You can use diet to reprogram cells without having to make any genetic alterations

Fasting diet 'regenerates diabetic pancreas'


Excerpt: "The pancreas can be triggered to regenerate itself through a type of fasting diet, say US researchers. Restoring the function of the organ - which helps control blood sugar levels - reversed symptoms of diabetes in animal experiments.

The study, published in the journal Cell, says the diet reboots the body. Experts said the findings were "potentially very exciting" as they could become a new treatment for the disease.

People are advised not to try this without medical advice.

In the experiments, mice were put on a modified form of the "fasting-mimicking diet". It is like the human form of the diet when people spend five days on a low-calorie, low-protein, low-carbohydrate but high unsaturated-fat diet.

It resembles a vegan diet with nuts and soups, but with around 800 to 1,100 calories a day.
Then they have 25 days eating what they want - so overall it mimics periods of feast and famine. Previous research has suggested it can slow the pace of ageing."

My comment: So far, we've been taught that Diabetes I and II are caused by genetic mutations. For example:


Seems again that genes are not drivers. There's not a single mutation that can be reliably associated with a certain heritable disease or trait. Mutations are results of bad diet, oxidation, stress and harmful chemicals. There are stronger agents that are capable of affecting insulin production; short and long non-coding RNA-molecules and numerous epigenetic markers in the RNA regulate and control the protein production.

Life is not driven by genes. Genes are driven by lifestyle. The theory of Evolution has no mechanisms. These clever mechanisms point to Creation and Intelligent Design.


Early-stage embryos with abnormalities can still develop into healthy babies

Early-stage embryos with abnormalities can still develop into healthy babies


Excerpt: "Abnormal cells in the early embryo are not necessarily a sign that a baby will be born with a birth defect such as Down’s syndrome, suggests new research from the University of Cambridge, the Wellcome Trust Sanger Institute and the University of Leuven, Belgium. In a study published today (29 March) in the journal Nature Communications, scientists show that abnormal cells are eliminated and replaced by healthy cells, repairing – and in many cases completely fixing – the embryo.

Researchers at the Department of Physiology, Development and Neuroscience at Cambridge report a mouse model of aneuploidy, where some cells in the embryo contain an abnormal number of chromosomes. Normally, each cell in the human embryo should contain 23 pairs of chromosomes (22 pairs of chromosomes and one pair of sex chromosomes), but some can carry multiple copies of chromosomes, which can lead to developmental disorders. For example, children born with three copies of chromosome 21 will develop Down’s syndrome.

Pregnant mothers – particular older mothers, whose offspring are at greatest risk of developing such disorders – are offered tests to predict the likelihood of genetic abnormalities. Between the 11th and 14th weeks of pregnancy, mothers may be offered chorionic villus sampling (CVS), a test that involves removing and analysing cells from the placenta. A later test, known as amniocentesis, involves analysing cells shed by the foetus into the surrounding amniotic fluid – this test is more accurate, but is usually carried out during weeks 15-20 of the pregnancy, when the foetus is further developed.

Professor Magdalena Zernicka-Goetz, the study’s senior author, was inspired to carry out the research following her own experience when pregnant with her second child. At the time, a CVS test found that as many as a quarter of the cells in the placenta that joined her and her developing baby were abnormal: could the developing baby also have abnormal cells? When Professor Zernicka-Goetz spoke to geneticists about the potential implications, she found that very little was understood about the fate of embryos containing abnormal cells and about the fate of these abnormal cells within the developing embryos.

Fortunately for Professor Zernicka-Goetz, her son, Simon, was born healthy.

In research funded by the Wellcome Trust, Professor Zernicka-Goetz and colleagues developed a mouse model of aneuploidy by mixing 8-cell stage mouse embryos in which the cells were normal with embryos in which the cells were abnormal. Abnormal mouse embryos are relatively unusual, so the team used a molecule known as reversine to induce aneuploidy.

In embryos where the mix of normal and abnormal cells was half and half, the researchers observed that the abnormal cells within the embryo were killed off by ‘apoptosis’, or programmed cell death, even when placental cells retained abnormalities. This allowed the normal cells to take over, resulting in an embryo where all the cells were healthy. When the mix of cells was three abnormal cells to one normal cell, some of abnormal cells continued to survive, but the ratio of normal cells increased."

My comment: The control and regulation of embryonic cells doesn't occur from inside the embryo. Short non coding maternal and paternal RNA molecules direct the embryonic and fetal development. Genes are not drivers or controllers. Traits are shared during the embryonic development after epigenetic reprogramming that erases all epigenetic markers except the methylation of the innate immune system associated genes. The mechanism is awesome and points to Intelligent Design and Creation.


"A myriad of locally produced factors into the microenvironment of the reproductive tract is regulated, not one-way but rather, through embryonic–maternal cross-talk. In this mini-review, we focused on the exosomes, which are cell-derived vesicles of 30–100 nm in diameter, as a communicating language facilitating this dialog. These nanovesicles are secreted from pre-implantation embryos, oviduct epithelium, and endometrium as well as from the placenta, and contain proteins, messenger RNA (mRNA), microRNA, and DNA cargoes, and have pleiotropic effects on both embryonic and maternal environments. A better understanding of the molecular mechanisms mediating this cross-talk will lead to the development of new regulating agents, with novel diagnostic, biological, and therapeutic potential for either supporting or hindering the normal reproductive functions."


