June 23, 2013

Dismissing Darwinist Lies - Answers to Anonymous in Kind...

Recently an anonymous commenter made a series of comments on my Dismissing Darwinist Lies series of posts. From his comments, he is a fairly new reader or else a recycled reader from the past who intends to take my time with his comments. I decided to answer him in kind, that is, statements with statements and thought to thought. I will let him (and you) research his point of view and mine and, if you are willing to not only go to propaganda sites like talk origins but also access sites like Creation.com and Access Research Network, you will hear from Darwinists, Creationists and Intelligent Design proponents. If you listen to all sides, you can then make an intelligent decision. But if you stick to the mainstream sources you will get one side only and will not be pursuing truth. Do not be afraid to get information from all sides and make up your own mind. This is what the Darwinists fear you will do and hope you will not do. But I DO want you to go to Darwinist and Creationist and ID sites and see what all sides assert. Then compare their stories and their view of the evidence and do the wonderful and amazing thing you have the power to do - make up your OWN MIND!!!

If he quotes me, it will be blued. His comments in black. Mine in this color.

As usual, quantity rather than quality, the usual refuge of the YEC.

One quick question: In what way is Genesis supposed to be an eyewitness account?

God created and was there. He gave the story of creation to Adam and Eve. The direct lineage of Adam to Noah is listed in the Bible. A very few remnants of human civilization found in coal tell us that man before the Flood was sophisticated and manufactured various things. It is silly to think that they could not write. In fact, while the earliest writing that is still found was by Semitic people (the lineage of Shem and also of course the Jews) it is hard to imagine that Noah and his family did not both read and write and that mankind was in possession of sophisticated knowledge but was stranded in a new world with no machines or factories or much of anything but drying muck and a mixture of rotting dead organisms left over from the Flood and new vegetation springing up all around. The probability of a written record that was passed down by the line of Noah through his descendants is rather large. If it was an oral history, it is remarkably coherent compared to the other global flood and creation stories from other cultures.

In any event, God ordered Moses to write down the family history of his lineage and the history of Creation from the beginning, as well as the order to record the activities of the lineage of Abraham down to the time of the life of Moses. At the time God called Moses to write down history from the past, he was also told to record the history of the Exodus events and the consequent history of the Children of Israel in the wilderness and eventually to the point of finally being ready to take back their Promised Land. Because God ordered Moses to write this down, even if the family history had been mistaken at any point, God Himself directed Moses to write Genesis and therefore it is the eyewitness account of the Creator Himself.

What I don't get - given the notion of an omnipotent and benevolent supernatural being - is why God would have chosen such a destructive mechanism as a global flood, causing tremendous pain and suffering and cruelty and death to so many innocent beings.

If his problem was with human beings, he could just as easily have had them all drop dead, except for the "starter kit" of Noah's offspring and their wives.

This commenter makes several statements along this line. Rather than deal with this over and over, let's be clear. He is dealing with the question of evil in the world. God is both absolutely just and yet merciful. He made a world that was good as He said Himself in Genesis, " And God saw that it was good."

Entire courses in philosophy classes deal with the problem of evil. This is not a question to be dealt with easily, so I will give an overview.

There was no evil in the world until Adam and Eve sinned. God had put man in charge of the entire world and man brought evil to the world, and therefore also suffering and death. Evil is not a positive thing, like a rock found on the ground, tangible and visible. It is the absence of Good. In every situation, every choice, every action there is the perfect thing to do and then there is everything else. If we do not do the right thing, we have missed the mark of perfection and thereby propagated evil.

Why did God allow man to sin? Well, do you wish to be a robot? Free will must include the ability to make choices. Every choice man had to make was allowed but for one - to eat from the tree of the knowledge of good and evil. Man was not perfect, but Eve was innocent (as was Adam) until she was convinced by Satan (a fallen angel who had also decided to disobey God) that God was withholding a great thing from her and she ate of the fruit. So God created innocent man and woman and they only had one choice to make that would be disobedient to God. One.

Adam knew better but he also ate. Perhaps he feared losing his wife? Did he fear being alone in the Garden if Eve was to die? We know what he did but we do not know every thought in his mind. What we know is that he had that same choice and he chose incorrectly.

The Fall of mankind involves both deception and rebellion. Mankind chose to rebel and the kingdom man had over Earth and his dominion over all creatures was ruined. Satan aka Lucifer, formerly an obedient angel aka spirit being was part of a rebellion against God among the angels and he determined to drag mankind down with him. Did Satan believe that God would allow him to go without punishment by subjecting man to the same potential punishment? One of Satan's hallmarks has been to overplay his hand. He actually pursued the death by crucifixion of Jesus Christ and thought this would be a victory for his side...only to find that Jesus overcame both sin and death and had taken dominion over all aspects of creation, including anything previously ceded by mankind. Jesus Christ is King of Kings and Lord of Lords. Satan is going to hell. Man does not have to join him.

Did God know what man would do? As God transcends time and space and has all wisdom and knowledge, He had to know and in fact did know. Had he started it all over it would have been the same thing. By giving mankind a choice, God made mankind free. But with a choice, mankind would eventually test the boundaries and once that happened, evil enters in and it all goes to pieces yet again. It would be nonsensical for God to keep making a Universe over and over again. Even knowing mankind would fall, God also made a plan for the salvation of all mankind through faith. The Bible asserts that Jesus Christ was the Lamb of God from the beginning. The Son of God breathed life into Adam and He would die on a cross in Jerusalem thousands of years later...but God knew this. Revelation 13:8- "And all that dwell upon the earth shall worship him, whose names are not written in the book of life of the Lamb slain from the foundation of the world."

Incidentally, the notion of the Noah's Ark myth is also falsified by the fossil record and current wildlife populations, in that these support organisms having evolved in place in different continents instead of having migrated from one central point about 4300 years ago.

Boilerplate propaganda. The fossil record makes no sense unless there was a global flood, and this is one point I have driven home in dozens of blog posts. There is really no evidence of any organism ever evolving at all at any time. All organisms reproduce after their kind. Pre-existing genetic information allows for speciation, so that we can have all sorts of different dogs or sturgeons. Observational science has studied this and Darwinists have worked so hard to get bacteria and fruit flies to evolve into ANYTHING else without success. Also scientists in labs have tried for many decades to come up with a scenario in which life would form from non-life or even to get the building blocks of life to be produced but these efforts have been epic failures.

"Speciation is not evolution."

What is your definition of evolution?

Evolution is the word used by those who claim a Big Bang created the Universe and they assert that the elements and stars and planets all evolved from this one event. This is in violation of the Laws of Thermodynamics. Evolution is the word that Darwinists use as they seek to disprove a scientific law we call Biogenesis. But if you wish to simply use the standard definition of evolution supposedly at work in organisms having ceded that life and all of the Universe is taken out of the equation? There is a full treatment of the subject here.

