Reasons why the theory of evolution is just a belief system

The theory of evolution has nothing to do with science

1. No one of the top scientists in the world has been able to prove evolution by using scientific methods.

True science means observable, repeatable, verifiable and measurable evidence. What kind of evidence does the theory of evolution need? Scientists should be able to show that random occurrence results in increase in biological information that leads to growth of structural or functional complexity of an organism.

This kind of phenomenon has never been observed. A few examples of so called novel structures were observed but they were due to epigenetic regulation of pre-existing biological information, such as rapid adaptation of Italian wall lizards. The reason for their rapid adaptational alterations was diet, that changed from insects to plants. Other examples of 'evolutionary changes' that are touted as clear evidence of evolution in public but were actually caused by epigenetic mechanisms and control are:
  • Blind cave fish
  • Butterfly wing color changes
  • Live birth in three-toed skinks
  • Darwin's finches
  • Owls that are changing plumage color
  • Stickleback fish adaptations

2. Genetic entropy is a biological fact.

The more adaptation and variation an organism experiences, the more genetic degradation happens in its genome. This results in faulty genes, heterochromatin formations in chromosomes, loss of functions, knocked out genes, susceptibility to diseases etc. In nature this can be observed as a huge number of endangered species. Genetic entropy touches also us humans; there are over 561,000 gene-disease associations in human genome at the whole world level but the number of random beneficial mutations is close to zero. Novel germline mutations are in rapid rise.

3. Evolution believers confuse with adaptational change and evolution.

Change in organisms is also a biological fact. It tells that organisms have potential to efficiently react and adapt into changing conditions. But adaptation always occurs due to epigenetic mechanisms and factors. At molecular biological level this means switching and regulation between alternative biological programs and it will never lead to any kind of information increase. Instead, errors in DNA typically occur when epigenetic information layers get modified. Organisms experience changes due to environmental input, such as diet, climate, stress factors, sensory stimuli, toxicants etc. Change in organisms is based on mechanisms, not on random mutations or selection.
4. The role of DNA is overemphasized
Organisms need the DNA primarily for building functional RNA molecules that mediate signals between cells and environment, encode for proteins or control and regulate cellular processes. Reading and transcription of the DNA is controlled by epigenetic mechanisms and factors. DNA itself is just a passive information library and it has no control over cellular processes. A stem cell has a perfect DNA but no epigenome. That's why it has no task, no identity and no programs needed for cellular differentiation. When an organism experiences adaptation and variation, then the epigenome gets modified. Sometimes this results in DNA errors (mutations).

There are only ~19,000 DNA strands in human genome used for protein encoding but the number of different proteins in a human body is up to several millions. This kind of efficient use of complex but optimal DNA grammar makes it possible for the cell to build a huge number of different mRNAs and proteins from a minimum amount of DNA.

5. Evolution by random chance?

Evolution proponents believe in random chance, but what's the probability of getting 288 amino acids in a perfect order (an average-sized protein molecule is composed of 288 amino acids

It's 1 of 10^300. There are apprx. 10^87 atoms in the whole Universe. THE PROBABILITY OF A PROTEIN BEING FORMED BY CHANCE IS ZERO!

6. Science has a serious replication crisis especially in the fields of biology and chemistry


"According to a 2016 poll of 1,500 scientists reported in the journal Nature, 70% of them failed to reproduce another scientist's experiments (50% failed to reproduce their own experiment). These numbers differ among disciplines:
  • chemistry: 90% (60%),
  • biology: 80% (60%),
  • physics and engineering: 70% (50%),
  • medicine: 70% (60%),
  • Earth and environment science: 60% (40%)."
Summary: Evolution believers are not able to address us scientific evidence for evolution. The theory of evolution has failed.


Small populations lose genetic diversity more rapidly than large populations

Populations only lose genetic diversity - Slower or faster - Genetic entropy is a biological fact


Excerpt from abstract: "Genetic diversity is necessary for evolutionary response to changing environmental conditions such as those facing many threatened and endangered species. To investigate the relationship between genetic diversity and conservation status, we conducted a systematic, quantitative review of vertebrate microsatellite data published since 1990: we screened 5165 previously published articles and identified 1941 microsatellite datasets spanning 17,988 loci that characterized wild populations distributed among five vertebrate classes. We analyzed these data in the context of conservation by comparing empirical estimates of heterozygosity and allelic richness between threatened and non-threatened species. We found that both heterozygosity and allelic richness are reduced in threatened species, suggesting that inbreeding and drift are both effective at removing genetic diversity in endangered populations. We then considered the criteria typically used to rank species of conservation concern (including declining population size, species range extent, and the number of mature individuals) to determine which of these criteria are most effective at identifying genetically depauperate species. However, we found that the existing criteria failed to systematically identify populations with low genetic diversity. To rectify this, we suggest a novel approach for identifying species of conservation need by estimating the expected loss of genetic diversity. We then evaluated the efficacy of our new approach and found that it performs significantly better than the existing methods for identifying species that merit conservation concern in part because of reduced genetic diversity." 

A few real life examples of genetic entropy:

Monitoring age-related trends in genomic diversity of Australian lungfish
 "They then compared empirical estimates of heterozygosity and allelic richness between threatened and non-threatened species, and found that genetic diversity is generally reduced in threatened species. However, when they considered which of the IUCN Red List Criteria (including declining population size, species range extent, and the number of mature individuals) are most effective at identifying genetically depauperate species, they found that the existing criteria failed to systematically identify populations with low genetic diversity ( Willoughby et al., 2015). Thus, threatened species generally show reduced genetic diversity compared to non-threatened ones (Spielman et al., 2004), but the IUCN Red List Criteria approach does not systematically prioritize the conservation of species with low genetic diversity ( Rivers et al., 2014;Willoughby et al., 2015). ..."
"... However, when they considered which of the IUCN Red List Criteria (including declining population size, species range extent, and the number of mature individuals) are most effective at identifying genetically depauperate species, they found that the existing criteria failed to systematically identify populations with low genetic diversity ( Willoughby et al., 2015). Thus, threatened species generally show reduced genetic diversity compared to non-threatened ones (Spielman et al., 2004), but the IUCN Red List Criteria approach does not systematically prioritize the conservation of species with low genetic diversity ( Rivers et al., 2014;Willoughby et al., 2015). Additionally, the genetic consequences of habitat degradation and fragmentation in relation to the IUCN Red List Categories remain largely unexplored. ..."