Evolution fast forward: Dog breeding

150 years of Dog breeding shows what evolution actually means. Dead end.

The following figure illustrates the huge differences between different breeds of dog skulls. Variation has occurred rapidly, mostly during the last 150 years as a result of so called artificial selection.

The skull morphogenesis, i.e. the determination of the shape of the skull, is based on epigenetic mechanism, mainly on certain histone methylation.

I have claimed that the variation is only caused by epigenetic factors and leads to sequence alterations that burden the genome and cause genetic degeneration and disease.

Now, can we have honest answers from the evolutionists? What condition might be the dog breed genome today?

You have just seen the evolution in Fast Forward. Dead end.


Missing Heritability is a serious problem for the theory of evolution

Message of the Missing Heritability Problem: Gene sequences don't determine traits


Excerpt: "The "missing heritability" problem can be defined as the fact that single genetic variations cannot account for much of the heritability of diseases, behaviors, and other phenotypes. This is a problem that has significant implications for medicine, since a person's susceptibility to disease may depend more on "the combined effect of all the genes in the background than on the disease genes in the foreground", or the role of genes may have been severely overestimated."

My comment: The Missing Heritability problem is a very inconvenient fact for evolutionists. There are several scientific facts pointing out that genetic variations don't correlate with diseases, behavior or any other heritable traits. For example, at least seven different lactase persistence gene alleles are known. Which one is the correct one?

There are about 200,000 disease-causing genetic mutations known in the human DNA but not a single mutation is reliably associated with certain disease. (http://www.hgmd.cf.ac.uk/ac/index.php)  About 1,000,000 SNPs (Single Nucleotide Polymorphism) in the human genome have been mapped but no one of them is linked to heritable traits. How is the Missing Heritablity problem solved?

Here's a brief summary of discoveries made by modern science that resolves the Missing Heritability problem:


- Variation of organisms is based on epigenetic control of gene expression.
- The most important factors influencing the epigenome are diet, climate, stress and toxins.
- microRNAs regulate gene expression, siRNAs transmit correct levels of methylation
- Aberrant methylation patterns trigger sequence changes.
- Sequence changes are genetic errors and they burden the genome. That's why they are hided by histone methylation, chromatin remodeling or chromosome loss.


- Embryonic cells undergo almost complete epigenetic reprogramming within vertebrates. Innate immune system is not erased.
- A cell that lacks the epigenetic layers and markers is a stem cell without a task.
- The epigenome is re-established by maternal and paternal miRNAs, piRNAs, siRNAs and other short non coding RNA molecules during embryonic development and pregnancy


- There are no mechanisms for large scale evolution. Loss of biological information is a scientific fact within all types of organisms.
- Rapid rates of variation and genomic degradation point to design and creation.


Mutations are often caused by poor nutrition in long term

Poor diet in long term is a reason for most mutations


Excerpt: "Eating a lot of fruit and vegetables is a natural way of increasing vitamin C blood levels, which in the long term may contribute to reducing the risk of cardiovascular disease and early death. You can get vitamin C supplements, but it is a good idea to get your vitamin C by eating a healthy diet, which will at the same time help you to develop a healthier lifestyle in the long term, for the general benefit of your health."

My comment: Vitamin C is very important for your epigenome and immune system. Lack of vitamin C disrupts your epigenome and makes your genome weaker causing genetic changes.

For years, scientists have studied only genetic changes associated with the cardiovascular disease. Modern scientists understand that actual reason for genetic alterations and the cardiovascular disease can be found in epigenetic factors.

Up to 10 portions of fruit and vegetables a day may prevent 7.8 million premature deaths, says the newest study:


Mutations are not random occurrences. Mutations are often results of poor nutrition. So, there is no such a thing as evolution driven by random mutations. Genes are driven by life(style). Take care of your epigenome. These clever mechanisms point to Creation and Design.


"It could be that all codons could be start codons."

Start codons in DNA may be more numerous than previously thought


Excerpt: "For decades, scientists working with genetic material have labored with a few basic rules in mind. To start, DNA is transcribed into messenger RNA (mRNA), and mRNA is translated into proteins, which are essential for almost all biological functions. The central principle regarding that translation has long held that only a small number of three-letter sequences in mRNA, known as start codons, could trigger the production of proteins. But researchers might need to revisit and possibly rewrite this rule, after recent measurements from a team including scientists from the National Institute of Standards and Technology (NIST).

The findings, to be published on February 21, 2017, in the journal Nucleic Acids Research by scientists in a research collaboration between NIST and Stanford University, demonstrate that there are at least 47 possible start codons, each of which can instruct a cell to begin protein synthesis. It was previously thought that only seven of the 64 possible triplet codons trigger protein synthesis.

"It could be that many potential start codons had remained undiscovered because no one could see them," said lead author Ariel Hecht, a team member at the Joint Initiative for Metrology in Biology, a research collaboration that includes NIST and Stanford.