The general theory of evolution? Here is a simple description: That organisms survive by acquiring mutations that give them a reproductive advantage and that these mutations become part of the genetic code of the organism. As mutations provide new features for natural selection to act upon, less complex organisms become more complex and evolve into new kinds of organisms. There are huge holes in this idea. First, natural selection was first described by a creationist and it does exist. Natural selection is the description of the process by which the most fit versions of a kind of organism passes on genetic information to offspring, depending on the environment. But we observe that usually only pre-existing information is involved in the process of natural selection.

When a mutation occurs in an organism the DNA strand has miniature machines designed to repair and eliminate the mutation. Mutations break things rather than build them. On occasion an mutation will confer an advantage in a very specific situation but the overall fitness of the organism is harmed thereby. Blind cavefish do not seek to use eyesight to navigate their environment and injuries to the unseeing eyes are not consequential. But should they be released into a normal pond or stream they would be extinct quickly. There is not one recorded instance of a mutation actually conferring an overall fitness advantage to an organism. Furthermore the irreducibly complex systems of organisms cannot be built one change at a time, so gradual evolution (even if it could happen) could never build the neck of the giraffe or the DNA strand or the ATP Synthase motor or the bombardier beetle's fascinating defense mechanism. Furthermore, there is the weighty problem of information. There is no natural source for information and organisms are full of it.

"The Big Bang is the idea that nothing made everything."

A singularity is not "nothing", and the theory doesn't state that the singularity "made" anything - or that "nothing made everything".

But a singularity does not come from nothing, does it? If you are a naturalist, tell me who or what made the singularity? Hawking claims that gravity gets credit, but before there is a temporal existence there is no mass, no energy, no laws of nature...he is simply assuming that all existence appears magically with no source for it at all. Quantum Mechanics is not helpful here. No matter whether matter or anti-matter would exist, they need a source of origin. Claiming that a singularity can be created without a Creator is logically absurd.

"The equation for that is nonsense and the makeup of the Universe also cannot fit into that scenario."

Since you lack most of the knowledge of the people who came up with these equations, I've got a hunch that you don't have a very educated refutation of the equation to hand.

You do not know what I do or do not know. Ad hominem arguments already? As it happens, the equations for the Big Bang include about 96% of nothing, less than nothing! Big Bangers claim there is a tremendous amount of Dark Matter and Dark Energy because they need these fudge factors to make their equations, based on suppositions that cannot be defended, come out as actual equations. If I made a proposal to a client that included only 4% of what he needed, I would certainly not be taken seriously! Yet Darwinists give us a singularity that has no cause, Planck Time with no scientific support and an equation that is 96% nothing. That is merely the beginning of their problems. The Universe does not appear to be what the Big Bang would be expected to be produced. Everything about the Universe other than the speed of light and the vastness of the expanse of it seems to be very young. Since God tells us that He both stretched and is continuing to stretch out the Universe, the idea of the whole of existence being merely around 7,000 years old becomes more and more viable through observation and the advance of human knowledge.

As I understand it, the entire Big Bang theory is based on drawing conclusions about the origin of the universe as we see it based on what we can observe. So how exactly does it fail to do that? How do you reckon that "the makeup of the Universe cannot fit into that scenario"?

The Big Bang is nonsense from the start. It is simply *poof* with no proof. It is creation without a Creator. It is a humbug.

"Evolution must also account for the formation of life itself (which it cannot)."

The theory of evolution doesn't have to account for the origin of life any more than the theory of gravity has to account for the origin of planets. It is valid as it stands, based on confirmed falsifiable statements and observed evidence. If you want to claim that some god-like supernatural being created life at the beginning of it, go right ahead. It wouldn't change the theory of evolution one bit.

There is no observed evolution at all. It is not based on confirmed falsifiable statements at all. We never observe it happening and the tree of life and the idea of transitional forms is dead in the water. The more we learn about the fossil record, the more evidence FOR creation rather than evolution.

Creationists like to harp on the question of origins because they can't falsify the actual theory of evolution (not the silly cartoon versions that Young-Earth Creationists have constructed over time).

What is there left to falsify? Real science has shown that life is designed, not evolved.

"Then after life is here, the claim is that mutations build organisms into the various kinds of organisms we have today. But mutations are mistakes."

Mutations are mistakes, correct. No controversy there.

"Darwin had it backwards. Life is devolving,"

A claim for which no creationist has ever managed to present any scientific evidence whatsoever.

Oh, you need to study genetics for awhile. Mutations are a big problem for higher organisms. As the human genome collects mutations it becomes less robust. We now have more diseases and maladies and allergies than ever. Bacteria are so simple (compared to higher animals) that mutations are not a big problem. They reproduce in large quantities and the unfit bacteria just die and are not missed. But with higher animals with a far more complex set of genetic instructions, the mutations will manage to be passed on now and then, enough to eventually kill us off entirely.

Must post one article here to put an end to your line of unreasoning:

Mutations: evolution’s engine becomes evolution’s end!

by Alex Williams

In neo-Darwinian theory, mutations are uniquely biological events that provide the engine of natural variation for all the diversity of life. However, recent discoveries show that mutation is the purely physical result of the universal mechanical damage that interferes with all molecular machinery. Life’s error correction, avoidance and repair mechanisms themselves suffer the same damage and decay. The consequence is that all multicellular life on earth is undergoing inexorable genome decay. Mutation rates are so high that they are clearly evident within a single human lifetime, and all individuals suffer, so natural selection is powerless to weed them out. The effects are mostly so small that natural selection cannot ‘see’ them anyway, even if it could remove their carriers. Our reproductive cells are not immune, as previously thought, but are just as prone to damage as our body cells. Irrespective of whether creationists or evolutionists do the calculations, somewhere between a few thousand and a few million mutations are enough to drive a human lineage to extinction, and this is likely to occur over a time scale of only tens to hundreds of thousands of years. This is far short of the supposed evolutionary time scales.

Mutations destroy

Photo stock.xchng

Ever since Hugo de Vries discovered mutations in the 1890s they have been given a central role in evolutionary theory. De Vries was so enamoured with mutations that he developed an anti-Darwinian saltationist theory of evolution via mutation alone.¹ But as more became known, mutations of large effect were found to be universally lethal, so only mutations of small effect could be credibly considered as of value to evolution, and de Vries’ saltationist theory waned. When the Neo-Darwinian Synthesis emerged in the 1930s and 1940s, mutations were said to provide the natural variations that natural selection worked on to produce all new forms of life.

