Nuclear genome has lost its function as the unique and exclusive determinant of inherited characteristics

Fresh Study minimizes the role of DNA in inheritance


Excerpt: "The development of epigenetic studies in recent years has profoundly enriched our view of genetic inheritance. Most significantly, the nuclear genome has gradually lost its function as the unique and exclusive determinant of inherited characteristics due to mounting waves of data revealing the complex epigenetic networks that heritably control genome expression. A comprehensive picture of epigenetic patterns is now emerging where DNA methylation, histone modification, chromatin patterning and RNA-mediated functions play key regulatory roles on a variety of cellular processes and on the programming of early embryonic development.

Growing evidence indicates that epigenetic states can be transmitted to the germline—most significantly via spermatozoa—and then delivered to the offspring at fertilization and inherited by the progeny (extensively reviewed by Lane et al.  and Rando). A fundamental role in this process is played by extracellular vesicles, heterogeneous membrane-coated particles that can transfer RNA, DNA, proteins and lipids between a broad range of cell types and across species. The cargo of extracellular vesicles is predominantly constituted by a wide range of RNAs including regulatory miRNA, tRNA, lncRNA, piRNA and snRNA, which collectively can modulate the expression of an ample spectrum of genes. In the past decade, extracellular vesicles, particularly exosomes, have emerged as crucial vehicles mediating intercellular communication in a variety of physiological and pathological processes. Extracellular vesicle-mediated intercellular trafficking is not restricted to somatic cells, but is also a phenomenon involving germline cells—most significantly, mature spermatozoa. During sperm maturation, the regulatory RNA content is selectively modified by the interaction with epididymosomes, a class of extracellular vesicles released from somatic epididymis that deliver their cargoes to epididymal spermatozoa. Some of these epididymal RNAs are essential for proper embryonic development.
In summary, a growing body of published data now supports the idea that spermatozoa provide an active system of soma-to-germline communication that crosses the Weismann barrier and contributes to epigenetic formatting of progeny development .

Extracellular vesicles are recognized as effective mediators of intercellular communication. They are released from diverse cellular sources and can pass many different RNA molecules, which may vary in response to stressing stimuli and with the health of the donors."

My comment: DNA is just a passive data base and it has no control over cellular processes. Organismal traits and characteristics are inherited mostly by non coding RNA molecules transferred by extracellular vesicles. These discoveries should help researchers solve the problems in missing heritability, for instance. There is no mechanism for evolution because epigenetic modifications never result in any kind of evolution. Don't get lost, my friends.


Nuclear Pore Complex points out the absurdity of the theory of evolution

Nuclear pore complex recognizes faulty DNA sequences

The nuclear pore complex is a highly complex protein machine that serves as a kind of gateway between the nucleus and cytoplasm. The nuclear pore complex is composed of 500-1000 proteins, making it one of the most complex cellular protein machines.

The Nuclear Pore Complex (NPC) has several important roles in the molecular transport between the nucleus and the cytoplasm. It checks that the cargo of mRNA transiting from the nucleus to the cytoplasm is in good order and that its grammar is correct. This process is a very important step in protein production. NPC is a cargo monitoring port that does not allow mRNA to leave the nucleus in case of cargo uncertainties.

Another interesting task of the NPC is to assist in repairing faulty DNA sequences. The cell has mechanisms by which it recognizes faulty DNA sequences. When it detects defective DNA, the cell most often hides the defective sections by methylating them and transferring them to regions called telomeres at the ends of the chromosomes. The tightly packaged, silenced DNA is called heterochromatin. The cell uses myosins, so-called motor proteins, two-legged transporter proteins, to move defective DNA sequences in the vicinity of nuclear pore complexes, where the DNA repair mechanisms modify the defective DNA sequences so that they can be reused by the cell.

