’s the organism controlling the DNA, not the DNA controlling the organism.

4. Random mutations and natural selection are the cornerstones of evolution.

This is utter nonsense. The change in organisms is based on epigenetic mechanisms and factors, and on reorganization of information due to information corruption. Every alleged evolutionary evidence has proven to be a change caused by epigenetic regulation of existing biological information, which even leads to a gradual corruption of information. Environmental signals are transmitted to the cells through the epigenome that directs the cell to use the most appropriate sequences from the passive DNA library for the production of functional RNA molecules.

Science is changing. Continually. The more serious science reveals cellular mechanisms and secrets of inheritance, the more it supports Biblical creation and the less it supports the theory of evolution.


Epigenetics will not save the pseudoscientific theory of evolution

Epigenetic modifications result in genetic degradation. Here's the evidence.

It's obvious that current plant/animal breeding techniques have reduced genetic diversity of food varieties. Breeding is kind of artificial selection of desired traits and characteristics. This can be done by epigenetic amplification or silencing of desired traits as in dog breeding. The most modern techniques try to manipulate genetic information in different ways. Scientists are even able to transfer genes between organisms. Results have been almost catastrophical; ~90% of food varieties have disappeared during the last 100 years. This is why farmers are looking for safer and more efficient techniques for plant/animal breeding.

Keywords:  breeding reduces genetic diversity, epigenetic breeding

The latest and the best solution is epigenetic breeding. But will it result in improvement of genetic diversity? No. Just like in the wild, epigenetic modifications result in genetic errors and low genetic diversity. This happens slower than in traditonal breeding techniques but anyway, it's an inevitable phenomenon. Here's the evidence. Changes in epigenetic information profiles result in genetic errors:

"Many studies have reported that CpG-SNPs are associated with different diseases, such as type 2 diabetes, breast cancer, coronary heart disease, and psychosis which show a clear interaction between genetic (SNPs) and epigenetic (DNA methylation) regulation."

"Loss of expression of the O6-methylguanine DNA methyltransferase (MGMT) protein is a frequent occurrence in many types of cancer, including 30–46% of sporadic colorectal cancers.9, 10, 11, 12, 13 This is almost invariably associated with methylation of the MGMT promoter.9 MGMT is a ubiquitously expressed DNA repair protein that protects against mutagenesis by repairing mutagenic O6-methylguanines within DNA. By direct cleavage of the methyl adducts, the enzyme can restore the affected guanine nucleotides to normal.14 If this fails to occur, O6-methylguanines can pair erroneously with thymine during DNA replication, resulting in G:C>A:T transitions in the DNA, which can be important in neoplastic transformation."
"Recently, MGMT methylation was found to be closely associated with the C>T SNP (rs16906252) within the first exon of MGMT in colorectal cancer."

Epigenetic marks respond to internal and environmental cues (A) resulting in various effects on chromatic conformation and gene expression.

"Surprisingly, hydroxymethylated sites are consistently associated with elevated C to G transversion rates at the level of segregating polymorphisms, fixed substitutions, and somatic mutations in tumors."

"DNA hypomethylation promotes genomic instability 4, in many cases leading to an increased mutational load and activation of proto-oncogenes."

"DNA methylation has been linked to mismatch repair (MMR) deficiency and genomic instability in multiple contexts, in both cell lines and in disease. In the HCT116 colorectal cancer cell line, ablation of catalytically active DNMT1 causes cell cycle arrest and apoptosis due to increased chromosomal instability. In mouse ES cells, loss of Dnmt1 also causes global hypomethylation and increased mutation rates."

"If we assume that CpHpG methylation also occurs in the germline, and that 5mC deamination can occur within a CpHpG context, then we might surmise that methylated CpHpG sites could also constitute mutation hotspots causing human genetic disease. To test this postulate, 54,625 missense and nonsense mutations from 2,113 genes causing inherited disease were retrieved from the Human Gene Mutation Database (http://www.hgmd.org). Some 18.2 per cent of these pathological lesions were found to be C > T and G > A transitions located in CpG dinucleotides (compatible with a model of methylation-mediated deamination of 5mC), an approximately ten-fold higher proportion than would have been expected by chance alone."

"Altered DNA methylation and genome instability: A new pathway to cancer"

"This increased genome instability is characterized by increased occurrences of mutations, cells with incorrect chromosome number, loss of heterochromatin and mistakes in transcription."

"A reduction in DNA methylation leads to genomic instability, accumulation of endogenous DNA damage, and sensitivity to DNA-damaging agents."

"CpG methylation reduces genomic instability."