However, directly contradicting mutation’s central role in life’s diversity, we have seen growing experimental evidence that mutations destroy life. In medical circles, mutations are universally regarded as deleterious. They are a fundamental cause of ageing,^2,3cancer^4,5 and infectious diseases.⁶

Even among evolutionary apologists who search for examples of mutations that are beneficial, the best they can do is to cite damaging mutations that have beneficial side effects(e.g. sickle-cell trait,⁷ a 32-base-pair deletion in a human chromosome that confers HIV resistance to homozygotes and delays AIDS onset in heterozygotes,⁸ CCR5–delta32 mutation,⁹ animal melanism,¹⁰ and stickleback pelvic spine suppression¹¹). Such results are not at all surprising in the light of the discovery that DNA undergoes up to a million damage and repair events per cell per day.¹²

Mutation physics

Neo-Darwinian theory represents mutations as uniquely biological events that constitute the ‘engine’ of biological variation. However, now that we can see life working in molecular detail, it becomes obvious that mutations are not uniquely biological events—they are purely physical events.

All multi-cellular life on earth is undergoing inexorable genome decay because the deleterious mutation rates are so high … and natural selection is ineffective in removing the damage.

Life works via the constant (often lightning-fast) movement of molecular machinery in cells. Cells are totally filled with solids and liquids—there are no free spaces. The molecular machines and the cell architecture and internal structures are made up of long-chain organic polymers (e.g. proteins, DNA, RNA, carbohydrates, lipids) while the liquid is mostly water. All forms of movement are subject to the laws of motion, yet the consequences of this simple physical fact have been almost universally ignored in biology.

Newton’s first law of motion says that a physical body will remain at rest, or continue to move at a constant velocity, unless an external force acts upon it. Think of a message molecule that is sent from one part of a cell to another. Since the cell is full of other molecules, with no empty spaces, the message molecule will soon hit other molecules and either slow down or stop altogether. This is the universal problem known as friction.

Friction events can result from many causes, but can be crudely divided into two types: one is referred to as ploughing and the other is shearing. Ploughing involves the physical displacement of materials to facilitate the motion of an object, while shearing arises from the disruption of adhesive interactions between adjacent surfaces.¹³

Molecular machines in cells owe a great deal of their structure to hydrogen bonds, but these are rather weak and fairly easily broken. For example, most proteins are long, strongly-bonded chains of amino acids, but these long chains are coiled up into 3-dimensional machine components, and the 3-dimensional structures are held together by hydrogen bonds.¹⁴ When such structures suffer mechanical impacts, the transfer of momentum can distort or break the hydrogen bonds and critically damage the molecule’s function.

The inside of a cell has a density and viscosity somewhat similar to yogurt (figure 1). The stewed fruit (dark colour) added to the yogurt during manufacture can be seen swirling out into the white yogurt. The fruit has not continued to disperse throughout the yogurt. It was completely stopped by the initial friction. This is like what happens in a cell—any movement is quickly dampened by friction forces of all kinds coming from all directions.

Figure 1. A transparent carton of fruit yogurt illustrates how friction in the viscous fluid stopped the motion initiated by mixing the fruit (dark colour) with the yogurt (white colour).

How do cells cope with this friction? In at least five different ways. First, there are motor proteins available all over the cell that attach to mobile molecules and carry them along the filaments and tubules that make up the cytoskeleton of the cell. Second, these motor proteins are continually re-energized after friction collisions by energy inputs packaged in the form of ATP molecules. Third, there are ‘address labels’ attached to mobile molecules to ensure they are delivered to the correct destination (friction effects continually divert mobile molecules from their course). Fourth, thin films of water cover all the molecular components of cells and provide both a protective layer and a lubricant that reduces the frequency and severity of friction collisions. Fifth, there is a wide range of maintenance and repair mechanisms available to repair the damage that friction causes.

The friction problem—and the damage that results from it—is orders of magnitude greater in cells than it is in larger mechanical systems. Biomolecules are very spiky objects with extremely rough and highly adhesive surfaces. They cannot be manufactured and honed to the smoothness that we achieve in our vehicle engine components such as pistons and flywheel pivots, nor can ball-bearings be inserted to reduce the surface contact area, such as we do in wheel axles. As a biological example, consider the rotary motor that drives the bacterial flagellum. The major wear surfaces are on the rotor (attached to the flagellum) and the stator (the housing for the rotor, attached to the cell wall). The stator consists of 22 molecules, set in 11 pairs. The wear rate is so great that the average residence time for a stator molecule in the stator is only about 30 seconds.¹⁵ The cell’s maintenance system keeps a pool of about 200 stator molecules in reserve to cope with this huge turnover rate.

Finding suitable lubricants to overcome friction is a major focus in the nanotechnology industry. A special technique called ‘friction force microscopy’ has been developed to quantitatively evaluate potential lubricants.¹⁶

This shows that the laws of physics, operating among the viscous components of the cell, both predict and explain the high rate of molecular damage that we observe in DNA. Between 50% and 80% of the DNA in a cell is continually consulted for the information necessary for everyday metabolism. This consultation requires numerous steps that each involve physical deformation of the DNA—moving around within the nucleus, winding and unwinding of the chromatin structures, unzipping the double-helix, binding and unbinding of the transcription machinery, re-zipping the double-helix, rewinding the chromatin structures and shuffling around within the nucleus. Each step of motion is powered by ATP discharges and inevitably causes mechanical damage among the components. While most of this damage is repaired, the repair mechanisms are not 100% perfect because they suffer mechanical damage themselves.¹⁷

Mutations rapidly destroy

Within neo-Darwinian theory, natural selection is supposed to be the guardian of our genomes because it weeds out unwanted deleterious mutations and favours beneficial ones. Not so, according to genetics expert Professor John Sanford.¹⁸ Natural selection can only weed out mutations that have a significant negative effect upon fitness (number of offspring produced). But such ‘fitness’ is affected by a huge variety of factors, and the vast majority of mutations have too small an effect for natural selection to be able to detect and remove them.

Furthermore, if the average mutation rate per person per generation is around 1 or more, then everyone is a mutant and no amount of selection can stop degeneration of the whole population. As it turns out, the mutation rate in the human population is very much greater than 1. Sanford estimates at least 100, probably about 300, and possibly more.

All multicellular life suffers

Two recent reviews of the mutation literature not only confirm Sanford’s claims, but extend them to all multi-cellular life.

In a review of the distribution of fitness effects (DFE) of mutations,¹⁹ the authors are unable to give any examples of beneficial mutations for humans. In their calculations regarding the rate of deleterious mutations (MD) and neutral mutations (MN), they use the equalities MD = 1 –MN and MN = 1 – MD which both imply that the rate of beneficial mutations is zero. They do give a few non-zero values for beneficial mutation rates in some experimental organisms, but qualify these results by noting the interference of other variables.