“Myosins are conveyed as a walking molecule because they have two legs,” Chiolo said. “One [leg] is attached and the other moves. It’s like a molecular machine that walks along the filaments.” 
The myosins pick up the injured DNA, walk along the filament road and then reach the emergency room, a pore at the boundary of the nucleus. 
“We knew, based on our prior study, that there was an emergency room — the nuclear pore where the cell fixes its broken DNA strands. Now, we have discovered how the damaged DNA travels there,” Chiolo said. “What we think is happening here is that the damage triggers a defense mechanism that quickly builds the road, the actin filament, while also turning on an ambulance, the myosin.”

These findings on the complexity and function of NPCs are extremely embarrassing for the evolutionary theory. At the same time, they help to understand the passive nature of DNA as a digital information library that the cell must read in order to produce active and functional RNA molecules. If the theory of evolution were true, it would mean that evolution would have developed a protein machine that is able to recognize what would be a valid DNA or RNA sequence in the cell. In other words, this machine recognizes and helps to correct mutations, i.e. genetic defects. If the hypothesized evolution were based on mutations and natural selection, it would also mean that the nuclear pore complex would have evolved to find and repair the mutations. Absurd!

A good question is how is it possible for NPCs to recognize faulty DNA sequences and also to detect whether a DNA or RNA sequence is a grammatically valid material. Such a machine of up to a thousand complex proteins could not have evolved by chance. The blind, uncontrolled process is unable to construct even one simple protein. The probability is nonexistent, 1: 10 ^ 202. Without functioning nucleus pore complexes, life would end after a few generations because defective proteins would lead to reproductive failures.

The nuclear pore complex points to Intelligent Design and Creation. NPC is designed to be a complete, functional entity. How could random mutations be able to create a machine that is able to recognize and repair random mutations?! Defects in the nuclear pore complex lead to many diseases because it is integral to cellular structure. Its ability to detect and recognize both valid and inaccurate information shows how incredibly complex structures are found in the cell. However, not all errors are repaired by the cell. Gradually everything decays. God has ordained the beginning, the life cycle, and the end of life. There are already hundreds of thousands of genetic defects in the human genome worldwide. Evolution never happened.


Assumed evolution of insect wings?

Evolution of insect wings?

Does the fossil record provide any examples of supposed evolution of insect wings? If the insect wings have evolved, we are expected to find signs of developing wings within flies, dragonflies, bees and wasps, in the fossil record.

Or are evolution believers so desperate that we can only find perfect and working wing structures in the fossil record?

And do we find within present insect species evidence for loss of biological information? Are there insects who have lost genetic information and lost their wings as a result?

Which one wins, evolution or genetic entropy?


Excerpt: "Scientists have sequenced the genome of the Antarctic midge (Belgica antarctica), which contains only 99 million base pairs of nucleotides, making it smaller than other tiny reported genomes, such as that of the body louse (105 million base pairs) or the winged parasite Strepsiptera (108 million base pairs). It is now the smallest insect genome described to date."


Excerpt: "The finding reveals that flightless species retain higher genetic differentiation among populations and comprise a higher number of genetically distinct lineages than flight-capable species, indicating high possibility for allopatric speciation."

There is no sign of evolving or developing wings in the fossil record. An idea of 'half-evolved' wings or 'stumped wings' is absurd. What would an insect do with 'half-evolved' wings? Nothing! They would only make moving difficult and consume energy. We can only observe fully functional wing structures in the fossil record and in the wild. That is a great evidence of Creation.


Parasitic organisms result from loss of information

Gene loss typically leads to parasitic organisms


Excerpt: "Nasonia females inject their eggs inside developing flies, leaving the young wasps to eat their way out. Studying Nasonia could help to improve the agricultural use of other wasps that behave in similar ways. Trichogramma, for example, is used to control pests on tomatoes, corn (maize) and apples.

The Nasonia genomes indicate that the wasps lack the genes required to synthesize certain amino acids, possibly owing to their exclusively carnivorous feeding habits."


Excerpt: "Tapeworms show the largest loss of developmental genes of any animal examined to date," claimed geneticist Dr. Pete Olson.


Excerpt: "Here we sequence the genome of Cuscuta australis. Our analyses reveal that the genome of C. australis experienced massive gene losses, including important genes involved in leaf and root development, flowering-time control, as well as defense against pathogens and insects."