"We thought we knew the rules, but it turns out there's a whole other level we need to learn about. The grammar of DNA might be even more sophisticated than we imagined."

My comment: Same start codons within different types of organisms has been used as an evidence for common descent. That's the end of the fairytale. This discovery points to Creation and Design.


Serious overestimation of species count

Serious overestimation of species count


Excerpt: "Computer programs that rely on genetic data alone split populations of organisms into five to 13 times as many species as actually exist, researchers report online January 30 in Proceedings of the National Academy of Sciences."

My comment: This is the result after false science and Darwinian heresy. Evolutionary biologists are lost with their definitions of species and with true reasons for adaptation and variation of organisms.

Let's figure it out what speciation actually means.

Organisms adapt into changing environment due to epigenetic regulatory mechanisms. Adaptation may lead to change in phenotype which is observed as variation. When the outcome has changed a lot, there have been significant epigenetic alterations in the organism's genome. These changes also influence the type of pheromones the organism produce. Pheromones control mating behaviour. Often the case is that an adapted and variated organism is able to reproduce with its ancestral type but due to pheromone control, it is not willing to. In zoos we can sometimes observe interesting phenomena, for example several types of hybrid animals. Modern scientists have also found out that odors of certain foods function as pheromones by controlling the mating behaviour.

From the perspective of Design, this goes by logic because due to pheromone controlled mating behaviour the biodiversity is maintained very rich.

After an organism has experienced a lot of epigenetic modifications that lead to adaptation and variation, it also experiences mechanism based sequence alterations. These mutations have no role in biodiversity except that they cause genomic deterioration. Faulty genes lead to chromatin remodeling and chromosome loss. These are often true barriers for reproduction especially when the number of chromosomes differ significantly.

This is observed by studying the so called evolutionary tree of any organism. Let's have an example. The Fox lineage:

Bat-eared fox 72 chromosomes
Gray Fox 66 chromosomes
Fennec Fox 64 chromosomes
Bengal Fox 60 chromosomes
Kit Fox 50 chromosomes
Tibetan sand fox 36 chromosomes
Red Fox 34 chromosomes

Just have a look at the evolutionary tree of the Foxes and note that chromosomes are typically lost in the nodes of branches in that tree:


Mutations cause loss of biological information. Large scale evolution has never been observed. Everything in beautiful nature points to Design and Creation. Don't get lost.


Plant miRNAs regulate gene expression

Ingested plant miRNAs regulate gene expression in animals


Excerpt: "The incidence of genetic material or epigenetic information transferred from one organism to another is an important biological question. A recent study demonstrated that plant small RNAs acquired orally through food intake directly influence gene expression in animals after migration through the plasma and delivery to specific organs.

Non-protein coding RNAs, and in particular small RNAs, were recently revealed as master chief regulators of gene expression in all organisms. Endogenous small RNAs come in different flavors, depending on their mode of biogenesis. Most microRNAs (miRNA) and short interferring RNAs (siRNA) derive from long double-stranded RNA (dsRNA) precursors that are processed into small RNA duplexes, 20 to 25-nt long, by RNaseIII enzymes called Dicer. One strand of small RNA duplexes is loaded onto an Argonaute protein that executes silencing by cleaving or repressing the translation of homologous mRNA. In certain species, RNA cleavage is followed by DNA methylation and/or histone modification, leading to heritable epigenetic modification.

Endogenous small RNAs play essential roles during development and stress responses, and control transposable elements and chromatin states. Small RNAs can also be produced in response to invasion by exogenous nucleic acids from viruses, bacteria, transgenes, etc. Under these circumstances, small RNAs act in defense mechanisms by directing the destruction of the invader. Importantly, exogenous small RNAs and some endogenous small RNAs are mobile within certain organisms. Moreover, exogenous small RNAs can be amplified during the defense mechanisms, allowing the spreading of RNA silencing from the cell where it is activated to the rest of the organism."

My comment: Diet is the most significant factor affecting the epigenetic control of gene expression within all animals. Random mutations have no role in variation and adaptation that organisms experience in nature. That study proves several claims and observation regarding diet induced epigenetic gene expression.

Diet strongly affects our heritable epitranscriptomes. By eating healthy food, we can influence the healthy condition of our genome too, because the epitranscriptome is directly linked to gene sequences. Harmful mutations occur due to poor nutrition, for example. These clever and complex mechanisms point to Intelligent Desing and Creation.

Here's a few examples of how diet microRNAs affect the gene expression. Note that these linked articles don't tell you anything about the mechanisms behind rapid adaptation, but they only try to maintain the heresy of Darwinian evolution. False science.

1. Italian wall lizards.

2. How does a lizard go vegetarian?

3. Butterflies' diet impact evolution of traits

4. Diet shift induced rapid evolution of size and function in a predatory bird.


Bird study reveals a key assumption in evolution theory is false

Bird study reveals a key assumption in evolution theory is false


Excerpt: "A new study of fifty bird species from the Andes now rules out any possibility of predicting evolution on a single genetic mutation.

The scientists wanted to study oxygen uptake in the blood at various altitudes, so these birds were the ideal test subjects.