Landscape Genomic Conservation Assessment of a Narrow-Endemic and a Widespread Morning Glory From Amazonian Savannas

... Such loss of evolutionary potential may increase the risk of extinction of local populations and degrade the persistence of the metapopulation (group of spatially structured local populations that may exchange individuals through migration, Frankham, 2005;Hanski, 1998). Hence, maintaining adequate levels of genetic diversity, within and among wildlife populations, is one of the main principles underlying the conservation T and management of threatened species ( Willoughby et al., 2015). ...

Low genetic diversity, limited gene flow and widespread genetic bottleneck effects in a threatened dolphin species, the Australian humpback dolphin

... The low variation that exists between the solenodon sequences is hardly surprising, because the theoretical consensus in conservation genetics predicts that small populations lose genetic diversity more rapidly than large populations [102], and measures of genetic diversity have been explicitly suggested to IUCN as a factor to consider in identifying species of conservation concern [103]. The historical N e for each subspecies was examined by our analysis (Figure 9), and showed lower levels recently in S. p. woodi.

Next-generation metrics for monitoring genetic erosion within populations of conservation concern

... Describing the patterns of distribution of genetic diversity can help define population units important for effective management and conservation[10]. Moreover, population genetic parameters can be used in a holistic framework to support recommendations regarding official international conservation rankings[11]. To date, while some primate groups have been more explored regarding their genetic structure, others remain poorly studied[12]. ...
... Based on the estimates of the effective population size obtained for the two biggest populations (Ne = 26 and 40), applying the equation for heterozygosity loss (Eqn. 4 in[11]), we can anticipate that the studied BGHM populations will lose heterozygosity below the 25% quantile of the current values in less than 50 generations. We also found that the populations at the southernmost limit of the species range have a reduced effective size and may be genetically depleted to face threatening events such as yellow fever outbreaks, which could rapidly affect all individuals in most of the species' distribution area. ...

 Genetic structure in the southernmost populations of black-and-gold howler monkeys (Alouatta caraya) and its conservation implications
... This is especially true for threatened species, which can sometimes be characterised by low levels of genetic variation, often due to inbreeding, population bottlenecks, or the disproportionate effects of genetic drift on small populations (e.g. England et al. 2003;Spielman et al. 2004;Allendorf 2005;Willoughby et al. 2015). ...

Genetic diversity and differentiation of the Western Leopard Toad (Sclerophrys pantherina) based on mitochondrial and microsatellite markers

... Genetic diversity is reduced in threatened taxa, relative to non-threatened taxa reflecting population bottlenecks and small population sizes [58][59][60][61]. We used data from the same section in the mitochondrial control region from a related and co-distributed finches to provide context for the measures of genetic diversity. ...

Three Molecular Markers Show No Evidence of Population Genetic Structure in the Gouldian Finch (Erythrura gouldiae)

... likely go to fixation when either N e or s are very large. In most endangered wildlife the former requirement is not met [30], thus selection will be of lesser importance than genetic drift for shaping genetic diversity in the population. Tasmanian devil populations with and without DFTD all had similar genetic diversity—a pattern that remained unaffected over time in DFTD populations (S1 File). ...
My comment:  Rapid and efficient ecological adaptation is based on epigenetic regulation of existing biological information. Switching and regulating between alternative epigenetic programs never lead to any kind of evolution, because it doesn't cause growth of biological information. Instead, shifting methylation patterns typically result in subtle errors in DNA sequences. That's why genetic entropy is a biological fact. There's a deletional bias within all kind of organisms. We can only observe loss of genetic diversity within every type of populations, smaller or larger. There is no mechanism for evolution. The only alternative is Creation and Intelligent Design. Of course it's a good question why organisms are only experiencing genetic degradation. To get the answer, we have to open the Bible. Don't be deceived.


Genetic degradation in nature - About 40,000 species become extinct every year

A team of scientists is trying to establish a global DNA bank for endangered animals to restore earlier levels of genetic diversity within species


Excerpts: "In our own lifetime, it’s estimated that 40,000 species become extinct every year. To help keep a record of this disappearing life, a team of scientists is trying to establish a global DNA bank for endangered animals.

Although banks containing animal genes are scattered throughout the world, this would be the first international effort to collect and compile tissue samples from all known endangered animal species.

Final Vestiges

Scientists currently must rely on studying fossils and other bits of data to understand extinct animals, like dinosaurs and woolly mammoths. A DNA bank would provide future generations with a more complete and accurate record of now-threatened species, such as black rhinos, giant pandas and tigers.

Oliver Ryder, a geneticist at the Center for Reproduction of Endangered Species, Zoological Society of San Diego, and lead author of the proposal, which was published in last week’s issue of Science, says, “The future will find uses for the information obtainable from DNA banks that we cannot presently imagine.”

While Jurassic Park-like recreations are remote at this point, experiments are under way to freeze the eggs and sperm of endangered species in a process called “cryopreservation.” An embryo may then be implanted into a non-endangered host animal, thus preserving the donor species.

If DNA samples are collected before a species’ population drops to dangerous lows, Ryder and his colleagues additionally believe that preserved cell lines for endangered animals could be replicated. Such nuclear replacement cloning might be able to restore earlier levels of genetic diversity within a species.

Ryder hopes that information from the samples could be available to scientists and conservationists worldwide via a single Web site, perhaps run by a multinational organization.