Excerpt: "Second, the human parasite Brugia malayi lost otherwise essential genes most probably owing to the mutualistic relationship with a bacterial endosymbiont."


Excerpt: "Parasites tend to evolve small and compact genomes, generally endowed with a high mutation rate, compared with those of their free-living relatives."


Excerpt: "Parasite genomes are often characterized by a reduction in size, loss of genes, and loss of functions as the parasite becomes more dependent on the host. A. ceratii has retained most of the genome functionality of a free-living species, with the exception of the biosynthesis of a few amino acids and, more significantly, isoprenoids, which appears to be related to the loss of plastid organelles."


Excerpt: "The reduction in plastid genome size and gene content in parasitic plants predominantly results from loss of photosynthetic genes."

Excerpt: "They also compared the C. australis genome with the genomes of similar but non-parasitic plants from the same family, the Convolvulaceae.

The research team found about 11.7% of genes commonly found in photosynthetic plants do not exist in the dodder genome.

Editorial comment: Regressive for sure, and yes gene loss does help to explain how this plant went from being independent to becoming a parasite, but it is not evolution. Gene loss in the opposite of evolution. What has happened here is a degenerative process, which has forced the plant to become completely dependent on another plant to keep it alive for a while, until the parasitized plant is ‘bled dry’ and can no longer sustain itself as well as the totally dependent dodder, then they both die. The dodder plant has not become extinct because it hasn’t lost its ability to form flowers and set seed before it dies.

These findings fit well with Genesis, which tells us that God created plants in separate kinds in a very good world, where there were no dependent parasites that destroyed other plants. However, after man sinned, God cursed the ground and many plants have degenerated since then in varied ways – from shrinking in size, to forming thorns, and some have become parasites as they lost the ability to make and process their own food. Overall, this parasitic plant with its deficient genome is reminder that the real history of the world is from created perfection to degeneration, or to put it more plainly, from good to bad to worse."


Highly predictable toxin resistance debunks evolutionary randomness

Predictable genetic changes point to Design, not evolution


Excerpt: "The caterpillar of the monarch butterfly eats only milkweed, a poisonous plant that should kill it. The caterpillars thrive on the plant, even storing its toxins in their bodies as a defense against hungry birds.

For decades, scientists have marveled at this adaptation. On Thursday, a team of researchers announced they had pinpointed the key evolutionary steps that led to it.

Only three genetic mutations were necessary to turn the butterflies from vulnerable to resistant, the researchers reported in the journal Nature. They were able to introduce these mutations into fruit flies, and suddenly they were able to eat milkweed, too.
Biologists hailed it as a tour-de-force that harnessed gene-editing technology to unscramble a series of mutations evolving in some species and then test them in yet another."

Similar genetic alterations in 47 taxa


Excerpt: "When Dr Ujvari and Dr Casewell’s team widened their investigation to include all 47 taxa that are resistant to cardiac glycosides (whether it was from a plant or an animal source), they found that resistance was due to two amino acid substitutions at just four positions: 111, 119, 120, or 122. Further, the team found that, of the 11 amino acids within this portion of the sodium-potassium exchange pump subunit, one specific amino acid site (111) must always change for resistance to evolve, whereas the second resistance-conferring change then occurs in one of three other amino acid sites (119, 120, or 122), which vary across species."
Other papers confirming these highly predictable changes:

My comment: By using keywords 'cardiac glycosides substitutions at positions 111 and 122' we will soon realize that these predictable changes happen in different types of organisms. Nothing to do with random mutations and selection. Nothing to do with evolution. Organisms are able to tweak their genomes by so called natural genetic engineering. There are several epigenetic mechanisms that make it possible for an organism to modify its own genome. They are typically controlled by the immune system, such as AID mediated deamination. This is ecological adaptation, not evolution. This is Design, not random mutations. Don't get lost.


Icons of Evolution refute the basic tenet of the Evolutionary Theory

Change in allele frequency results in genetic degradation and species extinction


Excerpt: "New research on these complex little birds demonstrates that our understanding of the genetic markers used to predict a species’ extinction is overly simplistic, a pressing problem at a time of unprecedented extinction rates around the globe.