“These birds live both at high altitudes and at sea level, so they’re a good case study. Our data show that haemoglobin in birds living at higher altitude can take up oxygen more effectively. And we wanted to study this difference at the genetic level,” says Fago.

The scientists took samples from 50 different species of birds that live at various altitudes in the Andes. They compared the blood analysis with the genes that are responsible for producing haemoglobin.

But what they discovered, was unexpected.

Birds living at high altitude, need to be specially adapted to cope with low levels of oxygen.

The scientists’ hypothesis was therefore that these birds would have a definite pattern of mutations that enabled them to do this.

“But we didn’t see any patterns in the birds’ genes. We thought there would be clear similarities among the high-altitude birds, but there’s clearly more than one recipe for this special haemoglobin [mutation],” says Fago.

Even though two individuals have the same mutation on one gene, it does not necessarily mean that they both have the same effect, says Zhang. So scientists will need to test the manifestation of these mutations in practice and not just rely on computer models.

This study warns us that we can’t draw direct links between genes and their function in individuals,” he says."

My comment: Hemoglobin production is based on several factors and it is regulated by epigenetic control of gene expression. The most significant factors in regulation of hemoglobin variants and their subunits are DNA methylation, histone methylation/acetylation and microRNA downregulation.

Keywords: hemoglobin gene expression splice variant


The most important observation was that genetic mutations didn't correlate with assumed hemoglobin variants. Random mutations didn't affect the phenotype as researchers had assumed. Then how those genetic mutations are explained?

Intensive adaptation changes epigenetic patterns and this leads to mechanism based sequence alterations. Methylated cytosines turn easily into thymine, guanines to adenine and hydroxymethylated cytosines into guanine. This kind of point mutations have no role for ecological adaptation except that they only burden the gene regulatory networks because faulty genes consume energy. RNA mediated cellular mechanisms try to hide and pack this kind of faulty genes from getting to transcription. This can be observed as chromatin remodeling and even chromosome loss. 

This same phenomenon can be observed in the human DNA: There are about one million SNPs, 200 000 disease-causing genetic mutations in the human genome. 10 000 new genetic errors are discovered every year.  Genetic entropy, rapid degradation of genomes within all organisms is an observable fact. 

Again, we have a clear example of how the gene centric evolutionary theory includes serious fallacies. Gene sequences alone don't determine traits. Genes are not drivers. There is no such a thing as a mutation driven evolution. Don't get lost.


Infertile Mom's Genetics, Via MicroRNAs, Get Passed On To Her Egg Donation Child

Infertile Mom's Genetics, Via MicroRNAs, Get Passed On To Her Egg Donation Child

Excerpt: "A new study from researchers at the Fundacion Instituto Valenciano de Infertilidad and Stanford University suggests infertile women who carry a child fertilized using a donor egg still impart an important genetic gift to their children. Molecules known as MicroRNAs that are secreted in the mother’s womb can change the genetic information of the child, the researchers say.

“The ‘Barker hypothesis’ suggests that ‘the womb may be more important than the home,’ emphasizing the concept that the maternal endometrium [or the mucus membrane of the womb] has a reprogramming effect on the embryo, fetus, and adult,” wrote the researchers, who believe their work supports this famous theory.

The heartbreak of infertility includes knowing you will never pass on your genes to your children. Nevertheless, many couples who cannot get pregnant spontaneously become parents through adoption or in vitro fertilization (using donor sperm or eggs). Rather than adopt, many infertile women choose to carry a baby fertilized with a donor egg, believing this will help them feel more connected to their future child.

Frequently these same mothers will say their donor-egg child shares some unexpected physical characteristic with them, said Dr. Felipe Vilella, a researcher the Spanish fertility clinic in a FIVI press release. Also it is believed many adult diseases originate from conditions occurring in the womb. There, endometrial fluid, which carries a variety of molecules from the mother (including microRNAs) serves as milk to a developing embryo.

Could the (pregnant) mother influence her developing baby's genetics, even though she used a donor egg?

Vilella along with Dr. Carlos Simón, FIVI’s scientific director, and their colleagues proposed microRNAs floating in a mother’s endometrial fluid might change the embryo. To investigate, the researchers examined 10 women at FIVI and measured the activity of genes within the fluid of her uterus. They found six of 27 specific, maternal miRNAs were expressed in the endometrial epithelium during the window of implantation and were released into the endometrial fluid.

Practically speaking, this means the mother’s DNA influences the way the baby develops. Her genetic material essentially helps to "decide" which of her baby's genes get turned on and off. Even more, it means the baby will acquire some DNA from the mother, even if the egg comes from another woman, as Dr. Nick Macklon, professor of obstetrics and gynecology at the University of Southampton, explained to Express.

No matter how she becomes pregnant, a woman performs an invaluable service by carrying the child. This new research suggests she also exerts a significant influence on her child's genetics, development, and lifelong health."

My comment: After the fertilization, almost all epigenetic markers are wiped out of embryonic cells. Genes linked to innate immune system are left to be methylated. Incredible design! Because epigenetic markers are wiped out, then also traits are wiped out of the embryonic cells. Paternal and maternal miRNAs, piRNAs and siRNAs are responsible for re-establishing the epitranscriptome and cellular differentiation of the embryonic cells. Gene sequences alone don't determine traits.