Project Could Save Species

Many scientists, including Ryder and Rodrigo Medellin, a professor at the Institute of Ecology, National University of Mexico, believe a world DNA bank may also save certain species from imminent extinction.

For example, California researchers already are using genetic information to help save the California condor, a species placed in captivity to prevent its extinction. By analyzing DNA samples, conservationists are able to identify kinship among the birds, which aids in the prevention of inbreeding and the spread of heritable diseases.

Conservationists also are attempting to revive Przewalski wild horse populations throughout the world, particularly in the majestic animal’s native land of Mongolia. In this case, breeders are attempting to preserve an extremely limited gene pool derived from 12 horses that were captured in the wild.
Genetic information is used to monitor commercial products, like canned fish, to make sure they do not contain meat from endangered mammals, such as blue whales and dolphins.

As science and technology advance, information in DNA animal banks might assist medicine and pharmaceutical development by helping to explain how certain genes work.

Medellin adds, “Maybe in the future, when we are wiser and perhaps fewer (in number), we might be able to do something to recover lost species.” "

Endangered Species' Genetic Diversity Explains their Decline


Excerpt: "Some species may face extinction when they are not able to adapt as easily to changing environments or defend against new diseases. To better identify or rank threatened and engendered species, researchers from Purdue University suggest using the animals' rate of genetic diversity loss.

"Genetic diversity is a key component to the long-term survival of a population," Janna Willoughby, a then-doctoral student in wildlife genetics, said in a statement. "The approach we developed identifies populations with limited genetic diversity that isn't going to be enough to allow the population to persist over time. We found that this method performs significantly better than current methods for identifying species in need of conservation efforts."

Willoughby, along with Andrew DeWoody, a professor of genetics, studied positions of genes on chromosomes in order to estimate genetic diversity loss among wildlife populations. From this they were able to develop a statistical approach for estimating the number of generations remaining before a species' genetic variation reaches a low threshold.

According to their study, researchers found a reduced genetic variation in threatened species. They attributed this to circumstances such as inbreeding, which can result when population sizes are small.

The researchers also acknowledged the many methods for determining that a species is either threatened or endangered, including the International Union for Conservation of Nature (IUNC). They examined the IUNC's Red List to see how effective it was at identifying poor genetic diversity in species; however, the researchers discovered that the organization's criteria was not closely related to genetic diversity.

"The criteria of many conservation organizations were formulated before the availability of genetic data we have today," DeWoody said in the release. "But genetic methodology has advanced so rapidly that factoring in genetic diversity is now pretty straightforward." "

My comment: This is the best scientific evidence against the evolutionary theory. Genetic entropy is a fact and it's happening all over nature, including us human beings. There are 561,119 gene-disease associations in human genome at the whole world level and the number of random beneficial mutations is close to ZERO. Evolution has no mechanism because any change in organisms is based on rapid and efficient epigenetic regulation of existing biological information OR gradual but inevitable corruption of information. Both adaptation and information loss occur very rapidly. Stories about millions of years of evolution are pure pseudoscience. Don't get lost.


Scientists Confirm: Darwinism Is Broken

Evolution believers need a new theory


Excerpts: "Darwinian theory is broken and may not be fixable. That was the takeaway from a meeting last month (11/2016) organized by the world's most distinguished and historic scientific organization, which went mostly unreported by the media.

The three-day conference at the Royal Society in London was remarkable in confirming something that advocates of intelligent design (ID), a controversial scientific alternative to evolution, have said for years. ID proponents point to a chasm that divides how evolution and its evidence are presented to the public, and how scientists themselves discuss it behind closed doors and in technical publications. This chasm has been well hidden from laypeople, yet it was clear to anyone who attended the Royal Society conference, as did a number of ID-friendly scientists.

Dr. Meyer, a Cambridge University-trained philosopher of science, writes provocatively in the book's Prologue:
“The technical literature in biology is now replete with world-class biologists routinely expressing doubts about various aspects of neo-Darwinian theory, and especially about its central tenet, namely the alleged creative power of the natural selection and mutation mechanism.
“Nevertheless, popular defenses of the theory continue apace, rarely if ever acknowledging the growing body of critical scientific opinion about the standing of the theory. Rarely has there been such a great disparity between the popular perception of a theory and its actual standing in the relevant peer-reviewed science literature.”
The opening presentation at the Royal Society by one of those world-class biologists, Austrian evolutionary theorist Gerd Müller, underscored exactly Meyer’s contention. Dr. Müller opened the meeting by discussing several of the fundamental "explanatory deficits" of “the modern synthesis,” that is, textbook neo-Darwinian theory. According to Müller, the as yet unsolved problems include those of explaining:
  • Phenotypic complexity (the origin of eyes, ears, body plans, i.e., the anatomical and structural features of living creatures);
  • Phenotypic novelty, i.e., the origin of new forms throughout the history of life (for example, the mammalian radiation some 66 million years ago, in which the major orders of mammals, such as cetaceans, bats, carnivores, enter the fossil record, or even more dramatically, the Cambrian explosion, with most animal body plans appearing more or less without antecedents); and finally
  • Non-gradual forms or modes of transition, where you see abrupt discontinuities in the fossil record between different types.
As Müller has explained in a 2003 work (“On the Origin of Organismal Form,” with Stuart Newman), although “the neo-Darwinian paradigm still represents the central explanatory framework of evolution, as represented by recent textbooks” it “has no theory of the generative.” In other words, the neo-Darwinian mechanism of mutation and natural selection lacks the creative power to generate the novel anatomical traits and forms of life that have arisen during the history of life. Yet, as Müller noted, neo-Darwinian theory continues to be presented to the public via textbooks as the canonical understanding of how new living forms arose – reflecting precisely the tension between the perceived and actual status of the theory that Meyer described in “Darwin’s Doubt.”
Yet, the most important lesson of the Royal Society conference lies not in its vindication of claims that our scientists have made, gratifying as that might be to us, but rather in defining the current problems and state of research in the field. The conference did an excellent job of defining the problems that evolutionary theory has failed to solve, but it offered little, if anything, by way of new solutions to those longstanding fundamental problems.