While the story of Darwin’s finches is often framed as a “eureka moment” in his understanding of the way organisms transform through natural selection, nothing could be further from the truth.

Darwin arrived at the Galápagos islands in September of 1835. The black lava of the island and the terrible heat caused him some distress, and he was only selectively attentive to the wonders around him.

He was captivated by the local mockingbirds that varied from island to island, but ignored the island-specific tortoises, preferring instead to shoot and eat them in serious numbers. He even rode on the back of one of the larger specimens for fun.

He had noticed the many finches in the dense growth of the islands’ lowlands but the variation in size, colour and habit left him in a state of “inexplicable confusion”. He collected samples of six species from three islands and stored and labelled them rather haphazardly.

On his return to England, he dumped this mess in the lap of the talented artist and ornithologist John Gould of the Zoological Society of London, and it was he that figured out (in only six days) that Darwin’s finches were actually a complexly interrelated group of 12 different species.
Over time, and in tandem with his consideration of the Galápagos mockingbirds, the finches helped Darwin to understand the process that we now call adaptive radiation, the way in which an ancestral species transforms into many new types, dependent on local environments, and thus evolution more generally.

Now it seems the finches, including some of the specimens Darwin himself collected in 1835, are helping science to understand the complexities of the process of extinction.

One of the common ways to test whether a population or species is likely to go extinct is to measure its genetic diversity: such testing is quick, easy and cheap. Each gene comes in a number of different forms, called alleles.

Genetic diversity refers to the number of different alleles in a population or species; greater diversity is thought to mean that the population or species will have the capacity to adapt should environmental conditions change.

With more diversity comes a higher likelihood that alleles exist in the population that will provide certain individuals with an advantage in changed conditions. These individuals will then outbreed the rest of the population and over time these alleles will become typical of the population or species. This is basically how evolution works. (My comment: This is how it was thought to work.)

"Typically, we would expect populations with high genetic diversity to have a greater potential for long-term survival," says Lawson. "Meanwhile, the low-diversity populations would be more likely to go extinct because that's a common pattern as populations decline to few individuals."

She and her colleagues set out to explore this indicator using Darwin’s finches, which provide a rare opportunity to test whether genetic diversity really is a predictor of extinction.

By looking at the genetic diversity of 212 tissue samples taken from both museum specimens and living birds, they could compare these to the reality that has played out in the islands’ finches, where “many populations went extinct, but far more persisted” over the last 100 years or so. The trio’s hypothesis was “that genetic variation was lower in populations that ultimately went extinct, relative to those that are still extant”.

What they found was the opposite.

Only one of the extinct finch populations, a species called the vegetarian finch, had lower genetic diversity compared to modern survivors. To make matters more confusing, most of the now extinct populations had indications of higher genetic diversity compared to surviving populations that migrated to other islands.

My comment: Change in allele frequency means just different repertoires of genetic errors. Despite of scientists' efforts to explain away these inconvenient findings, Darwin's Finches prove that genetic mutations never result in any kind of evolution. Adaptation and variation within organisms is based on epigenetic modifications that cause minor genetic errors. High genetic diversity means a higher rate of harmful DNA mutations. Along the needs of adaptation these genetic errors are silenced by epigenetic mechanisms. This can be observed as higher amounts of heterochromatin. Further, if population size decreases, gene pool is reduced to a critical level and the final step is extinction.

There is no mechanism for evolution. Any change in organisms is based on epigenetic regulation of pre-existing biological information OR corruption of information. Don't get lost.


Scientific evidence for human genetic degeneration

Scientific evidence for human genetic degeneration (Mutational load)


Excerpt: "Other scientists at Harvard and the Broad Institute have been working on an even more daring tweak to the Crispr system: editing individual base pairs, one at a time. To do so, they had to design a brand-new enzyme—one not found in nature—that could chemically convert an A-T nucleotide pairing to a G-C one. It’s a small change with potentially huge implications. David Liu, the Harvard chemist whose lab did the work, estimates that about half of the 32,000 known pathogenic point mutations in humans could be fixed by that single swap." 