In a review of mutation rate variations in eukaryotes,²⁰ the authors admit that all multicellular organisms are undergoing inexorable genome decay from mutations because natural selection cannot remove the damage.²¹ Their Box 2 and Table 1 list deleterious mutation rates for a wide range of multicellular organisms, noting they are all underestimates, with the possible exception of those for the fruit fly Drosophila melanogaster with a value of 1.2. The value given for humans is ‘~3’.

Thus, all multicellular life on earth is undergoing inexorable genome decay because the deleterious mutation rates are so high, the effects of the most individual mutations are so small, there are no compensatory beneficial mutations, and natural selection is ineffective in removing the damage.

The wheels have come off the neo-Darwinian juggernaut!

How long to extinction?

How long could multicellular life survive in the face of universal genetic degradation? This is a very important question, and I will attempt to answer it by using several different lines of evidence.

Human ageing and cancer

We have recently discovered that there is a common biology in cancer and ageing—both are the result of accumulating molecular damage in cells.²² This confirms the arguments outlined above, that for purely physical reasons molecular machinery suffers extremely high damage rates, clearly evident within the lifespan of a single human. Every cell has a built-in time clock to limit this damage and minimize the chance of it becoming cancerous. At every cell division, each telomere (the caps on both ends of a chromosome that stop the double-helix from unravelling) is shortened by a small amount, until they reach the Hayflick Limit—discovered in 1965 to be a little over 50 cell divisions. The cells then stop dividing and they are dismantled and their parts are recycled.

By adding the enzyme telomerase, the telomere shortening problem can be circumvented, but that then exposes the cell to a greater risk of becoming cancerous because of accumulating damage elsewhere in the cell. The overall balance between protection from damage and the need for longevity determines fitness (reproductive success) and life span.²³ The body’s normal reaction to increasing genome damage is to kill off the damaged cells via programmed senescence (of which the telomere clock with its Hayflick limit is but one part). But cells become malignant (cancerous) when mutation disables the senescence mechanism itself, which then enables the damaged cells to proliferate without limit.²² The Hayflick limit of around 50 cell divisions for humans seems to provide the optimum balance.

Fifty human generations of 20 years each gives us only 1,000 years as a timescale over which a human lineage would begin to experience a significant mutation load in its genome. This is alarmingly rapid compared with the supposed evolutionary time scale of millions and billions of years.

Reproductive cells

Figure 2. Schematic representation of human life expectancy (—), male fertility (∙∙∙), and risk of fetal abnormality with mother’s age (---). Despite the protective Hayflick limit on cell divisions and life expectancy, very significant molecular damage accumulates in humans even during the most productive years of life. Mutations do even more damage than the Hayflick limit and associated cancer rates suggest.

Ever since August Weismann published The Germ-Plasm: A Theory of Heredity²⁴ in 1893, a discrete separation has been shown to exist between body cells (the soma) and germ-line cells (germplasm). Germ-line cells were thought to be more protected from mutation than other body cells. However, another recently discovered cause of ageing is that our stem cells grow old as a result of heritable DNA damage and degeneration of their supporting niches(the special ‘nest’ areas in most organs and tissues of the body where stem cells grow and are nurtured and protected). The telomere shortening mechanism—intended to reduce cancer incidence—appears to also induce the unwanted side-effect of a decline in the replicative capacity of certain stem-cell types with advancing age. This decreased regenerative capacity has led to a ‘stem-cell hypothesis’ for human age-associated degenerative conditions.²⁵

Human fertility problems suggest that the decline in niche protection of stem cells also applies to our gametes (eggs and sperm). For males, fertility—as measured by sperm count, sperm vigor and chance of conception—begins to decline significantly by age 40 and the rate of certain paternal-associated birth defects increases rapidly during the 30s (figure 2).²⁶ For females, the chance of birth defects increases rapidly from around the mid-30s, particularly because of chromosome abnormalities (figure 2). In the middle of the most productive part of our lives, our bodies are therefore showing clear evidence of decline through accumulation of molecular damage in our genomes.

Do germ-line cells really suffer less damage?

When DNA was discovered to be the carrier of inheritance, Weissman’s germ-plasm theory gave rise to the ‘immortal strand hypothesis.’ When the DNA of an embryonic stem cell replicates itself, it was thought that the ‘old’ strand would remain with the self-renewing ‘mother’ stem cell, while the newly constructed daughter strand proceeds down the path of differentiation into a body cell. In this way, the ‘old’ strand would remain error free—because it has not suffered any copying errors—and thus becomes effectively immortal.

However, a research team at the Howard Hughes Memorial Institute recently tested this theory using the stem cells that produce blood, and found that they segregate their chromosomes randomly.²⁷ That is, the ‘immortal strand hypothesis’ is wrong. If stem cells are not given this kind of preferential treatment then it is reasonable to conclude that germ-line cells are also subject to the same molecular damage as somatic cells. This is confirmed by the observation that human fertility exhibits damage long before age-related diseases take over.

A single human lifetime is enough to show very significant mutation damage, even in our reproductive cells.

Haldane’s dilemma

The severe contradictions that these findings pose for neo-Darwinian theory corroborate what has become known as Haldane’s dilemma. J.B.S. Haldane was one of the architects of neo-Darwinism who pioneered its application to population biology. He realized that it would take a long time for natural selection to fix an advantageous mutation in a population—fixation is when every member has two copies of an allele, having inherited it from both mother and father. He estimated that for vertebrates, about 300 generations would be required, on average, where the selective advantage is 10%. In humans, with a 20-year generation time and about 6 million years since our last common ancestor with the chimpanzee, only about 1,000 such advantageous mutations could have been fixed. Haldane believed that substitution of about 1,000 alleles would be enough to create a new species, but it is not nearly enough to explain the observed differences between us and our closest supposed relatives.

The measured difference between the human and chimpanzee genomes amounts to about 125 million nucleotides, which are thought to have arisen from about 40 million mutation events.²⁸ If only 1000 of these mutations could have been naturally selected to produce the new (human) species, it means the other 39,999,000 mutations were deleterious, which is completely consistent with the reviews showing that the vast majority of mutations are deleterious. Consequently, we must have degenerated from the apes, which is an absurd conclusion.

According to Kirschner and Gerhart’s facilitated variation theory,²⁹ life consists of two main components—conserved core processes (the structure and machinery in cells) and modular regulatory processes (the signalling circuits and switches that operate the machinery and provide a built-in source of natural variation). The 40 million ‘mutation’ differences between humans and chimps are therefore much more reasonably explained as 40 million modular differences between the design of chimps and the design of humans.

Quantitative estimates of time to extinction

There are a number of different ways to estimate the time it would take for relentlessly accumulating mutations to send our species to extinction.