...This largely semantic, or classificatory, issue obscured a deeper question that few, if any, of the presentations confronted head on: the issue of the origin of genuine phenotypic novelty – the problem that Müller described in his opening talk.

Indeed, by the end of Day 3 of the meeting, it seemed clear to many of our scientists, and others in attendance with whom they talked, that the puzzle of life's novelties remained unsolved – if, indeed, it had been addressed at all. As a prominent German paleontologist in the crowd concluded, “All elements of the Extended Synthesis [as discussed at the conference] fail to offer adequate explanations for the crucial explanatory deficits of the Modern Synthesis (aka neo-Darwinism) that were explicitly highlighted in the first talk of the meeting by Gerd Müller.”

In “Darwin’s Doubt,” for example, Meyer emphasized the obvious importance of genetic and other (i.e., epigenetic) types of information to building novel phenotypic traits and forms of life. The new mechanisms offered by the critics of neo-Darwinism at the conference – whether treated as part of an extended neo-Darwinian synthesis or as the basis of a fundamentally new theory of evolution – did not attempt to explain how the information necessary to generating genuine novelty might have arisen. Instead, the mechanisms that were discussed produce at best minor microevolutionary changes, such as changes in wing coloration of butterflies or the celebrated polymorphisms of stickleback fish.

Moreover, the mechanisms that were discussed – niche construction, phenotypic plasticity, natural genetic engineering, and so on – either presupposed the prior existence of the biological information necessary to generate novelty, or they did not address the mystery of the origin of that information (and morphological novelty) at all.

Unfortunately, however, the conference will be remembered, as Suzan Mazur intimated in her coverage, for its failure to offer anything new. In particular, it failed to offer anything new that could help remedy the main “explanatory deficit” of the neo-Darwinian synthesis – its inability to account for the origin of phenotypic novelty and especially, the genetic and epigenetic information necessary to produce it.

These are still problems that evolutionary theory tells us little about – constituting, in our judgment, an invitation to scientists to consider the alternative of intelligent design.

(Dr. Paul Nelson and Mr. David Klinghoffer are Senior Fellows with Discovery Institute's Center for Science & Culture.)

My comment: Any change in organisms is due to epigenetic regulation of existing biological information or gradual but inevitable corruption of information. Darwinism is broken. Why to build theories that don't work? The truth can be found in the Bible.

DNA doesn't determine phenotype or individual characteristics - cloning example

Nuclei transplantation proves that DNA doesn't dictate skeletal characteristics of an organism


Excerpt: "In previous studies of nuclear transplantation, most cloned animals were obtained by intraspecies nuclear transfer and are phenotypically identical to their nuclear donors; furthermore, there was no further report on successful fish cloning since the report of cloned zebrafish. Here we report the production of seven cross-genus cloned fish by transferring nuclei from transgenic common carp into enucleated eggs of goldfish. Nuclear genomes of the cloned fish were exclusively derived from the nuclear donor species, common carp, whereas the mitochondrial DNA from the donor carp gradually disappeared during the development of nuclear transfer (NT) embryos.

The somite development process and somite number of nuclear transplants were consistent with the recipient species, goldfish, rather than the nuclear donor species, common carp. This resulted in a long-lasting effect on the vertebral numbers of the cloned fish, which belonged to the range of goldfish. These demonstrate that fish egg cytoplasm not only can support the development driven by transplanted nuclei from a distantly related species at the genus scale but also can modulate development of the nuclear transplants."


Excerpt: "Surprisingly, however, the number of vertebrae in the clones was that of the species providing the recipient egg. Thus the egg cytoplasm, and not the genetic code of the transplanted nucleus, affected this skeletal characteristic in the offspring."

My comment: This is a great example of how the cell uses DNA material. DNA has no control over cellular processes, phenotypes, individual characteristics or body plan. Epigenetic reprogramming of stem cells is needed for embryonic development. This complex reprogramming procedure is mediated by non coding RNA molecules that transfer necessary epigenetic markers for histone tails and DNA bases (cytosine and adenine methylation). There is no such thing as mutation driven evolution. Variation of organisms is based on epigenetic regulation of existing biological information and it will never lead to any kind of evolution. Adaptation and change are scientific facts but shifting between alternative epigenetic programs don't result in evolution, but gradual and inevitable genetic degradation only. Don't be deceived.

p.s. Thanks to Jorge Rodriguez for addressing me this interesting find. He told that researchers who made this study didn't get further funding for being able to continue this research. Surprise.


More than half a million disease-gene associations

More than half a million disease-gene associations - The lack of random beneficial mutations will ruin the theory of evolution

DisGeNet maintains a database of human genetic diseases and disorders. In May 2017, their database contained a collection of 561,119 disease-gene associations, that is, a disease associated with a genetic mutation. The site is currently one of the most important databases used by researchers who try to develop medicines and therapeutic treatments for humans suffering from rapid human genetic degradation.

Evolutionists have not a single convincing example of a random beneficial mutation. And even if there are some candidates, disease-causing genetic mutations will in any case be so numerous that it is perfectly clear that evolution is not happening and it never happened. In addition, harmful mutations arise so rapidly that the fairytales of millions of years of evolution have proved to be the most serious heresy of our time.


Same genome can yield very different animals

Chemical modifications to histone tails affect how available genes are to be transcribed


Excerpt: "The bee genome has a superpower. Not only can the exact same DNA sequence yield three types of insect—worker, drone, and queen—that look and behave very differently, but, in the case of workers, it dictates different sets of behaviors.

