Mutations & Natural Selection

“Whoever thinks macroevolution can be made by mutations that lose information is like the merchant who lost a little money on every sale but thought he could make it up on volume.”  Lee Spetner¹

Superstition, tradition and personal bias crept into research prior to tools of sophisticated technology.  Not only did 1859 era scientists lack access to electron microscopes, laboratories did not bask under the warm glow of electric light bulbs.  Language filtered through the stentorian tones of an elegant English accent helped bridge yawning gaps between supposition and fact.

Primitive investigative naturalists lacked the first clue about complex life codes vested in a cell’s DNA. They studied what they could see—embryos and bones. Striking similarities were erroneously interpreted as relatedness. Embryonic transformation from misunderstood simple cells to a fully developed animal encouraged conjecture that comparable transformations of any simple cell could lead eventually to most any complex creature—given spin the bottle luck and mega years of evolutionary gestation.

Theories of origin came burdened with the same medieval hot air that floated spontaneous generation fallacy. Darwinists looked in the wrong direction—toward fully developed life forms and their fossils. The world might have been spared specious speculations had molecular biology been a nineteenth-century science.

When Darwin opted for life by random chance accident rather than by design, his perception of the living cell smacked of the superstitious mystical.  He lacked the faintest perception of the cell’s origin and its complexity, much less awareness of its DNA.  In his quest to explain the evolutionary process he differentiated between somatic cells and germ cells and latched on to what he described as “gemmules” to work the unexplainable that his idea invited.

Darwin sought a mechanism that would preserve and pass along acquired physical traits to descendant generations.  He latched on to gemmules as the magical potion to carry acquired physical traits from somatic cells to germ cells.  Bit-by-bit, these gradual changes accumulated, underwriting evolution, or so the theory supposed. Forget for a moment that gemmules didn’t exist except in the imagination of someone walking in la-la land.

The hopeful guru seized upon the towering neck of the giraffe, a top ten attraction at animal zoos, as prime evidence of the pangenesis process.  Fairy tale logic manufactured uncorroborated fiction.

When persistent droughts dried the fields of grass grazed by the giraffe’s less elongated ancestor, survival hinged on stretching its neck to nibble tree leaves.  The animal’s bone and muscle structure managed to preserve each stretch of the neck and forward each miniscule change to the next generation, thanks to gemmules.  These modest adaptations eventually resulted in the long-necked giraffe that populates zoos.

The myth suffered from at least two major-league flaws.  Why didn’t other animals that grazed the same African landscape, like the zebra, evolve similar long necks?  And of course, the fact that gemmules don’t exist demolished the theory.

Scenarios of giraffe’s neck-stretching allegedly transporting elongation to the next generation proved untenable.  Pangenesis bit the proverbial dust. If the idea were valid, a muscle builder like Arnold Swartznegger could pass along a set of magnificent muscles to his children.

Gregor Mendel’s Garden 

The legacies of two European contemporaries of the mid-nineteenth century launched ripples impacting origin science that resonate in century twenty-one.  Gregor Mendel (1822-1884), an obscure Czech monk and Darwin contemporary, discovered genetic principles in the quietude of a monastery garden while Englishman Charles Robert Darwin postulated relentless change in life forms driven by natural selection picking from a smorgasbord of improved traits acquired by random chance.

Mendel’s experiment revolutionized knowledge of the mechanism of inheritance. He bred several generations of peas focusing on its seven basic characteristics.  What he discovered about hybrids clashed head-on with Darwinian theory.

Mendel published his findings in the Journal of the Brünn Society for the Study of Natural Science in 1865---six years after Darwin published Origin.  This Journal edition was distributed to 120 libraries including some in England and eleven in the United States. His work, either ignored or overlooked, was referenced in the Encyclopedia Britannica’s 1892 edition.²

When the twentieth century dawned, the stage was set for a direct assault on a core component of the Darwinian notion that had fascinated late nineteenth century academia.