My comment: C>T-mutations are mostly caused by changing methylation patterns or by oxidative stress that triggers deamination at methylated cytosines. This same phenomenon is very observable in the wild: 


Excerpt: "In a plant study, for example, epigenetic modifications were found to be responsible for delaying flowering during the cold winter months, until spring, when temperatures are more favourable.

"At a CpG site, a methylated "C' is only one chemical reaction away from becoming a "T'—a different base entirely. So, while environmentally induced epigenetic modifications do not cause mutations per se, the chance of a permanent C-to-T mutation is much greater at CpG sites."

"Such 'single nucleotide polymorphisms," or SNPs for short, can change the function of a gene or even lead to genetic diseases. The so-called "breast cancer gene" BRCA1, for example, is linked to mutation at a CpG site." 

My comment: Within Icelanders, for example, there are over 20 million SNPs in their genome that has led to loss of 1,171 'genes'. 

Evolution never happened. It's all epigenetics OR loss of information.


Passive DNA helps us understand why evolution never happened

Passive DNA helps us understand why evolution never happened

The following facts should help us realize that the DNA is just a passive data base. I wrote about passive DNA for the first time in 2017 and slowly this understanding is taking place in modern science. 

1. There are ~250 different cell types in a human body. Every cell (except neurons and T-cells) is maintaining the exactly same DNA. A question arises: Why is your skin cell different to your liver cell? They both have the same DNA sections so how is the identity of the cell determined? Obviously not by the DNA 'genes'.

The answer: The identity of the cell is determined by epigenetic mechanisms and factors. This is called epigenetic programming of the cell. Epigenetic mechanisms control transcription (reading) of the DNA; Where the reading starts and where it ends, how actively the reading is processed and when and how often the reading is done.

Keywords: cellular differentiation epigenetic programming

2. There are only ~19,000 DNA sections used for protein production in human genome but the number of different proteins in a human body is up to several millions. By reading (transcribing) just one section of the DNA, then generating a temporary pre-mRNA molecule and modifying it, the cell is able to produce thousands of different proteins. This complex mechanism is called Alternative splicing and it's regulated by epigenetic mechanisms and factors.

Keywords: alternative splicing DNA methylation, alternative splicing histone epigenetic, alternative splicing microRNAs

3. A Stem cell has no identity, no task, no differentiation. It has no job because it lacks epigenetic programs. It has an entire DNA but without epigenetic information it doesn't know what to do.

Keywords: stem cell epigenetic programming

4. There are no single 'genes' in the genome. Sections of the DNA can be read (transcribed) from different locations of the genome, sections may overlap, be embedded and locate even in different chromosomes. Epigenetic factors and mechanisms guide the cell to find appropriate DNA sections for further processing.

Keywords: gene concepts

5. The cell is able to modify its DNA. The most significant modification occurs in DNA repair at several levels but there are other DNA modifying mechanisms such as AID mediated deamination.

Summary: Because the DNA is just passive data base and it has to be activated by epigenetic mechanisms in order to have a purpose, it's obvious that all adaptation within organisms occurs through epigenetic mechanisms and factors = epigenome. Changing epigenetic profiles never result in any kind of evolution, vice versa. Changing methylation patterns often result in subtle genetic errors. That's why genetic degradation is a biological fact. This can be observed: There are 628,685 gene-disease-associations in human genome worldwide but the number of beneficial mutations is close to zero.

Evolution never happened. Don't get lost my friends.


Ancient coins and Noah's ark

Several ancient coins tell us about Noah's ark

1. https://www.baslibrary.org/biblical-archaeology-review/7/5/2

"New evidence for the antiquity of the tradition associating Mt. Ararat in Turkey with the landing place of Noah’s Ark comes to us in the form of a unique coin on display at the Israel Museum. This large bronze medallion was struck 1700 years ago at Apameia Kibotos in Asia Minor (modern Turkey) near the mountains of Ararat where, it is said, Noah’s Ark came to rest after the flood.