Life is not driven by genes. Genes are driven by life. This points to Intelligent Design and creation.


Epigenetic factors regulate key signalling pathways in early body plan formation

Dynamic DNA methylation and demethylation crucial to regulation of key signalling pathways in early body plan formation

Excerpt: "Mammalian genomes undergo epigenetic modifications, including cytosine methylation by DNA methyltransferases (DNMTs). Oxidation of 5-methylcytosine by the Ten-eleven translocation (TET) family of dioxygenases can lead to demethylation. Although cytosine methylation has key roles in several processes such as genomic imprinting and X-chromosome inactivation, the functional significance of cytosine methylation and demethylation in mouse embryogenesis remains to be fully determined. Here a collaboration of researchers from China and the US show that inactivation of all three Tet genes in mice leads to gastrulation phenotypes, including primitive streak patterning defects in association with impaired maturation of axial mesoderm and failed specification of paraxial mesoderm, mimicking phenotypes in embryos with gain-of-function Nodal signalling.

...Taken together, their results show that TET-mediated oxidation of 5-methylcytosine modulates Lefty-Nodal signalling by promoting demethylation in opposition to methylation by DNMT3A and DNMT3B. These findings reveal a fundamental epigenetic mechanism featuring dynamic DNA methylation and demethylation crucial to regulation of key signalling pathways in early body plan formation."

My comment: Morphogenesis and body plan have long been difficult problems for molecular biology. Darwinists have claimed that gene sequences determine these very fundamental traits of organisms. They are wrong. Morphogenesis and body plan are both regulated by epigenetic factors. This is done at early stages of embryonic development. And because epigenetic markers are wiped out of embryonic cells   right after the fertilization, it's obvious that maternal and paternal short and long RNA molecules (siRNAs, miRNAs, piRNAs, lncRNAs) are in response of doing this job. Embryonic development occurs in control of maternal and paternal mechanisms of reproduction.

Gene sequences are not drivers. There is no such a thing as a mutation driven evolution. Genes are not your destiny. The evolutionary theory is a major lie. Don't get misled.


Claims about convergent evolution are absurd

Claims about convergent evolution are absurd

Excerpt: "Get a load of this: Darwinians claim that complex features arose independently multiple times by an unknown process called “convergent evolution.”

Giving a name to something is not the same as explaining it. Darwinians have learned how to manipulate language to create vacuous terms that masquerade as explanations. For instance, if two organisms that share the same assumed ancestral line have similar traits, they are called “homologous” traits in Darwinese. But if the traits are similar and are not on the same ancestral line, they call them “analogous” traits. When evolution splits traits apart, they call it “divergence.” When evolution brings separate organisms together, they call it “convergence.” Evolutionists confabulate and confibulate to pretend they are doing science, when they’re actually just playing Jargonwocky. Let’s look at some examples that demonstrate how convergence—an essential ingredient in Darwin Flubber—operates according to the Stuff Happens Law.
It is a brilliant example of convergent evolution, where unrelated organisms independently evolve similar adaptations (for example, the wings of birds and bats). In this case, it is an animal that looks like a plant that imitates a carnivorous plant that feeds like an animal."
My comment: Let's have a closer look at these crazy claims about convergent evolution cases. Remember, the claim is that each case is independent from each other. They have no relationship or causality with each other. The craziest claims so far by darwinists:

1. C4 photosynthesis. According to 'science' it has evolved 60 times independently. Scientists have not succeeded in building an autonomous photosynthesis system. But evolution has done this for 60 times! Seems to be easy!

2. Eye 35 times. Think about the complex mechanism and signaling pathways that are connected with brain. And according to 'science' humans and squids evolved same eyes using same genes. What a coincidence!

3. Giving birth, 150 times. Piece of cake for evolution. Very convincing. 

4. Carnivorous plants. Nitrogen-deficient plants have in at least 7 distinct times become carnivorous. 

5. Hearing. 30 times. Bats and dolphins separately evolved same sonar gene. What a surprise! (Do they really think that one gene is sufficient for developing a sonar ability?)

6. Bioluminescence is quite a mystery for science. According to darwinists it has independently evolved even 27 times! 

7. Magnetite for orientation, magnetically charged particles of magnetite for directional sensing have been found in unrelated species of salmon, rainbow trout, some butterflies and birds.

8. Electric organ in some fishes. 6 times. Independently from each other. Sure.

9. Parthenogenesis. Some lizards, insects, fishes and rodents are able to reproduce asexually, without males. 

Seems that evolution is very intelligent. No, seriously. These absurd claims regarding convergent evolution are absolutely false science. Clever mechanisms observed in nature point to Design and Creation. Don't get misled.


Mutation status alone is not specific enough when predicting effectiveness of drugs against cancers

Mutation status alone is not specific enough when predicting effectiveness of drugs against cancers


Excerpt: "If a group of tumours could be successfully treated using a drug, the scientists looked for typical biomarkers for this tumour type. Up to now, doctors have decided for and against the use of a drug directed against the EGF receptor mainly based on gene mutations. However, the mutation status alone is not specific enough.