The landmark findings of Gregor Mendel, dormant and virtually unnoticed since his 1866 presentation to the Natural History Society of Brunn, Austria, were translated and published in English in 1900.   Driving force pushing the release was 39-year-old British biologist, William Bateson (1861-1926), founder of the science of genetics, and eventual president of the British Association for the Advancement of Science, admired Mendel’s scholarship.

The publication of these simple garden experiments rocked intellectual circles with the fury of a bombshell blast.

There is speculation as to whether Darwin’s theory of evolution would have “evolved” and seen the light of day had he studied Mendel’s findings. Bateson, a biologist, expressed doubts. “…Darwin would never have written the Origin of Species if he had known Mendel’s work.”³

Maybe “yes,” maybe “no,” but we’ll never know!

What we do know is that contemporary knowledge about the cell and its DNA correlates with Mendel’s law of heredity and does nothing to corroborate Darwin’s theory. Darwin’s collaborator and co-evolutionist, Alfred Russel Wallace, viewed Mendel’s findings as a threat to evolutionism. “On the general relation of Mendelism to evolution, I have come to a very definite conclusion.  That is, that it is really antagonistic to evolution.”⁴

Eventually Mendel’s pioneer research anchored the science of genetics confirming life forms function through precisely expressed codes with predictable results.  Mendel’s law of genetic inheritance blows the cover off empty rhetoric embellishing make-believe and opened doors to discoveries of genes, chromosomes, and DNA—the master genetic templates that determine and distinguish life prototypes.  “Cell biologists identified chromosomes as the carriers of Mendel’s heredity factors, and in 1909 Wilhelm Johanssen named them ‘genes.’”⁵

Darwin lacked knowledge of genes.  As a result, he went looking for endorsement of his theory in all the wrong places.  His belief that acquired physical traits could be passed on to offspring proved to be gross error.  His hope that evidence from fossil fields would reveal a chain of organic life, continuous from simple to complex, fell apart on the rocks.  He relied on the visible for support!

Knowledge as to ancestry and origins lay obscured in data invisible to the naked eye.  In time, the science of molecular biology would open doors closed to nineteenth century understanding.

Genetic “Abnormalities”

What Mendel did with garden peas, Hugo deVries tried with the primrose.  He reported flowers rising “…suddenly, spontaneously, by steps, by jumps.  They jumped out among the offspring.” He observed the Intra-Genomic Adaptability of the primrose.  He described variables as “new species” which he designated as “mutations.” Eventually, “mutations” joined evolutionism’s lexicon attempting to explain changes in nature.⁶

In 1908, Russel Wallace dismissed Mendel’s discovery and discounted mutations as minimally significant.  “As playing any essential part in the scheme of organic development, the phenomena seem to me to be of the very slightest importance.  They arise out of what are essentially abnormalities, whether called varieties, ‘mutations,’ or sports.”

He saw “…their extinction under natural conditions more certain and more rapid, thus preventing the injurious effects that might result from their competing with the normal form while undergoing slow adaptive modification…Any species which gave birth to a large number of such abnormal and unchangeable individuals would be so hampered by them whenever adaptive modification became necessary that the whole species might be in danger of extinction.” Wallace scorned these abnormalities as “refuse material of nature’s workshop, as proved by the fact that none of them ever maintain themselves in a state of nature.”⁷

His analysis of these genetic “abnormalities” as “refuse material” rings true a century after the fact!  Inadvertently, and apparently unforeseen by Wallace, his negative appraisals of mutations ran diametrically counter to the subsequently postulated neo-Darwinism: the Modern Synthetic Theory of Evolution!

Wallace was not the only man of influence reluctant to jump for joy when confronted with Mendel’s law of genetic inheritance. The news shook the faith of other evolutionists candid enough to doubt.