This coin, depicting the events of the story of Noah’s Ark related in Genesis 6–8, is the only coin-type known to bear a Biblical scene.

Apameia Kibotos was a Phrygian city established by Antiochus I (280–261 B.C.) who named it after his mother, Apameia. At that time, there were at least two other cities in the region named Apameia, one in Bithynia (northern Turkey) and the other in Syria. The addition of the word kibotos, which means “ark” in Greek, differentiates this particular Apameia from the others."

2. https://blogs.warwick.ac.uk/numismatics/entry/noahs_ark_in/

"The above coin is one of a series of exceptional coins from ancient Apamea, Phrygia. On the obverse we have a Greek inscription naming the emperor as Philip I (AD 244-249), and a bust of the emperor looking to the right wearing a laurel crown, cloak and cuirass. Philip, commonly known as Philip the Arab, was an emperor of Syrian origin,and he is best remembered to history for his sympathetic view of Christianity, and potential conversion, as discussed by Christian writers such as Eusebius, Jerome and Orosius."

3. https://www.mintageworld.com/media/detail/74-Noah%E2%80%99s-Ark-Depicted-On-Ancient-Coin/
"Bronze coins of Apameia in Phrygia depict Noah’s Ark. This was probably due to a large, prosperous Jewish population that resided in the town. A mountain nearby had been identified as the one where the ark is supposed to have rested; hence, it is obvious that the story would be commemorated on local coins.
    The coin depicts the ark, which is prominently labelled ‘NOE’ (Noah in Greek), which is in the form of a box barely big enough to hold Noah and his wife, who are depicted on the coin. The couple is seen observing a dove to the left, returning with a green olive branch as a sign that the flood has abated. 

    Coins of this type were issued under Septimus Severus, Macrinus, Gordian III, Philip, and Trabonianus Gallus."

    4. https://creation.com/roman-coin-ark

    "As the coins weren’t minted until AD 192, some have considered that the primary influence responsible for their minting may have been a Christian one. One reason is that for Jews, “A strict interpretation of the numerous prohibitions against idolatry in Scripture precluded the depiction of ‘graven images’ and thus any human or animal form on coins.”
    Adding to this possibility of a Christian influence is the fact that the only other similar image known from antiquity, i.e. depicting only Noah and his wife in the Ark, was produced by Christians in Roman catacombs.

    The obverse of the coin (see images right) carries the image and name of the Emperor, which obviously changes depending on the time of minting, but the core features remain essentially the same. On the reverse side it depicts Noah and his wife inside the box-shaped Ark with waves lapping at the bottom of it. Noah’s name in Greek, ΝΩΕ(Nōe), can be clearly read in the middle of the Ark. On top of the Ark on the right is the raven, and on the top left is the dove with an olive branch in its mouth. On the left side of the coin Noah and his wife are again shown, standing outside the Ark on solid ground with their hands raised upwards to God in praise. This important feature shows that they recognized that God remembered them (Genesis 8:1), bringing them safely through the global Flood.

    Of particular interest is the shape used for Noah’s Ark on the coin, which is clearly that of a chest—exactly what the Greek word kibōtos (κιβωτός) means. There is no element of the typical hydrodynamic boat shape or any tailfin added to the design that is so often seen now. The box/chest shape is very distinct in all the earliest representations of Noah’s Ark.

    5. Noah's ark labelled on French Royal Jeton 1742.

    GERMANY 1649 GOLD DUCAT “NOAH’S ARK” GERMANY, REGENSBURG “FREE CITY” DISPLAYING NOAH’S ARK sailing upon the Stormy Waters with a Dove Flying left below the Rainbow with a branch in its mouth and the Coat of Arms below. Certainly one of “THE” most beautiful Gold Coins in the World!!! This reverse of this Lustrous Golden Ducat is inscribed in eight lines within the wreath “Commemorating the PEACE of WESTPHALIA” and the end of the 30 YEARS’ WAR. The ARK is symbolic of Europe amid the tempestuous currents of the War. Under the Peace and Serenity of GOD (represented by the dove and rainbow), Europe is delivered unto safety, the terribly destructive conflict of the Thirty Years’ War finally being ended.