This means that rather than relying on the mutation status alone, we now have much more information on which to base decisions about treatment," explains Yaspo. The scientists now know the molecular profile of the tumours, which are more likely to be successfully treated with these drugs."

My comment: Only 5–10% of all cancer cases can be attributed to genetic defects. Successful cellular differentiation is based on epigenetic control of gene expression. Cancer means unsuccessful cellular differentiation. That's why the reasons for them can be found in elements regulating gene expression, such as non coding RNA molecules.

Genetic mutations are just results of epigenetic factors, not reasons for cancers. That's why they are not leading to any kind of evolution. Use your logic.

DNA methylation is directed by RNA

Cellular differentiation, adaptation and variation of organisms is directed by RNA, not DNA

Excerpt: "RNA-directed DNA methylation (RdDM) is a nuclear process in which small interfering RNAs (siRNAs) direct the cytosine methylation of DNA sequences that are complementary to the siRNAs. In plants, double stranded-RNAs (dsRNAs) generated by RNA-dependent RNA polymerase 2 (RDR2) serve as precursors for Dicer-like 3 dependent biogenesis of 24-nt siRNAs. Plant specific RNA polymerase IV (Pol IV) is presumed to generate the initial RNA transcripts that are substrates for RDR2. siRNAs are loaded onto an argonaute4-containing RISC (RNA-induced silencing complex) that targets the de novo DNA methyltransferase DRM2 to RdDM target loci."

My comment: There are only a few chemical modifications discovered on the DNA and histones; especially methylation and acetylation. But the list of different epigenetic markers on the RNA is remarkable; there are over one hundred of different chemical modifications discovered on the RNA. So far, most of these epigenetic tags are mysterious for science, but what is already found, is that genes don't regulate these tiny markers.

Instead, small interfering RNAs direct the cytosine methylation of DNA sequences and histones. The cell uses the cytosine and histone methylation for gene expression, it means at what level the genes are silenced or activated. This mechanism is the most significant factor in determining the outcome of an organism, the phenotype. SiRNAs are derived by the specific nucleotide cleavage of larger double-stranded RNAs, which means they are not copied from the DNA. Modern science is talking about target genes, not source genes.

The most significant share of biological information of an organism is utilized in RNA-mediated cellular mechanisms. Genes are just very rough libraries for these clever mechanisms. There is no such a thing as mutation driven evolution. These complex mechanisms point to Creation and Intelligent Design.


Only 5–10% of all cancer cases can be attributed to genetic defects

Cancer is a Preventable Disease that Requires Major Lifestyle Changes

Excerpt: "After sequencing his own genome, pioneer genomic researcher Craig Venter remarked at a leadership for the twenty-first century conference, “Human biology is actually far more complicated than we imagine. Everybody talks about the genes that they received from their mother and father, for this trait or the other. But in reality, those genes have very little impact on life outcomes. Our biology is way too complicated for that and deals with hundreds of thousands of independent factors.

Genes are absolutely not our fate. They can give us useful information about the increased risk of a disease, but in most cases they will not determine the actual cause of the disease, or the actual incidence of somebody getting it. Most biology will come from the complex interaction of all the proteins and cells working with environmental factors, not driven directly by the genetic code.

This statement is very important because looking to the human genome for solutions to most chronic illnesses, including the diagnosis, prevention, and treatment of cancer, is overemphasized in today’s world. Observational studies, however, have indicated that as we migrate from one country to another, our chances of being diagnosed with most chronic illnesses are determined not by the country we come from but by the country we migrate to. In addition, studies with identical twins have suggested that genes are not the source of most chronic illnesses. For instance, the concordance between identical twins for breast cancer was found to be only 20%. Instead of our genes, our lifestyle and environment account for 90–95% of our most chronic illnesses."

- Tobacco

- Alcohol
- Bad diet
- Obesity
- Infectious agents
- Environmental pollution
- Radiation

My comment: Epigenetic factors are associated with genetic changes. Modern scientists already understand how your epitranscriptome is regulated. We all can contribute to our own gene expression and healthy, stable epigenome. Doing so, we also contribute to our children and even their grandchildren because epigenetic alterations are inheritable through several generations.

Gene centric 'science' is false science. Genes are not drivers. Instead, they are followers and libraries for RNA mediated cellular processes. A sequence alteration is a consequence and a result, not a random reason for assumed evolution. There are about 200,000 disease-causing genetic mutations in the human DNA but not a single one is proven to be effective on human adaptation. There are only a few candidates, like lactase persistence and high altitude adaptation. However, these genetic markers don't increase the amount of biological information. And mechanisms involved in those complex adaptations are not regulated by one sequence change.

To have some perspective on how genes are used in most organisms, consider this:

There are only 19 000 protein coding genes in the human DNA. But there are even one million of different proteins in a human body. You can learn more about mechanism called alternative splicing from here:


This mechanism is incredibly complex and it's affected by several factors, like microRNA:s, histone, DNA and multifaceted RNA methylation.