Binomial estimates

Some very rough estimates can be derived from the Binomial distribution, which can predict the likelihood of multiple mutations accumulating in an essential genetic functional module. A binomial model of a mutating genome could consist of the cell’s DNA being divided into N functional modules, of which N_e are essential; that is, the lineage fails to reproduce if any of the essential modules are disabled. For any given mutational event, p = 1/N is the probability of being ‘hit’, q is the probability of being ‘missed’, and p q = 1.

What is the likely value of N? We can derive two estimates from the knowledge that there are about 25,000 genes, plus the discovery from the pilot study report of the ENCODE project that virtually the whole human genome is functional.³⁰

For the first estimate, the average protein contains a few hundred amino acids and each amino acid requires three nucleotides of code, so the average gene would take up about 1,000 nucleotides of exon space (an exon is the protein-coding part of a gene). There are about 3 billion nucleotides in the whole human genome, so if we assume that the average protein represents an average functional unit then N = 3 million.

The second estimate comes from the ENCODE report that gene regions produce on average 5 RNA transcripts per nucleotide, and the untranslated regions produce on average 7 RNA transcripts per nucleotide. There are about 33 times as many nucleotides in the untranslated regions as in the genic regions. Assuming that transcript size is approximately equal in each region, then there are 25,000 x 5 = 125,000 gene transcripts and 25,000 x 33 x 7 = 5,775,000 untranslated transcripts, making N= 5,900,000 in total. Our two estimates of N are therefore 3 to 6 million in round figures.

What is the likely value of Ne? Experiments with mice indicate that 85% of genes can be knocked out one at a time without lethal effects.³¹This is due to the robustness and failure-tolerance through fallback processes built into the genomic designs. That means any one of those remaining 15% genes will be fatal if disabled. Multiple mutations occur however, so the likely value of Ne when exposed to multiple mutations will be much higher than 15%. The maximum possible value is 100%. In a study of 2,823 human metabolic pathways, 96% produced disease conditions when disrupted by mutation,³² so if we take an average between this value and the minimum 15% then we get about 60% of functional units being essential.

How many random mutations are required on average to disable an essential functional module? In rare cases, a single mutation is enough to disable a person’s ability to reproduce. A two-hit model is common in cancer. In a study of cell signalling networks, these two hits usually knocked out: (i) the programmed death system for dealing with damaged (cancerous) cells, and (ii) the normal controls on cell proliferation—so the damaged cancer cells can proliferate without limit. The proportion of cancer-associated genes was also found to increase with the number of linkages between genes. When a healthy gene is linked to more than 6 mutated genes, ~80% of all genes in the network are cancerous. Extrapolating from this, we find that by the time a normal gene is linked to about 10 mutated genes, then the whole network has become cancerous.³³

Almost 70% of known human genes can be causal agents of cancer when mutated.³⁴ Cancers can result from as little as a single mutation in a stem cell, or multiple mutations in somatic cells.³⁵ The minimum possible value of 1 is known to be rare, so the more common occurrence of the 2-hit model makes it a reasonable best-estimate minimum. But it may require 10 modules to receive two hits each for the whole network to become dysfunctional.

The maximum number of hits required to disable a single module may be 100 or more, but if the average functional module only contains 1,000 nucleotides then this figure, at 10% of the whole, seems rather large. An order-of-magnitude average is perhaps more likely to be 10 random mutations per functional module.

To provide some context for these estimates, recent work shows that the cell-cycle checkpoint damage repair system is activated when 10 to 20 double-strand breaks accumulate in a cell undergoing division.³⁶ That is, life will tolerate only 10 to 20 DNA breaks per cell before it starts repair work, whereas we are examining scenarios in which there are thousands and millions of damage events per cell. Our numbers are clearly up in a region where the cell’s repair mechanisms are working at their hardest.

What then is the likelihood of accumulating either 2 hits in 10 modules, or 10 hits in one module, in any one of either 15% or 60% of the 3 to 6 million functional modules? The binomial distribution in Microsoft Excel was used to make the following calculations, making the further assumption that the likelihood of the unit being a critical one must exceed 50% for extinction to be more likely than not in the next generation.

Assuming 60% essentiality, only one functional module needs to be disabled for the probability of its essential status to exceed 50%. For the 2-hit model, about 6,000 to 12,000 mutations are required to disable ten of the 3 to 6 million functional modules. For the 10-hit model, 3 to 6 million mutations are required to disable one functional module.

Assuming 15% essentiality, four modules need to be disabled before the probability of at least one of them being essential exceeds 50%. For the 2-hit model, 250,000 to 500,000 mutations are required to disable ten modules with four mutations each among the 3 to 6 million functional modules. For the 10-hit model, 3.7 to 7.5 million mutations are required to disable four functional modules.

If every individual produces 100 new mutations every generation (assuming a generation time of 20 years) and these mutations are spread among 3 to 6 million functional modules across the whole genome, then the average time to extinction is:

1,200 to 2,400 years for the 2-hits in 10 modules model and 60% essentiality
50,000 to 100,000 years for the 2-hits in 10 modules model and 15% essentiality
600,000 to 1,200,000 years for the 10-hit model and 60% essentiality
740,000 to 1,500,000 years for the 10-hit model and 15% essentiality.

Truncation selection

Evolutionary geneticist Dr James Crow argued that humans are probably protected by ‘truncation selection’.²⁶ Truncation occurs when natural selection preferentially deletes individuals with the highest mutation loads. Plant geneticist John Sanford put Crow’s claims to the test by developing a computer simulation of truncation. His assumptions were: 100 individuals in the population, 100 mutations per person per generation, 4 offspring per female, 25% non-genetic random deaths per generation, and 50% selection against the most mutant offspring per generation. He assumed an average fitness loss per mutation of 1 in 10,000. His species became extinct in only 300 generations. With a generation time of 20 years this corresponds to 6,000 years.³⁷

Sanford’s assumptions are somewhat unrealistic, but there are other ways to approach the problem. Mutations are pure chance events that follow a Poisson distribution, and this behaves like the normal curve when the average expected value is greater than about 30.³⁸ In a Poisson distribution, the variance is equal to the average expected value, and the standard deviation is the square root of the variance. When the expected average value is 100, the standard deviation will be 10. The normal curve now tells us the following:

Half the people will suffer about 100 mutations or more, and half the people will suffer about 100 mutations or less.
About 84% of people will suffer 110 mutations or less, and so the remaining 16% of people will suffer 110 or more mutations. Alternatively, about 16% of people will suffer 90 or less.
About 97.7% of the population will experience 120 mutations or less, and the remaining 2.3% will suffer 120 mutations or more. Alternatively, 2.3% will suffer 80 or less.
About 99.9% of the population will suffer 130 mutations or less, and the remaining 0.1% will suffer 130 or more mutations. Alternatively, 0.1% will suffer 70 or less.