    Confirmed Creationist Predictions

    Confirmed Creationist Predictions

    Creationists have predicted that evolution is not happening, never was and that there's no need for millions of years for current biodiversity to have arisen.

    1. The blind cavefish

      Creationists have claimed that random mutations and selection have nothing to do with loss of eyes within the cavefish. We were right. The eyes loss and recovery are due to epigenetic regulation, which occurs rapidly. Stories of millions of years are ridiculous pseudosciences.

    2. Fisher's theorem.

      Evolution believers have claimed that random mutations and selection result in evolution. Creationists, particularly those mentored by Dr John Sanford, have argued that genetic mutations typically cause rapid genetic degeneration, disease and extinction. Today every biologist knows the fact about heavy mutational load; Every newborn brings 100-200 genetic errors in the germline.

    3. The Junk-DNA theory.

      Evolutionists have argued for decades that about 98% of human DNA is evolutionary junk. Creationists have always believed that the vast majority of DNA is meaningful and important. Newest research has revealed that >90% of the human genome is transcribed to functional RNA molecules.

      "In addition, there has been an explosion of research addressing possible functional roles for the other 98% of the human genome that does not encode proteins. In fact, >90% of the human genome is likely to be transcribed yielding a complex network of overlapping transcripts that include tens of thousands of long RNAs with little or no protein forming capacity; they are collectively called non-coding RNA."

    4. Lenski's experiment. The bacterial experiment started by Richard Lenski in 1988 was intended to prove evolution. Today, after over 65,000 generations of bacteria, we know that no evolution has occurred. Indeed, much has happened in terms of genetic degradation and loss of function. Evolutionists' best bet was that E. Coli was able to utilize citrate under acidic conditions. Later, it has become clear that this adaptive change was also based on a reorganization of existing biological information.
      Here we show why it probably was not a speciation event… We conclude that the rarity of the LTEE mutant was an artifact of the experimental conditions and not a unique evolutionary event. No new genetic information (novel gene function) evolved.” (Journal of Bacteriology)
    5. Human Eye

      According to evolution believers, the human eye is poorly 'designed'. Evolutionary biologists thought that photons should pass through several layers before they reach the light-sensitive cells, called rods and cones. Nowadays, it is known that this is not the case; The so called Müller cells collect photons and direct the activity of rods and cones. Later, research has confirmed the optimal structure of the retina of the eye. Here too creationists were right.

    6. Vestigial organs

      After Darwin developed his theory, evolution believers have claimed that there are so called vestigial organs, some kind of evolutionary remnants in a human body. The list of vestigial organs in humans has shrunk from 180 in 1890 to 0 in 1999. Creationists were right. Again.

    Position of evolution believers has become very desperate. The total lack of scientific evidence for evolution points out that the theory of evolution is nothing more but a belief system, a religion. Observed change in organisms is due to epigenetic regulation of pre-existing (built-in) biological information OR corruption of information. Don't get lost, my friends.


    Overwhelming scientific evidence against the theory of evolution

    Overwhelming scientific evidence against the theory of evolution

    The leading Evolutionary biologists:

    "If much more than 3% of genome is functional, evolution becomes primarily a destructive process." (PZ Myers, 2015)

    "If any more than a small percentage of DNA has a meaningful sequence, such a mutation rate causes more than 1-2 harmful mutations per generation, and evolution becomes primarily a destructive process." (Larry Moran, 2014)

    "Mutational load considerations lead to the conclusion that the functional fraction within the human genome cannot exceed 25%, and is probably considerably lower." (Dan Graur, 2017)
    Modern science has revealed that there's no junk-DNA in the genome:


    "In addition, there has been an explosion of research addressing possible functional roles for the other 98% of the human genome that does not encode proteins. In fact, >90% of the human genome is likely to be transcribed yielding a complex network of overlapping transcripts that include tens of thousands of long RNAs with little or no protein forming capacity; they are collectively called non-coding RNA."