We are not what our genes are. We are what our epigenome is. These clever mechanisms point to creation and Intelligent Design.


Genes are not our fate

DNA is no master controller, nor is it even at the centre of biology


Excerpt: "Test your understanding of the living world with this simple question. What kind of biomolecule is found in all living organisms? If your answer is “DNA”, you are incorrect. The mistake is very forgiveable though. The standard English-language biology education casts DNA (DeoxyriboNucleic Acid) as the master molecule of life, coordinating and controlling most, if not all, living functions. This master molecule concept is popular. It is plausible. It is taught in every university and high school. But it is wrong. DNA is no master controller, nor is it even at the centre of biology. Instead, science overwhelmingly shows that life is self-organised and thus the pieces are in place for biology to undergo the ultimate paradigm shift.

To take a ruthless look at that question is thus the purpose of this article. Does DNA have any claim to being in control? Or at the centre of biological organisation?

The answer is that DNA is none of the things Watson, Lander, and Collins claim, and that even the standard nuanced biologist’s view of life is wrong. This is provable in many ways but mainly by a new science of life that is emerging from almost complete obscurity. This new science explains the features of living beings in productive new ways that DNA-centric, genetic determinist, biology has not, and cannot.

...RNA also has four bases (A, C, G, and U). But cells make more than one hundred comparable chemical modifications to them. The roles of these modifications are essentially a mystery, but presumably they help RNA perform its many cellular tasks.

RNA is also misunderstood. In a typical human cell, less than 1% of it makes proteins. The remaining 99% has a huge variety of structural, regulatory, and enzymatic functions. Most biologists though might as well be slaves to the central dogma in thinking that RNA is just the intermediate between DNA and protein. Only recently has RNA begun emerging from the shadow of DNA as a far more interesting molecule.

“Human biology is actually far more complicated than we imagine. Everybody talks about the genes that they received from their mother and father, for this trait or the other. But in reality, those genes have very little impact on life outcomes. Our biology is way too complicated for that and deals with hundreds of thousands of independent factors. Genes are absolutely not our fate. They can give us useful information about the increased risk of a disease, but in most cases they will not determine the actual cause of the disease, or the actual incidence of somebody getting it. Most biology will come from the complex interaction of all the proteins and cells working with environmental factors, not driven directly by the genetic code”. (Anand et al., 2008)

My comment: Modern scientists understand that the DNA is not the master controller of life. Genes are just libraries for RNA-mediated cellular processes. Genetic alterations are results of cellular mechanisms impacted of RNA-molecules, proteins, epigenetic factors and several other contributors. DNA is not the centre of evolution. This is why we can observe only variation of organisms but not large scale evolution. All of this is in perfect harmony with Biblical creation and Intelligent Design.


Human mutations don't occur randomly

Epigenetic factors are linked to genetic changes

About 200,000 disease-causing genetic mutations have been discovered in the human DNA. Are these alterations random changes? Let's figure it out.

Excerpt: "Human mutations don't occur randomly. In fact, transitions (changes from A <-> G and C <-> T) are expected to occur twice as frequently as transversions (changes from A <-> C, A <-> T, G <-> C or G <-> T).

One of the most surprising features of many variant lists in humans is that C->T changes (C reference, T variant) are more frequent than T->C changes. Likewise, G->A changes are more frequent than A->G changes.

At first, this might seem a bit puzzling. For example, perhaps we might expect that the two counts should be extremely similar. However, the reference makes perfect biological sense -- and the explanation below is due to Tom Blackwell.

The major mechanism for new mutations (in warm-blooded animals) is deamination of 5'-methyl C to uracil (equivalently T) producing (C -> T) or, on the complementary strand, (G -> A). This was first studied for CpG dinucleotide sites, but it also occurs at lower rates throughout the genome at any C whether followed by G or not."

My comment: So, if an unmethylated cytosine deaminates, it turns to uracil and glycosylase, the repair enzyme, fixes this error. But if the same phenomenon occurs within methylated cytosine turning it into thymine, then glycosylase bypasses that alteration and also a G --> A transition occurs during next replication procedure. This is a mechanism.

It's clear that the level and patterns of methylation affect human genetic alterations. The most interesting phenomenon occurs at CpG dinucleotides and especially in CpG islands, genomic regions
 with a high frequency of CpG sites. Interesting is also, that human immune system genes typically have a clear CpG island. Seems that they were designed to experience alterations. Sounds logical.

Can we do something to keep our genes normally methylated and by this way, reduce the possibility to genetic changes? Yes, we can. Factors that mostly affect your epigenome are:

- Diet
- Stress
- Toxins
- Viruses and other pathogens

So, we can try to change our life habits by eating healthy food, avoiding stress, 
doing physical exercise and avoiding toxins (alcohol, smoking, chemicals etc.). It's our own choice.

Human genetic mutations don't occur randomly. Interesting is that this same mechanism is functional in almost every organism in nature. However, it will not lead to large scale evolution but it can be associated with some 
changes linked to the immune system . This mechanism is the most significant reason for genetic degradation. The evolutionary theory is a big lie. Don't get lost.