If we remove the most mutant—those above 130 mutations per person per generation—then we will only remove 0.1% of the population and it will make virtually no difference. If we removed the most mutant 50% of the population that would not solve the problem either, for two reasons. First, the great majority of the remaining people still suffer between 70 and 100 mutations per person per generation, far above the value of 1 that ensures inexorable decline. Second, removing half the population each generation would send it extinct in a few dozen generations.

Estimated number of generations and years to extinction for populations of various sizes, when fitness declines by 1.5% in each generation.

Table 1. Estimated number of generations and years to extinction for populations of various sizes, when fitness declines by 1.5% in each generation.

Synergistic epistasis and population size

None of the above models include the effect of synergistic epistasis (if one gene is mutated, its impact is ameliorated by the coordinated activity of other genes) or of population size. We can include these by using Crow’s estimate that the fitness of the human race is currently degenerating at a rate of about 1 to 2% per generation. If we use an average value of 1.5% then only 98.5% of the next generation will produce reproductively viable offspring. The next generation after that will only have 98.5% of those survivors able to produce reproductively viable offspring, and so on.

For any given stable population size N, the size of the next generation that can produce reproductively viable offspring will be 98.5% of N ,and for any given number of generations G, the number of survivors able to produce reproductively viable offspring will be (98.5%)^G of N.

Table 1 shows the approximate numbers of generations after which the population degenerates to extinction (only one individual is left, so breeding cannot continue). No population can sustain a continual loss of viability of 1.5%.

Like rust eating away the steel in a bridge, mutations are eating away our genomes and there is nothing we can do to stop them.

The above model assumes that right from the beginning there will be 1.5% loss of fitness each generation. However, the binomial simulations earlier showed that individuals can tolerate somewhere between a few thousand to a few million mutations before the damage critically interferes with their ability to reproduce. This means that synergistic epistasis is a real phenomenon—life is robust in the face of mutational assault. Instead of the immediate loss of 1.5% every generation, the general population would remain apparently healthy for a much longer time before the damage became apparent.

However, the rate at which mutations accumulate will remain the same because the cause remains the same—mechanical damage. This means that most people will be apparently healthy, but then approach the threshold of dysfunction over a much shorter period, creating a population crash rather than a slow decline.

Either way, however, the time scales will be approximately the same because the rate of damage accumulation remains approximately the same.

Summary

Mutations are not uniquely biological events that provide an engine of natural variation for natural selection to work upon and produce all the variety of life. Mutation is the purely physical result of the all-pervading mechanical damage that accompanies all molecular machinery. As a consequence, all multicellular life on earth is undergoing inexorable genome decay because the deleterious mutation rates are so high, the effects of the individual mutations are so small, there are no compensatory beneficial mutations and natural selection is ineffective in removing the damage.

So much damage occurs that it is clearly evident within a single human lifetime. Our reproductive cells are not immune, as previously thought, but are just as prone to mechanical damage as our body cells. Somewhere between a few thousand and a few million mutations are enough to drive a human lineage to extinction, and this is likely to occur over a time scale of only tens to hundreds of thousands of years. This is far short of the supposed evolutionary time scales. Like rust eating away the steel in a bridge, mutations are eating away our genomes and there is nothing we can do to stop them.

Evolution’s engine, when properly understood, becomes evolution’s end.

Related Media

A 'mountain of evidence' for evolution? -- Creation Magazine LIVE! (2-18)

References

De Vries, H., The Mutation Theory, German edition 1900–03, English edition 1910–11; De Vries, H., Species and Varieties: Their Origin by Mutation, 1905, , 11 August 2007. Return to text.
Niedernhofer, L.J. et al., A new progeroid syndrome reveals that genotoxic stress suppresses the somatotroph axis, Nature 444:1038–1043, 2006. Return to text.
Kudlow, B.A., Kennedy, B.K. and Monnat, R.J. Jr, Werner and Hutchinson–Gilford progeria syndromes: mechanistic basis of human progeroid diseases, Nature Reviews Molecular Cell Biology 8:394–404, 2007. Return to text.
Eccleston, A. and Dhand, R., Signaling in cancer, Nature 441(7092):423, 2006. Return to text.
He, X.C. et al., PTEN-deficient intestinal stem cells initiate intestinal polyposis, Nature Genetics 39:189–198, 2007. Return to text.
Casanova, J-L. and Abel, L., Human genetics of infectious diseases: a unified theory, The EMBO Journal 26:915–922, 2007. Return to text.
Carroll, S.B., The Making of the Fittest: DNA and the ultimate forensic record of evolution, Norton, New York, pp. 174–179, 2006. Return to text.
Guilherme, A. and Pacheco, F., CCR5 receptor gene and HIV infection, , 11 August 2007. Return to text.
Lamb, A., CCR5–delta32: a very beneficial mutation, Journal of Creation 20(1):15, 2006. Return to text.
Carroll, S.B., Endless Forms Most Beautiful: The new science of evo devo, Norton, New York, Ch. 9, 2005. Return to text.
Carroll, S.B., The Making of the Fittest: DNA and the ultimate forensic record of evolution, Norton, New York, Ch. 8, 2006. Return to text.
, January 29, 2008. Return to text.
Leggett, G.J., Brewer, N.J and Chong, K.S.L., Friction force microscopy: towards quantitative analysis of molecular organisation with nanometre spatial resolution, Phys. Chem. Chem. Phys. 7:1107–1120, 2005. Return to text.
Most organic macromolecules contain numerous hydrogen atoms bonded to carbon atoms. Because hydrogen has only one (negative) electron and one (positive) proton, the ‘cloud’ of electron trajectories tends to be easily skewed towards the stronger electromagnetic fields in the core of the carbon chain, thus giving the hydrogen atom a small net positive force, which is then available to form a ‘hydrogen bond’ with electron-rich (negative) sites on other nearby molecules, or on adjacent folds in its own chain. Return to text.
Leake, M.C. et. al., Stoichiometry and turnover in single functioning membrane protein complexes, Nature 443:355–358, 2006. Return to text.
Leggett, G.J., Brewer, N.J. and Chong, K.S.L., Friction force microscopy: towards quantitative analysis of molecular organisation with nanometre spatial resolution, Phys. Chem. Chem. Phys. 7:1107–1120, 2005. Return to text.
Copy fidelity varies with the different DNA copying systems that are present in all eukaryote cells, with the different kinds of errors that can occur, and with the different stages at which errors can occur. A couple of errors in ten million is fairly typical, but mutant cells may produce a hundred to ten thousand times this value. E.g. Pursell, Z.F., Isoz, I., Landström, E-.L., Johansson, E. and Kunkel, T.A. Regulation of B family DNA polymerase fidelity by a conserved active site residue: characterization of M644W, M644L and M644F mutants of yeast DNA polymerase ε, Nucleic Acids Research 35(9):3076–3086, 2007. Return to text.
Sanford, J.C., Genetic Entropy & The Mystery of the Genome, Elim Publishing, New York, 2005. Return to text.
Humans have lived on earth for about 6,000 years and about 250 generations. For a population size of 1 million people, an average rate of one mutation per 20 people per generation is sufficient to ensure that everyone today is a mutant. I.e. (0.054)²⁵⁰ x 1 million people < 1. If the supposed 300,000 generations since the split with apes is assumed, then a rate of only 1 mutation in 21,000 people per generation is enough to ensure that everyone today is a mutant.Return to text.
Eyre.-Walker, A. and Keightley, P.D., The distribution of fitness effects of new mutations, Nature Reviews Genetics 8:610–618, 2007. Return to text.
Baer, C.F., Miyamoto, M.M. and Denver, D.R., Mutation rate variation in multicellular eukaryotes: causes and consequences, Nature Reviews Genetics 8:619–631, 2007. Return to text.
Two important difference between multicellular organisms and bacteria and viruses in this regard are: (a) effective population size (trillions in the latter); (b) the latter have higher tolerance for mutations and are able to actively use them to their own advantage when required. E.g. Wagner, J. and Nohmi, T.,Escherichia coli DNA Polymerase IV mutator activity: genetic requirements and mutational specificity, Journal of Bacteriology 182(16): 4587–4595, 2000.Return to text.
Finkel, T., Serrano, M. and Blasco, M.A., The common biology of cancer and ageing, Nature 448:767–774, 2007. Return to text.
Serrano, M. and Blasco, M.A., Cancer and ageing: convergent and divergent mechanisms, Nature Reviews Molecular Cell Biology 8:715–722, 2007. Return to text.
Weismann, A., The Germ-Plasm: A Theory of Heredity, Charles Scribner’s Sons, 1893. On-line version: .