Princeton’s Prof. Scott complained the findings “…rendered but little assistance in making the evolution process more intelligent, but instead of removing difficulties have rather increased them.”⁸

The Chair of Evolution for the University of Paris, aired his concerns to a 1916 Harvard audience.  “It comes to pass that some biologists of the greatest authority in the study of Mendelian principles of heredity are led to the expression of ideas which would almost take us back to creationism…The data of Mendelism embarrasses us quite considerably.”⁹

The year of the 1925 Scopes Trial, an English Zoology Professor, E.W. McBride, reminisced for Science Progress, January, 1925.  His words betrayed a touch of nostalgia laced with disappointment.  He recognized Mendel’s law as something of a wet blanket cast over evolution theory after first being greeted with “enthusiasm.”  His disappointment echoes.  “We thought at last the key to evolution had been discovered.  But as our knowledge of the facts grew, the difficulty of using Mendelian phenomena to explain evolution became apparent, and this early hope sickened and died.  The way that Mendel pointed seemed to lead into a cul-de-sac.”¹⁰

Eventually, evolutionists grasped reality: “gemmules” represented fantasy.  If giraffes had to keep stretching to munch on tree leaves to survive, how did zebras escape the same result?

“Pangenesis,” burdened with the flawed idea that acquired physical traits could be passed on to another generation, qualified as pure poppycock. The dismal surmise broke down completely under the scrutiny of Gregor Mendel’s irrefutable findings.  Natural selection was left stranded high and dry, without anything viable to select.

Given the shaken faith of the devout, the stage beckoned for solid evidence reconfirming evolutionism.  But its a quantum leap to suggest a string of DNA from human cells stretching 50 billion kilometers into space could be built by multi-millions of random chance abnormalities flowing from the first ever life form as postulated by Darwinism.

By the mid-1930s, serious evolutionists recognized the untenable  Pangenesis myth as anything but the magic elixir teaming with natural selection to propel transitions of one life kind to a new and  different body plan. Confronted with the absurdity of a primitive superstition, the time arrived to review, retrench and revise.  And not a moment too soon---a crescendo of doubting voices could be heard reacting negatively to the theory’s eroding credibility.

“[T]he theory suffers from grave defects, which are becoming more and more apparent as time advances. It can no longer square with practical scientific knowledge, nor does it suffice for our theoretical grasp of the facts…No one can demonstrate that the limits of a species have ever been passed. These are the Rubicons which evolutionists cannot cross…Darwin ransacked other spheres of practical research work for ideas…But his whole resulting scheme remains, to this day, foreign to scientifically established zoology, since actual changes of species by such means are still unknown.”¹¹

Theodosius Dobzhansky floated a theoretical life preserver in 1937 postulating that “mutations and chromosomal changes…constantly and unremittingly supply the raw materials for evolution.”¹² Dobzhansky’s idea attracted attention despite its failure to explain the source of the “raw materials” allegedly delivered to a corrupted genetic code.

Synthetic “Science”

In 1941 leading evolutionists, such as Julian Huxley and George Gaylord Simpson, put their heads together in an effort to salvage Darwinian thought without dumping the baby with the bathwater. Evolutionism’s movers and shakers grasped Dobzhansky’s straw in the wind, discarding the gemmule embarrassment and replacing the void with mutations, a new patch on a threadbare cape.

Looking to mutations as the “raw materials for evolution” seems as fanciful as picturing the equivalent of a Niagara Falls in a Mojave Desert mirage. Regardless, ignoring the information shortfall while fleeing the discredited gemmule pathway to nowhere, evolutionists seized upon the notion of gene mutations providing the “raw material” for natural selection to do its thing.

Embracing mutations, neo-Darwinism tried reinventing itself by blazing a trail within the shifting sands of genetic mistakes.  Those dedicated to life’s origin without input from intelligence, massaged Darwin’s dogma by awarding it the grand title: Modern Synthetic Theory of Evolution, or neo-Darwinism.  Hugo deVries didn’t live long enough to realize his aptly-named “mutations” surfaced in time to temporarily resuscitate a theory struggling to survive in prebiotic slime!