"As well, DNA methylation is thought to be a major contributor of point mutations leading to human genetic disease, when it precedes deamination of 5-methylcytosine (m5C) present within CpG dinucleotides. CpG dinucleotides are hypothesized to be a hotspot for mutations in a variety of genes, where a substantial proportion of intragenic single base-pair mutations (35%) occur in CpG dinucleotides and are the result of C>T or G>A transitions. Consequently, the rate of transitions at CpGs is suggested to be 20-fold higher than transitions at non-CpG sites."

"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, however, the product, thymine, is not repaired by DNA repair enzymes."

"I show that sites methylated by the Dcm enzyme exhibit an 8-fold increase in mutation rate in natural bacterial populations. I also show that modifications at other sites in various bacteria also increase the mutation rate, in some cases by a factor of forty or more."

"The architecture of the chromatin itself and its level of condensation can greatly impact the expression of genes as well as the sensitivity of the DNA to damage."

"For example, DNA is more highly methylated, and therefore compacted, in areas that contain repetitive sequences to prevent the expression of non-coding DNA, induction of double-stranded breaks (DSBs), transposable elements and inappropriate recombination events likely to occur at repetitive DNA sequences. These events can lead to mutations, genome instability and cancer development."

"When chromatin is more 'open,' major genetic disruption is more likely.  And when the researchers inhibited an epigenetic modifier called G9a, they found that chromatin accessibility, or openness, increased substantially."


Histone database and human traits and characteristics

Histone database and human traits and characteristics

Epigenetic markers of histones are still a relatively recent discovery in science, but studies of their relevance to individual characteristics are beginning to be found. Histones are DNA packing proteins, a type of protein cylinders around which DNA is wrapped.


Excerpt: "Histones pack and order DNA into structures known as nucleosomes so that it fits within a cell’s nucleus. Each nucleosome contains two subunits, both made of histones H2A, H2B, H3 and H4 – known as core histones – with the linker histone H1 acting as a stabilizer."

Histone subunits have a histone tail that can attach a broad combination of different types of epigenetic markers such as methylation, acetylation, phosphorylation, ubiquitination, sumoylation, etc.
Histone markers control many cellular events, particularly protein synthesis and production of different RNA molecules. Their main function is to control the transcription of DNA either by closing the chromatin tight so that the DNA sequences do not end up into transcription or by opening, thereby allowing the cell to read the DNA for transcription. The histone markers also control alternative splicing procedure, thus allowing the cell to produce up to tens of thousands of different proteins using the same DNA sequence as a template file. In addition to transcriptional regulation, the histone database controls post-translation. Serious science is constantly finding new, complex regulatory functions for histone markers.

Keywords: histone transcription regulation, alternative splicing histone, histone post-translational regulation

There are writers, readers, and erasers for the epigenetic markers of histones. Thus, the entire histone database is a fully dynamic information library, allowing organisms to adapt efficiently under changing conditions. Reversible histone modifications are just regulation of existing biological information. That's why epigenetic regulation has nothing to do with evolution. Turn the lights on and off, turn the lights on again, did evolution happen?

Serious science has found several regulatory functions for histone markers that control and regulate a number of individual characteristics. For example, cranial and skeletal morphology is regulated by deacetylation of certain histone markers. Similarly, human height. In the bee colony, deacetylation of histone markers controls whether the larvae develops into a workers or a queen. Histone markers affect sex determination. In men, the X chromosome must be suppressed to prevent feminine traits from becoming dominant. Epigenetic markers of histones are responsible for this task. Mouse hair coloration is a trait controlled by histone markers. Accurate transcription timing and regulation in embryo development is a process driven by histone markers, etc. Science is constantly finding new roles for histone markers. It already seems obvious that histone markers form a complex biological database that plays a decisive role in an organism's characteristics and health.

Because the characteristics of an individual are inherited, a serious scientist have to make a question: What mechanisms affect the inheritance of the epigenetic markers of histones? There's a lot of research about this. Writing, reading and erasing of histone markers is mediated by non-coding RNA molecules such as miRNAs, lncRNAs, piRNAs, siRNAs, rRNAs and tRNAs. So is it possible that similar mechanisms control the inheritance of histone markers during reproduction and embryo development? Yes. For example, human sperm contains tens of thousands of different non-coding RNA molecules that deliver epigenetic information to embryonic cells. 

Keywords: embryonic cell development histone non coding rna

Thus, evolution does not occur in epigenetic switching. Change in organisms is not based on random mutations and selection but accurately controlled readers, writers and erasers driven by signals from environment. Serious science has also found that when the nucleosome and DNA wrapped around histone open for transcription, the DNA is prone to genetic errors=mutations. Not all errors are repaired by the cell, so genetic degradation is a biological fact.