Sharpless, N.E. and DePinho, R.A., How stem cells age and why this makes us grow old, Nature Reviews Molecular Cell Biology 8:703–713, 2007. Return to text.
Crow, J.F., The high spontaneous mutation rate: is it a health risk? Proceedings of the National Academy of Science 94:8380–8386, 1997. Return to text.
Kiel, M.J. et al., Haematopoietic stem cells do not asymmetrically segregate chromosomes or retain BrdU, Nature 449:238–242, 2007. Return to text.
DeWitt, D.A., Chimp genome sequence very different from man, Journal of Creation 19(3):4–5, 2005. Return to text.
Kirschner, M.W. and Gerhart, J.C., The Plausibility of Life: Resolving Darwin’s Dilemma, Yale University Press, New Haven, CT, 2005. Return to text.
Williams, A., Astonishing DNA complexity uncovered. Return to text.
, 14 August 2007. Return to text.
Ma, H., et al., The Edinburgh human metabolic network reconstruction and its functional analysis, Molecular Systems Biology 3, Article number 135; published online, 2007, . Return to text.
Cui, O. et al., A map of human cancer signaling, Molecular Systems Biology 3, Article number 152, 2007. Return to text.
Kim, L., Accumulation of mutations: cancer or molecule-to-man evolution? Journal of Creation 21(2):77–81, 2007. Return to text.
He, X.C. et al., PTEN-deficient intestinal stem cells initiate intestinal polyposis, Nature Genetics 39(2):189–198, 2007. Return to text.
Löbrich, M. and Jeggo, P.A., The impact of a negligent G2/M checkpoint on genomic instability and cancer induction, Nature Reviews Cancer 7:861–869, 2007.Return to text.
Sanford, ref. 18, p. 113. Return to text.
Arnold, S.F., Mathematical Statistics, Prentice Hall, NJ, Table 6, 1990. Return to text.

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If you like real science and actual evidence, the true effect of mutations shows us that Darwinism cannot account for life on Earth at all. Organisms are devolving, not evolving.

"just as the Laws of Thermodynamics show us that the entire Universe is running downhill from order to disorder or, if you will, from heat to cold."

If your argument is that the LOT tell us that entropy must always increase uniformly everywhere, then you're barking up the wrong tree. There are plenty of local decreases of entropy. It is only the overall entropy that never decreases.

My argument is that entropy increases and energy decreases. Natural processes reflect this regularly. The only way to fend off this process is to bring in work and intelligence to the table, which only comes from an intelligent mind.

"Not one example of evolution has ever been observed"

I suspect you have to stick to some meaning of the term "evolution" that differs significantly from the actual theory of evolution to make such a claim.

I have made it abundantly clear what I mean and will not have to say more. The article on mutations falsifies the concept of mutations being organism-builders. Without mutations to be the engines for evolution, evolution is dead in the water.

"since Darwin regurgitated the old Pantheistic myth of the Universe making itself and all within it. Mother Nature, in other words. That is a silly and unscientific idea."

Your cartoonish rendition certainly is a silly and unscientific "idea". More accurately, it is a strawman argument, which is - guess what - a logical fallacy.

You do not intend to discuss things reasonably, that is your choice. But evolution requires mutations as a method of building organisms when we have shown that in fact they break them down. I did not erect a strawman, I simply revealed a key fallacy of Darwinism - that mutations are a mechanism for building new systems while they are, in fact, destructive. There is really nothing else to say about this. Your worldview is fatally flawed in many ways and this is just one of them.

The observation that the distribution of species among the continent is explained by mainstream science but unexplainable in the YEC/Noah's Ark narrative seems obvious to me. I don't recall reading it anywhere, though I'm sure I'm not the first to have thought of it.

There is nothing in the Biblical account that does not fit the scenario. Studies of speciation show that very rapid speciation can and will occur and I mean by the various combinations of pre-existing genetic information available to the kinds that were preserved on the Ark. It also applies to all the organisms that were expected to withstand the Flood and did in fact survive. All creatures big and small are easily demonstrated to have been designed. All creatures have the ability to speciate rapidly. Therefore organisms spread rapidly throughout the world, at first able to cross from continent to continent via land bridges that were available until the snow-created glaciation on the Northern portions of the great continents began to melt and raise the sea levels around the world.

No doubt you will evade and obfuscate about this issue as you have evaded phenomena that are equally unexplainable by YECs, for example the sorting of fossils in the fossil record and the alleged recalibration of radiometric dating data that would make existing data line up with YEC predictions - all of which falsify YEC and for which YECs like yourself have no coherent reply.

Oh, not only me but lots of YECs have plenty to say...cue Ian Juby:

So much for the sequential order of fossil rocks and fossils...

I have presented real science as evidence for my assertions already on this blog. The fossil record is full of organisms amazingly preserved by rapid and anaerobic burial, supporting the Flood model. We now find flesh and blood remains in all sorts of fossils, including dinosaurs, which greatly undercuts the myth of long ages. The so-called standard geological column is also mythical, being found in less that 0.5% of the world's exposed sedimentary layers and even then never in uniform layers as depicted in textbooks.