Darwinists met in Chicago in 1959 to celebrate the centennial anniversary of the publication of The Origin of Species.  Sir Julian Huxley, grandson of the 19th century Huxley that ran interference for Darwin, waxed eloquent.   According to Sir Julian, “Darwin’s theory…is no longer a theory but a fact…We are no longer having to bother about establishing the fact of evolution…” He ruled out “either need or room for the supernatural…”¹³

Huxley’s whistling-in-the dark mentality might better have been an obituary for a fragile and obsolete idea confronting its death throes. Despite Huxley’s chest thumping, evolutionism’s delicate threads had begun to unravel, reminiscent of Darwin’s own words signaling unease.  The envisioned partnership linking mutations to natural selection could not salvage a bankrupt theory.  Yawning, genetic chasms separating distinct kinds of organic formats have never been bridged by the combo---even in a bazillion years.

Even after neo-Darwinism attempted to patch up glaring “holes” and “flaws” in the theory, vigorous dissent echoed loud and clear.  "The Darwinian theory of descent has not a single fact to confirm it in the realm of nature. It is not the result of scientific research, but purely the product of imagination."¹⁴ “…Let it be stated in no uncertain terms that there is no evidence that evolution ever has occurred or ever can occur across the kinds.”¹⁵ “No matter how numerous they may be, mutations do not produce any kind of evolution….There is no law against day dreaming, but science must not indulge in it.”¹⁶

Despite redundant clichés citing changes in finch beaks, fruit flies, and bacteria as proof of evolutionism, the variations confirm only the adaptation potential within a preexisting genetic code. Bacteria replicate prodigiously as bacteria…ad infinitum. Thousands of generations later, fruit flies remain fruit-flies (albeit possibly crippled and deformed).  No change blazes an upward genetic trail to some other new and different life-kind or “class.”

Intra-genomic adaptability (IGA) does not equate neo-Darwinism! There is not a scintilla of evidence that any mutation or series of mutations have joined with natural selection to activate random chance mandates.  Insurmountable hurdles block the route.

Mutations never provide the new information to a genetic code enabling a “bear” to “evolve into something as monstrous as a whale.” Mutations are overwhelmingly deleterious, typically handicapping the genome by inducing a corruption or a loss of genetic information that weakens the organism. Even in the rare case of an arguably “good” mutation, new information is not added to the genetic code.  Accumulated mutations typically degrade overall fitness leading to possible extinction.

A diminished gene pool assures decline in diversity—never a leap linking one life form to an entirely new and different prototype. Changes wrought by mutations paired with natural selection may shift a descendant organism down or laterally within the basic genome but never a vertical change up the down staircase to a different class or order with a distinctly new body plan kind.

Mutations themselves are subject to an organism’s self-correcting mechanism, thanks to twelve enzymes. If the repair system itself mutates, the organism’s survival could be jeopardized.  Mutations are much too slow to accomplish their conjectured mission.

Dr. Henry M. Morris, visionary scientist investigating origins from the creationist perspective, tackles the issue head-on. “Mutations take place, but they are either reversible, deteriorative, or neutral. Recombinations of existing genes…are ‘horizontal’ changes that do not result in reproductive isolation. Natural selection takes place, but this is a conservative phenomenon, which weeds out defective mutants and keeps the population stable. Adaptations take place, but these are horizontal changes which conserve the species against extinction, but do not produce new species.”¹⁷  “…If one must depend on mutation and natural selection to produce new species---let alone, new families, orders and phyla as evolutionists assume, then not even billions of years would suffice.”¹⁸

The mutation silver bullet, intended to salvage evolutionism, more closely resembles an executioner’s shot aimed at its heart.  Burdened with the baggage of abnormalities, evolutionism’s revised idea dubbed the Modern Synthetic Theory of Evolution, might appropriately be named, Medieval Synthetic Science.

Natural Selection

Natural selection is genuine! 