A key to the genome’s versatility seems to be epigenetic changes—chemical tags that, when added or removed from DNA, change the activity of a gene. Previous studies had shown distinct patterns of tags known as methyl groups on the genomes of bees performing different roles within their hives.

In a study published in Genome Research last month, Paul Hurd, an epigenetics researcher at Queen Mary University of London, and colleagues looked at a different type of epigenetic change: histone modifications. DNA wraps around histones, and chemical modifications to these proteins are thought to affect how available genes are to be transcribed.

In their new study, the researchers report that queen and worker bees each have characteristic patterns of histone modifications on their genomes, and that these differences emerge very early in development, suggesting they may be key to determining the insects’ fates.
The very different individuals that arise from hive members’ identical genomes have made the honeybee “one of the most well-known and striking examples of phenotypic plasticity,” says Gene Robinson, a genomicist at the University of Illinois who was not involved in the study. Bees are a model, he says, for “understanding how environmental signals are transduced and then trigger these alternate developmental pathways.”

Larvae are sent down different developmental pathways from the time of hatching by nurse bees (a type of worker), which tailor the insects’ diets according to their future castes. Worker bees that tend to queen larvae and mature queens make their special food, so-called royal jelly, themselves, and it contains a compound known to directly influence histone modifications, the authors note in their paper.

No previous studies had examined whether histone modifications might help steer development in bees, even though, Hurd notes, unlike methyl tags, which are restricted to certain stretches of DNA in honeybees, “the histones are all over the genome.” To investigate their role, the research team collected worker and queen bee eggs and larvae from Apis mellifera hives and sampled the larvae 96 hours after they hatched. The team then analyzed the bee genomes for the positions of three different types of histone modifications.

At 96 hours, the researchers found, the genomes of future workers and queens already had “striking differences” in their patterns of histone modifications, says Robert Lowe, a computational biologist at Queen Mary University of London and one of the paper’s authors. And the locations of the histones that were modified differently in workers and queens corresponded with the sites of genes that have different expression levels between the two populations.

The authors suggest that the histone modifications drive differences in gene transcription among bees of different castes, which in turn guide them down different developmental paths.

Elena Torlai Triglia, who studies chromatin modification and transcriptional regulation at the Broad Institute in Massachusetts and was not involved in the study, says the relationship between histone modification and gene transcription in honeybees is “still a bit of a mystery.” To nail down cause and effect, she suggests, a study would need to alter the histone marks and see whether changes in gene transcription and phenotype occurred as a result—a step the authors didn’t take, but plan to in future experiments, Hurd says.

Lowe notes that unlike the popular lab insect Drosophila, bees have all the same types of epigenetic marks humans do, making them useful subjects for understanding those modifications. One question they’d like to look into, Hurd says, is whether pesticides affect bees’ epigenetic marks."

My comment: DNA has no control over cellular processes. C
hemical modifications to histone tails affect how available genes are to be transcribed into functional RNA products. This is how passive DNA is used by clever cellular mechanisms. Available DNA is transcribed along to rules affected by epigenetic factors and mechanisms. 'Available genes' describes well the polyfunctional and optimized DNA code. Histone code is a complex biological database and it has a major role in determining organismal characteristics. When organisms experience adaptation and variation, the histone code and other epigenetic code is altered. Sometimes shifting between alternative epigenetic programs results in genetic errors and this is why DNA mutations often occur. Mutations never result in any kind of evolution but genetic degradation, faulty genes, loss of information, diseases, disorders etc. Don't get lost.


Israeli teachers discouraged from teaching evolution

Israeli teachers discouraged from teaching evolution


Excerpt: "Many students in the Israeli school system are not learning about evolution and the Education Ministry is discreetly encouraging teachers to avoid the subject in primary school biology courses, a local media report found on Wednesday.

A handful of Israeli teachers told Channel 10 that the Education Ministry promotes the avoidance of the theory of Charles Darwin who said all living things evolved from common ancestry. The teachers reportedly said they are not trained to teach the subject and are instead encouraged to teach other subjects within the sciences.

Israeli children in kindergarten through elementary school do not receive biology lessons on the origins of mankind, according to the report. Only when they reach middle school do teachers vaguely refer to evolution during general classroom discussion, it added.

Before the Israeli high school curriculum was changed five years ago, it included one unit on evolution, the teachers said.

This unit was replaced by subjects like genetics, species survival, and environmental adaptation, according to the three biology teachers who spoke to Channel 10.
The Education Ministry reportedly responded to the news saying, “Learning the principles of adaptation to the environment is compulsory in middle school. The theory of evolution itself is taught as an optional class in high schools.”

A 2016 survey found secular Israelis are more inclined than Orthodox Israelis to see a contradiction between science and religion.

The Pew Research Center found that approximately half of Israelis believed in evolution."

My comment: The theory of evolution is just a hypothetical model and it has nothing to do with science. The Education Ministry of Israel has done a wise solution because the theory of evolution has too many scientific controversies and gaps. Btw, did you know that Jews are the most intelligent people in the world? Look at the facts:

"As of 2017, Nobel Prizes have been awarded to 892 individuals, of whom 201 or 22.5% were Jews, although the total Jewish population comprises less than 0.2% of the world's population."


Lactose tolerance is regulated by epigenetic factors

Methylation at the LCT promoter and enhancer is highly predictive of lactase enzymatic activity


Excerpts: "On the other hand, although it is generally accepted that there is a strong association between the ancestral -13910*C allele with lactase non-persistence and the variant -13910*T allele with lactase persistence in people of European descent, in some cases these genotypes are not completely predictive of the phenotype. Yet, the physiological change in lactase gene expression occurs in the context of a stable DNA sequence. This suggests the presence of dynamic mediators of LCT regulation such as epigenetic modifications and/or transcriptional changes."

"DNA methylation also plays an important role in regulation of human LCT. This was confirmed by Labrie et al. who identified epigenetically controlled regulatory elements where differential DNA methylation accounted for inter-individual differences of lactase mRNA level in a Lithuanian cohort of individuals."