The fossil rocks include megabreccias, unconformities, paraconformities, polystrate fossils, fossils sorted by flow, fossils buried in situ, mixed fossil environments in which both land and sea creatures and plants are all jumbled in together. Some fossil layers only contain animals without plants. How could entire ages exist without plant life? Some fossil layers have lots of tracks but few fossils. What kind of age was that, the age of invisible but heavy feet? All the lower rock layers are sedimentary and show signs of being formed by massive floodwaters. The sheer magnitude of some rock formations that span continents and contain millions of tons of rock falsifies any local flood myth. The stark flat borders usually found between layers show no signs of age. I have been to many places where the rock layers look like layer cake. Flow patterns of floods can produce these things but long ages of life would not.

Sequential fossils is another myth. The general overview of the rock layers is that organisms are sorted first by habitat, second by specific gravity, third by the ability of higher organisms to evade the initial onslaught of water (organisms not living in the areas where the Flood waters were started by many possible means). The post-Flood rocks reflect a different ecosystem entirely, the world after the Flood in which an ice age was formed and then as the planet began to stabilize and the ocean waters cooled, the glaciers began to melt and then dike breaks further changed the face of the Earth. Some fossils in these layers resulted from vast loess storms, some from mudslides and volcanic activity and there were other dynamic forces at work that factor in, such as tar pits that bubbled up from below the surface of the new Earth after the waters abated.

Lazarus taxa have helped put the kibosh on evolution as well. If the organisms appear in the rock records and then disappear, Darwinists called them ancestors of other organisms. But we keep finding organisms that disappear from the rock records for sometimes hundreds of millions of supposed years only to be found alive and well now. So much for the sequential rock records. We actually have been able to reproduce the sedimentary layers of fossil rocks as they are observed today using flume technology. Furthermore, miniature laboratories have occurred in nature, such as Mt. St. Helens, which helped us understand the formation of the Grand Canyon and similar structures, demonstrated the means by which trees are mineralized and preserved as multi-level false forests and also showed us that so-called varves could be formed in minutes rather than years.

Honestly, we see that in the real world a fossil is not likely to form. It takes special circumstances to preserve soft-bodied jellies, flesh and bone remains in dinosaurs and living organisms found in formations supposedly tens and hundreds of millions of years old. On top of all that is the tendency of Darwinists to give different scientific names to the same organisms found in different rock layers. Even worse, the careless or deliberately fraudulent naming of dinosaurs. With the ability to study the physiology of dinosaurs we now see that many dinosaurs with different names were simply specimens of varied age of the exact same kind of dinosaur. With so many deliberate deceptions that Darwinists have tried to use to fool the public over time, from Huxley to Haeckel to Gingerich and many others, it is hard to trust what Darwinist scientists present to the public as evidence. LUCY aka Australopithecus afarensis has been extensively promoted as a hominid ancestor, but those who present this fossil as evidence have added to the actual fossil remains with human-like features not found and even deliberately altered the evidence to make an ape look somewhat human. Like other so-called ancestors of humankind, they always turn out to be apes.

"I do object to the fake fallacy of argument from incredulity. It is a complete farce, an attempt to evade both logic and evidence by simply running away with a fallacious fallacy."

You object to it, I understand that, but you have no logic to oppose it. Saying something is too complex for you to imagine at this point that there could not possibly be a scientific answer to it is an actual logical fallacy that has been exposed time and time again. Pointing out a logical fallacy is not "running away", committing one is.

Well, now you are deceptive or deceived, one. Darwinists hide behind this so-called fallacy as modern real science has demonstrated conclusively that organisms are designed, that information in abundance is found in organisms and information does not arise from nature. Furthermore the information is complex and specified. Within organisms are algorithms and systems mankind is copying to make life better for man. How is it that organisms have a far superior coding system than man has devised? How is it that they are packed with information, and information is not material in form or substance? If you study the cell, you find myriad well-designed machines and processes more complex and efficient than any factory mankind has ever built. Information is not produced naturally. Furthermore life is not found naturally and the Law of Biogenesis has never been violated.

The so-called fallacy of argument from incredulity is a liar's resort. We do not claim that organisms are simply too complex to imagine them having arisen by chance, we assert that all the hallmarks of intentional design are reflected in organisms, including built-in processes to provide redundancy and processes and information to allow for many contingencies. Just as a space capsule has redundancies and has tools and parts and spare systems to contend with various contingencies that can be imagined in order to preserve the lives of the astronauts, God made organisms with sophisticated systems and rich genetic libraries from which to choose so that by natural selection the various kinds of organisms could be preserved.

Beyond that, more than one kind of organism was designed that could fill the same space in an ecosystem so that if one kind of organism would go extinct, another kind could fit into the overall ecosystem. There are many varieties of grazing animals that can provide food and often milk and cheese for people. There are varieties of organisms for any niche you can name. We have found organisms that depend on minerals that are extruded from beneath the sea bottoms, smokers/seeps in both hot and cold water that dispense methane or sulfur in forms that support entire small ecosystems that are entirely independent of the Sun-plant-carbon ecosystem we are used to observing on the planet. Not only does this compound the problems of common descent (which had been blown to smithereens anyway) but it again provides a signature of a Designer capable of being remarkably creative.

We may find dinosaurs in the Congo. We may find trilobites alive somewhere on the ocean floor. We have explored very little of the ocean and there are still large portions of deep jungles that, as we inspect them, reveal more new organisms as well as revealing more Lazarus organisms. Someone stumbles upon a stand of Wollemi Pines. A fisherman catches a coelecanth. A naturalist finds a Lazarus rat at a food vendor's table. Meanwhile real science detects design in organisms.

Last and enough for today, the massive problems of Darwinist dating methods have been covered thoroughly on this blog. For now, it is enough to say that our measurements of the Earth's magnetic field (which is decaying) dating back to the 17th Century (with knowledge of its degradation going back 1,000 years before then) limits the age of the Earth to around 10,000 years and the fact that C-14 and C-12 in the atmosphere has not reached equilibrium yet limits the Earth to less than 25,000 years. Helium extant in granitic zircons limit the Earth to an age of 6-8,000 years old. Finally, the presence of C-14 in all fossils in all rock layers precludes long age dating. Lyell deliberately fudged his data when he first wrote on the age of the Earth. I fear there are too many Lyells and too many uncritical thinkers swallowing nonsense whole.

Mr. Anonymous, you have not researched ID and Creation science to any extent and have accepted all sorts of Darwinist myths without question. If you do not allow yourself to consider that your so-called facts are unsupported by evidence, then you will keep the same opinion and presumably be happy with it. Hoping to have at least led you to reconsider some of your assumptions and moving forward from here. Happy Sunday!

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