    These facts are in concordance with OBSERVED evidence:

    • There are 628,685 gene-disease associations in human genome worldwide but the number of beneficial mutations is close to zero.
    • In the wild, a strong deletional bias shapes organisms' genomes. This can be observed as growing amounts of heterochromatin, chromosome fusions and decreasing numbers of chromosomes.
    • There are two main reasons for speciation:
      • Epigenetic modifications. 
      • Corruption of genetic information that results re-organization of information. 

    So, as Dan Graur has said: "If ENCODE is right, evolution is wrong."

    ENCODE is more than right, there's no junk-DNA. Evolution is wrong.


    A Striking similarity between the Chicxulub (Yukatan) crater and the Santorini volcano crater

    Dinosaurs were not killed by an asteroid


    Excerpt: "The whole debate about the genesis of drilled melt and breccias in the Chicxulub crater is conducted with wrong assumptions. The Chicxulub "impact" crater is in fact the caldera of a supervolcano that is created by a huge gas explosion. The volcanic origin is by drilled pure andesite in the center of the structure no doubt proved. The bedrock was blasted in a great extent and widely distributed.

    Gravimetric investigations on Yucatan, suggest that the former magma chamber is not limited under the center of the Chicxulub crater. Possibly the dioritic magma chamber reach far to south. It is possible that the crater to south is open (no boreholes). That would be one explanation for the thick breccia units in Guatemala and South-Mexico.

    The ascending andesitic melt in the center of the explosion had only a low eruptive potential. There is no evidence of eruptive melt in the breccias outside the crater on the Yucatan peninsula (questionable Y-5A). The caldera after the gas explosion was immediately covered with falling-back debris. The detection of dykes or veins in the bedrock (Ya-1) indicates lateral intrusions from the yet not cooled andesitic melt body (mixed with breccia). In two wells (C-1, Y-1) were found "ash with glass" in depths between 1300 and 1400 m. This is mysterious and would be worth a new analysis.

    There are two different types of breccias from the ruined bedrock. There are breccias above the intact bedrock and breccia above the igneous andesite. The breccias above the bedrock has no contact with the melt and are unchanged. The breccias above the andesite (S-1, C-1, Y-1 wells) are melted or are in contact with melt, in decreasing intensity upwards. Possibly the lowest parts of falling-back debris are already fallen in the andesitic melt. A sorting the breccias (called units) make not sense because convective movements in the melt are expected. In the upper part of the breccia-package are smaller components of falling-back debris concentrated and have already stratification. Glass fragments in the melted breccias-package are geochemically different. These fragments belong as the breccia to the falling-back debris after the explosion. Presumably, these glasses come from a mixed melt of igneous andesite and bedrock on top of the eruptive vent. All the others in Central America found glassy spherules and glass fragments have probably not a connection with the Chicxulub event.

    The occurrence of shock-generated features is not only an indicator for an impact event, because this is also proved by finds in volcanic structures."

    Picture 1. Horseshoe Basin in the western Gulf of Mexico, as compared using (left) the historic NOAA bathymetry map and (right) BOEM’s new map. The basin contains a salt dome at its center and is flanked by salt sheets. Movement of the salt is evident from the network of faults and rifts expressed on the seafloor around the basin, as well as from the sediment debris flows seen falling down the slopes of the basin and onto its floor. Credit: BOEM

    Picture 2. Digital elevation model (DEM) reconstruction of Santorini comparing (a) the present-day topography and (b) the proposed topography prior to the Minoan eruption. The latter shows the reduced size of a Pre-Kameni island, a smaller and shallower caldera harbour restricted to the north, a possibly smaller caldera outlet (dotted blue line) in the north, and a continuous southern caldera rim connecting Thera and Therasia through Aspronisi.

    My comment: Gen. 7:11 "In the six hundredth year of Noah's life, in the second month, the seventeenth day of the month, the same day were all the fountains of the great deep broken up, and the windows of heaven were opened."


    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.