"Through regression modeling we show that DNA methylation in the enhancer and promoter site of the LCT gene, rather than differential regulation of intestinal transcription factors, e.g. CDX2, POU2F1, GATA4/6 or HNF1α, is predictive of lactase persistence/non-persistence."

"Most importantly, however, cross-validation analysis revealed that methylation at the LCT promoter and enhancer was highly predictive of lactase enzymatic activity, and the persistence/non-persistence phenotype. The predictive power outperformed the hitherto existing genotype at rs4988235, which fails prediction for the C/T genotype."
"In summary, we have investigated the contribution of epigenetics to the lactase persistence/non-persistence phenotypes, including lactase gene expression and enzymatic activity. We have identified putative lactase meQTLs, which are differentially methylated between lactase persistent and lactase non-persistent individuals."

My comment: C>T alteration is a common alteration in DNA and it typically occurs as a result from deamination of a methylated cytosine base. This study proves that methylation levels of MCM6 and LCT genes are more predictive for lactose tolerance phenotype than genetic mutations. That's why DNA mutations are often results from epigenetic modifications.

This study didn't take into account other regulatory mechanisms, such as miRNA upregulation, lncRNA regulation, histone epigenetic markers, gut bacteria, immune system etc. But this study shows that evolutionists' claims regarding random beneficial mutations are pseudoscientific claims. Random DNA mutations never result in any kind of evolution. Don't be deceived.


Observed facts refute the theory of evolution

The theory of evolution is just a hypothetical model and it has nothing to do with observed science

  1. Random mutations lead to genetic degradation, loss of genes, loss of information, loss of function and they are associated with huge number of genetic diseases. The number of observed and scientifically verified random beneficial mutations is extremely low compared to the huge number of harmful mutations. For example, there are 224,642 disease causing genetic mutations (08/2018)  in human genome at the whole world level. Annual increase was more than 20,000. One in five 'healthy' adults may carry disease-related genetic mutations. Most of known rare beneficial mutations are not scientifically verified and they typically are SNPs, which means they are only small changes at one nucleotide level. They don't lead to increase of biological information.

    Most of so called random mutations are not actually random. Instead, most of them are based on mechanisms, such as methylated cytosines are prone to turn into thymines in deamination caused by oxidative stress. DNA repair mechanisms don't touch this alteration due to methyl marking on the base.

  2. Natural selection is a fictional force that is assumed to be able to select beneficial changes and weed out harmful ones. Evolution theorists also talk about 'negative selection' or 'purifying selection' meaning that assumed natural selection is able to weed out harmful mutations. In reality there's no natural force being able to select harmful mutations out. Most of so called neutral mutations are so subtle that they don't directly affect cell's ability to produce necessary proteins or regulate cellular functions. But in long run they cause corruption in the integrity of genetic language and grammar. It's like fragmentation of a hard drive; the computer still works but there are some problems in normal functions.

    The cell is able to reorganize genetic information. Faulty genes are located at the ends of chromosomes in telomeres. Healthy DNA will remain in euchromatin close to centre of a chromosome. Reorganization of biological information after information loss often results in interesting changes in an organism.

    Imaginary pictures and stories are necessary for maintaining
    pseudoscientific theories. 
    Because there's no NS weeding out harmful mutations, scientists try to repair genomes of organisms. Serious scientists know that genetic entropy is a scientific fact and human genome must be repaired in order to reproduction be possible.


    Excerpt: "About half of the 32,000 mutations associated with human genetic diseases are this type of C-G to T-A change, says Liu, a Howard Hughes Medical Institute investigator at Harvard University. Until now, there was little anyone could do about it, he says."

  3. "Survival of the fittest" is a phrase that originated from Darwinian evolutionary theory as a way of describing the mechanism of natural selection. The biological concept of fitness is defined as reproductive success. In Darwinian terms the phrase is best understood as "Survival of the form that will leave the most copies of itself in successive generations." (Wikipedia)

    Modern science has revealed that ecological adaptation is based on epigenetic mechanisms. A good example is the blind cave fish. Genetic mutations or selection were not the reasons why the cave fish lost its eyes. You can read about this energy efficient epigenetic mechanism more from here:


    The strongest, fastest and fittest in a population means an organism who has the healthiest epigenome, which means inheritable epigenetic cellular memory.

  4. DNA similarities between organisms. According to the latest studies, human and dog genomes are 95% similar at the whole genome level. That percentage is about the same between humans and chimps, pigs, kangaroos, dolphins etc. But if we really want to study possible relationships between organisms, then this should be done at RNA level. For example, there are over 60,000 long non coding RNA molecules in human sperm which is over three times more than DNA strands used for protein encoding. These RNAs are the true functional informational units and information carriers that are responsible for transmitting epigenetic information layers during embryonic development. Similarity of lncRNAs between humans and chimps is less than 50%, probably close to 30%. Mutations in lncRNAs are associated with serious diseases.

    Conclusion: Genetic entropy is a scientific fact. There is no mechanism for evolution. Organisms experience changes but the change never results in evolution. Scientists are not allowed to criticize the theory of evolution but we individuals are free to make our own conclusions. Don't get lost.

A new mechanism identified that links epigenetic changes to memory reconsolidation

Epigenetic mechanisms control both transcription and translation


Excerpt: "Understanding the mechanics of how memories form and are retrieved has applications to psychiatric, neurological and neurodegenerative disorders, and may be helpful to attenuate maladaptive memories in psychiatric disorders.