Sickle cell mutation is not beneficial

Scientists try to fix the mutation that causes sickle cell disease

Excerpt: "Scientists have taken an important step toward using CRISPR-Cas9 genome-editing to cure sickle cell disease, repairing the disease-causing mutation in blood-forming cells taken from patients. Some edited cells, injected into lab mice, both survived in the animals’ bone marrow and turned into red blood cells — a hint that CRISPR’d cells would would produce healthy hemoglobin in people. This is the first such experiment to get levels of healthy hemoglobin that might be high enough to cure patients.

Sickle cell is a painful and sometimes fatal disease that affects about 100,000 people in the US. Many scientists consider it an embarrassment that, although the mutation responsible for sickle cell was discovered in 1949, the revolution in molecular biology and genetics has hardly touched it.

That is finally changing. Researchers at Dana-Farber/Boston Children’s Hospital and elsewhere have reported enough progress in cell and animal experiments with virus-based gene editing to plan a human study of at least one genome-editing strategy in a few months. The new study, published on Wednesday in Science Translational Medicine, takes a different approach, increasing the chance that something will eventually be able to engineer blood cells so they produce healthy hemoglobin rather than the mutated, sickled kind.

CRISPR did as it was programmed to. In about one-quarter of cells, the guide RNA made a beeline for the mutation, Cas9 snipped out the mutation, and the cell used the repair template to insert a healthy version. In the other cells, the editing didn’t take, which is typical for CRISPR."

My comment: Why do scientists try to eliminate the sickle cell mutation? Because it's very harmful when inherited from both parents. Millions of people suffer from SCD worldwide and it causes heavy costs for the economy:


"SCD is a major public health concern. From 1989 through 1993, an average of 75,000 hospitalizations due to SCD occurred in the United States, costing approximately $475 million.

There is not such a thing as a beneficial random mutation. But scientists have discovered about 200,000 genetic mutations that cause diseases within humans. 10,000 new genetic disease causing mutations are discovered every year, but there are no signs of human evolution. The evolutionary theory is a major lie. Don't get lost.

200,000 disease causing genetic mutations known in the human DNA

About 10,000 new genetic mutations discovered annually in the human DNA

"Study shows 400,000 children with (new) developmental disorders born each year globally"

There's no doubt that human genome is rapidly degrading. The human gene mutation database proves this fact. Conclusions are obvious:

- Human genome is very young, only a few thousands of years.
- Rapidly increasing number of mutations form a logarithmic curve, which means that mutations make the genome weaker and new mutations arise even rapidly than before.
- Not a single beneficial mutation is observed. This means evolutionary theory is a major lie.
- Scientists urgently need efficient gene editing techniques. That's why they are focusing on CRISPR/Cas9 and other techniques.

Total entries
Gene symbol
The gene description, gene symbol (as recommended by the HUGO Nomenclature Committee) and chromosomal location is recorded for each gene. In cases where a gene symbol has not yet been made official, a provisional symbol has been adopted which is denoted by lower-case letters.
cDNA sequence
cDNA reference sequences are provided, numbered by codon.
Genomic coordinates
Genomic (chromosomal) coordinates have been calculated for missense/nonsense, splicing, regulatory, small deletions, small insertions and small indels.
HGVS nomenclature
Standard HGVS nomenclature has been obtained for missense/nonsense, splicing, regulatory, small deletions, small insertions and small indels.
Single base-pair substitutions in coding regions are presented in terms of a triplet change with an additional flanking base included if the mutated base lies in either the first or third position in the triplet.
Mutations with consequences for mRNA splicing are presented in brief with information specifying the relative position of the lesion with respect to a numbered intron donor or acceptor splice site. Positions given as positive integers refer to a 3' (downstream) location, negative integers refer to a 5' (upstream) location.
Substitutions causing regulatory abnormalities are logged in with thirty nucleotides flanking the site of the mutation on both sides. The location of the mutation relative to the transcriptional initiation site, initiaton codon, polyadenylation site or termination codon is given.
Small deletions
Micro-deletions (20 bp or less) are presented in terms of the deleted bases in lower case plus, in upper case, 10 bp DNA sequence flanking both sides of the lesion. The numbered codon is preceded in the given sequence by the caret character (^).
Small insertions
Micro-insertions (20 bp or less) are presented in terms of the inserted bases in lower case plus, in upper case, 10 bp DNA sequence flanking both sides of the lesion. The numbered codon is preceded in the given sequence by the caret character (^).
Small indels
Micro-indels (20 bp or less) are presented in terms of the deleted/inserted bases in lower case plus, in upper case, 10 bp DNA sequence flanking both sides of the lesion. The numbered codon is preceded in the given sequence by the caret character (^).
Gross deletions
Information regarding the nature and location of each lesion is logged in narrative form because of the extremely variable quality of the original data reported.
Gross insertions
Information regarding the nature and location of each lesion is logged in narrative form because of the extremely variable quality of the original data reported.
Complex rearrangements
Information regarding the nature and location of each lesion is logged in narrative form because of the extremely variable quality of the original data reported.
Repeat variations
Information regarding the nature and location of each lesion is logged in narrative form because of the extremely variable quality of the original data reported.