Two broad findings have been acknowledged regarding memory reconsolidation, which is the retrieval and strengthening of a recent memory. The first broad finding is that, during the process of memory reconsolidation, changes in translational control – whereby new proteins are formed from activated genes – occur in areas of the brain related to memory formation. The second broad finding is that epigenetic mechanisms – various molecular modifications known to alter the activity of genes without changing their DNA sequence – are also somehow actively involved during memory reconsolidation or strengthening.
Now, researchers at the University of Alabama at Birmingham have described a novel mechanism that links epigenetic change to translational control. They report how several particular epigenetic changes in the hippocampus of the rat brain control downstream regulation of translation in brain neurons during fear memory reconsolidation, acting through a gene called Pten. The downstream target affected by changes in PTEN enzyme levels is the AKT-mTOR pathway, one of the main translation control pathways involved in memory reconsolidation. PTEN was already known to be a potent inhibitor of AKT-mTOR, but was not previously linked to epigenetic control of memory.

Commenting on what these findings could mean for the medical community, Farah D. Lubin, PhD, associate professor in the UAB Department of Neurobiology, said: “These findings could be critical in treatment of memory disorders, such as post-traumatic stress disorder.

Memory consolidation is the process that stabilises a memory after it is first acquired in the brain. Memory reconsolidation occurs when that memory is retrieved, at which point the memory may be modified or strengthened.

In the study led by Lubin, researchers found that retrieval of a contextual fear memory in rats briefly increased levels of the enzyme EZH2, an enzyme known to add methyl groups to histones. Histones are proteins that help package and order DNA in the chromosome, and also play a role in epigenetic gene regulation. Along with the increased EZH2, the researchers found increased methylation of histone H3; specifically, the addition of three methyl groups to the lysine 27 amino acid of histone H3. That trimethylation of the histone by EZH2, known as H3K27me3, correlated with decreased levels of PTEN enzyme.

Examination of the DNA encoding for the Pten gene showed increased levels of H3K27me3 bound to the DNA, as well as DNA methylation, across the promoter and coding regions of the Pten gene. DNA methylation is another form of epigenetic control, and both the histone epigenetic change and the DNA epigenetic change indicated transcriptional silencing of the Pten gene.

The UAB researchers next used small interfering RNA (siRNA) to knock down genes. Through knockdown experiments, they showed that levels of H3K27me3 and PTEN appear to directly control the AKT-mTOR pathway.

Knockdown of the gene for the H3K27me3 methyltransferase enzyme, Ezh2, in the hippocampus – the memory-consolidating region of the brain – prevented decreases of PTEN and activation of AKT-mTOR during memory reconsolidation. However, when the Ezh2 and Pten genes were knocked down at the same time, the AKT-mTOR pathway was activated.

“In the present study, we found that H3K27me3 regulated Pten repression necessary for mTOR phosphorylation during memory reconsolidation,” Lubin said. “As a result, we have identified a novel epigenetic pathway critical for regulation of translational control mechanisms during memory reconsolidation.” "

My comment: Both DNA methylation patterns and especially histone code, a complex biological database, strongly affect transcription and translation of genetic code. These mechanisms and factors are dynamic, reversible and inheritable. The histone code is established during first phases of embryonic development mostly by lncRNAs that transmit the necessary information for developing embryo for its cell differentiation programs.

Epigenome controls DNA that is only a passive information library that the cell uses for being able to build RNA-molecules. A stem cell has a perfect DNA but it does nothing without epigenetic information layers. Stem cell needs to be programmed with epigenetic programs to have an identity and a task.

This is why any change in organisms is due to epigenetic regulation of existing biological information OR gradual but inevitable corruption and loss of information. There is no mechanism for evolution. Don't be deceived.


Multiple overlapping and poly-functional DNA reduce the probability of beneficial mutation

DNA is already optimized - Beneficial mutations are extremely rare - However, mutations happen and they result in genetic degradation


Excerpt from abstract: "There is growing evidence that much of the DNA in higher genomes is poly-functional, with the same nucleotide contributing to more than one type of code. Such poly-functional DNA should logically be multiply-constrained in terms of the probability of sequence improvement via random mutation. We describe a model of this relationship, which relates the degree of poly-functionality and the degree of constraint on mutational improvement. We show that: a) the probability of beneficial mutation is inversely related to the degree that a sequence is already optimized for a given code; b) the probability of beneficial mutation drastically diminishes as the number of overlapping codes increases.

The growing evidence for a high degree of optimization in biological systems, and the growing evidence for multiple levels of poly-functionality within DNA, both suggest that mutations that are unambiguously beneficial must be especially rare. The theoretical scarcity of beneficial mutations is compounded by the fact that most of the beneficial mutations that do arise should confer extremely small increments of improvement in terms of total biological function. This makes such mutations invisible to natural selection. Beneficial mutations that are below a population’s selection threshold are effectively neutral in terms of selection, and so should be entirely unproductive from an evolutionary perspective. We conclude that beneficial mutations that are unambiguous (not deleterious at any level), and useful (subject to natural selection), should be extremely rare."
A model nucleotide sequence of 100 bases that encodes 12 partially overlapping codes. Each sub-section represents the positions of the Genome Section that participate in that particular code. For example, only the first 10 positions of the Genome Section participate in Code 1 whereas all except the last 5 positions of the Genome Section participate in Code 12. Nucleotide positions of the Genome Section that do not fall into any code are considered entirely neutral with respect to those codes, since they play no part in what the function of those codes may be. In that regard, these neutral positions are not part of the functional genome (at least with respect to those specific codes). (G. Montañez, R. J. Marks II, J. Fernandez and J. C. Sanford)
Excerpt 2: "Each biological specification is encoded by strings of characters (nucleotides or amino acids) that are very specific (and hence very unlikely), with each character having meaning only in the context of many other characters — like letters in a book or like the binary bits comprising a computer code. Any random change in such a set of specifications causes some loss of useful information — with a very high degree of probability. The more that each character is contextually interactive with other characters, the less feasible it becomes to improve a set of specifications via random character changes, because each character is multiply constrained by its many contextual relationships.

The discovery of ubiquitous poly-functional DNA is profound, and forces us to reassess our understanding of the degree of genetic specificity and the probability of beneficial mutation."

My comment: Evolutionists need beneficial mutations to be able to scientifically prove their theory. But as we know, the number of known random beneficial mutations is extremely rare, that it is not possible for evolution to happen. This is because neutral (critical) and harmful mutations are so common. For example, there are 224,642 disease-causing genetic mutations in human genome at population level. This same genetic degradation, genetic entropy, is a phenomenon occurring rapidly all over nature. You can read about it more from here:



Identical DNA, similar outcome? Forget it.

Cloning won’t resurrect your pet because DNA doesn't determine characteristics


Excerpt: "There are some unique coat color variations in cats, particular calico cats. On December 22, 2001, a kitten named CC made history as the first cat—and the first domestic pet—ever to be cloned. But CC was a black and white tiger tabby and Rainbow was a calico. How is that possible?

“The answer lies in the X chromosome. In cats, a gene that helps determine coat color resides on this chromosome. Both CC and Rainbow, being females, have two X chromosomes. (Males have one X and one Y chromosome.) Since the two cats have the exact same X chromosomes, they have the same two coat color genes, one specifying black and the other specifying orange. Very early in her development, each of Rainbow’s cells “turned off” one entire X chromosome, thereby turning off either the black or the orange color gene. This process, called X-inactivation, happens normally in females, in order to prevent them from having twice as much X-chromosome activity as males.""


"Meet CC, short for Carbon Copy or Copy Cat (depending on who you ask). She was the world’s first cloned pet."

CC was genetically identical to Rainbow, the cat who donated the genetic material. But the cats looked different because coat patterns and other features can be determined in the womb.

Although CC was a clone of Rainbow, she grew up as her own unique self, with her own look and personality."

My comment: The information required for variation already exists in the cell. No mutations were needed for these cats to have different phenotypes. Reading of DNA is controlled by epigenetic factors and mechanisms. X-inactivation is regulated by certain histone epigenetic markers. Genetic mutations disrupt biological information leading to faulty genes, information degradation and diseases. DNA is just a passive information library controlled by the epigenome. More about this can be read from here:


Epigenetic Patterns Can Change Physical Characteristics at the Organismal Level

"For example, mice with methylation at the agouti gene are obese and yellow in color, while their unmethylated counterparts have normal weight and have brown coats. Note that these two mice are genetically identical and only differ epigenetically (i.e., different DNA methylation patterns).The coat color difference relates to the expression of different types of skin pigment.

DNA methylation is an epigenetic mechanism that can alter gene expression by binding to promoter regions and suppressing gene expression within specific genomic regions. It does this by blocking the ability of transcription factors (blue dots) from binding to the DNA and allowing transcription (the formation of RNA) from occurring."


Fathers pass on four times as many new genetic mutations as mothers

Faults in male DNA are a driver for rare childhood diseases - more reasons for genetic degradation


Excerpt: "Children inherit four times as many new mutations from their fathers than their mothers, according to research that suggests faults in the men’s DNA are a driver for rare childhood diseases.

Researchers studied 14,000 Icelanders and found that men passed on one new mutation for every eight months of age, compared with women who passed on a new mutation for every three years of age.

The figures mean that a child born to 30-year-old parents would, on average, inherit 11 new mutations from the mother, but 45 from the father.

Kari Stefansson, a researcher at the Icelandic genetics company, deCODE, which led the study, said that while new mutations led to variation in the human genome, which is necessary for evolution to happen, “they are also believed to be responsible for the majority of cases of rare diseases in childhood.”

My comment: How could evolution happen after DNA damage? DNA mutations are not the reason for human variations.

"Scientists know from previous research that children born to older fathers have a greater risk of developing certain disorders, including intellectual disabilities, autism and schizophrenia. New mutations are a likely factor, given that more genes are active in the brain than in any other organ in the body.
Children inherit new mutations when they build up in the father’s sperm and the mother’s eggs. Men pass on more mutations than women because they make sperm throughout their lives, using a process that is not perfect at copying DNA. And so, as the man ages, his sperm accumulate more and more mutations. Women pass on fewer mutations because they tend to be born with their full complement of eggs.

In the study published in Nature, the researchers analysed the DNA of 1,500 Icelanders and their parents and, for 225 people, at least one of their children. They found that new mutations from mothers increased by 0.37 per year of age, a quarter of the rate found in men. While the vast majority of new mutations are thought to be harmless, occasionally they can disrupt the workings of genes that are important for good health.

My comment: Most of mutations are so subtle that they are not weeded out by any selection.

"The scientists also found that in some parts of the genome, new mutations were overwhelmingly passed on from mothers. In one section of chromosome 8, for example, the researchers found 50 times more mutations from the mother than in any other part of the genome. The scientists speculate that the cluster of mutations reveals an ancient Achilles heel in the genome: a region where the chromosome can easily break in two, but can be patched up, leaving mutations as a genetic scar.

“It seems that when a chromosome breaks in an egg, it can sometimes be repaired, avoiding a chromosomal catastrophe but leaving a scar of small mutations,” said Martin Taylor, a geneticist at the University of Edinburgh.

Allan Pacey, professor of andrology at Sheffield University, said: “We have known for many years that the risk of having a child with a medical condition of genetic origin increases noticeably with the father’s age at conception. It is for this reason that there is a recommended upper age limit for sperm donors, currently 40 years in the UK. Put simply, the genetic quality of sperm from younger men, in terms of new mutations, is generally much better than that of older men.” "

My comment: All human beings are 99.9 percent identical in their genetic makeup. Differences in the remaining 0.1 percent hold important clues about the causes of diseases.


There are even 224,642 disease-causing genetic mutations in the human genome at population level. Annual increase was more than 20,000. But the number of verified random beneficial mutations is close to zero. This is why the theory of evolution is the most serious heresy of our time. Don't be deceived.