But don’t hold your breath for evolutionary change if the selection relies on mutations.  Natural selection works counter to the other half of the equation by normally screening out harmful mutations.  “Natural selection can serve only to ‘weed out’ those mutations that are harmful, at best preserving the ‘status quo.’”¹⁹

“Natural selection can act only on those biologic properties that already exist; it cannot create properties in order to meet adaptational needs.”²⁰ “No one has ever produced a species by mechanisms of natural selection.”²¹ Natural selection offers no more than tautology’s circular reasoning.  “…The Darwinian theory of natural selection, whether or not coupled with Mendelism, is false.”²²

No question, the law of gravity stands secure as an irrefutable landmark in the science of physics.  No less a fact of biology, is Mendel’s law of genetic inheritance.  Evolutionists like Wallace, Scott and McBride reacted with concern, recognizing that Mendel’s law not only didn’t track with the theory of evolution but also threw a monkey-wrench into its mechanism.

So, which approach deserves the respect of objective scholars? The irrefutable findings of Gregor Mendel?  Or the conjectured  role of mutations as stand-ins for discredited gemmules?

Mutations 

Punching a single digit error on a telephone keypad misdirects the intended connection.  Area code 212 reaches New York; 213 accesses California; 202 connects nowhere to nothingness. As with electronic communications, the gene machine demands precision. Mutations are genetic mistakes that access wrong numbers!

There is belief that genetic codes are vulnerable to assault from radiation and chemical reactions.  The ultimate villain may be virus parasites that invade cells and wreak havoc on nuclei.

“When a virus penetrates a cell, it disappears inside the nucleus for four to eight hours, giving the outward appearance of complete normalcy.  Then the viral particles that the cell has been coerced into making suddenly burst forth, shattering the host.”²³

While some argue “…that viruses were involved very early on in the evolutionary emergence of life,”²⁴ the contrary view questions just how such insidious, disease-causing critters could contribute anything other than genetic flaws. DNA mistakes degrade the genome. They bring no new information to the party, only a corruption or reshuffling of the old.  Genetic errors, duplications, translocations, and deletions in the genetic machinery trigger debilitation and susceptibility to disease.

This reality deserves billboard attention: if mutations provide the “raw materials” from which natural selection is to “select,” neo-Darwinism faces bleak times!  “Major functional disorders in humans, animals and plants are caused by the loss or displacement of a single DNA molecule, or even a single nucleotide within that molecule...There is no evidence for beneficial spontaneous genetic mutations.”²⁵

Crippling mutations respect no person!

A once monster of a man, now twisted and bent almost in half, totters feebly aided by a walker.  Parkinson’s disease, the insidious scourge, laid low the robust physique of the former football star.  A mutated gene stands accused as the culprit!²⁶

Mutations unload a bleak litany of physical flaws and debilitating diseases on the genome!  Mutations have plagued humans with a list of 4,500 already identified bad results—and still counting. Harmful gene mutations discovered in 1996 alone, cast a pall.  The roster disconcerts!

Progressive myoclonus epilepsy is caused by a gene mutation on chromosome 21. Treacher Callins Syndrome, hemochromatosis, is linked to a defective gene on chromosome 6. A gene mutation on chromosome 5 generates deformities of the face, ears, down-slanting eyes, and deafness. Progressive blindness described as retinitis pigmentosa is a disorder linked to a gene from the X chromosome. A chromosome 9 gene mutation causes skin cancer. A mutated gene on chromosome 16 is tied to fanconi anemia, affecting children who rarely live past their sixteenth birthday. A gene missing from chromosome 7 causes Williams Syndrome. Anhidrotic ectodermal dysplasia, resulting from a mutation on the X chromosome, can afflict victims with baldness, loss of teeth, or deprive them of ability to sweat.²⁷

“…Not one mutation that increased the efficiency of a genetically coded human protein has been found. Instead of a ‘blind watchmaker,’ the mutations behave like a ‘blind gunman,’ a destroyer who shoots his deadly ‘bullets’ randomly into beautifully designed models of living molecular machinery. Sometimes the ‘bullets’ only cause minor damage; sometimes they maim and cripple; sometimes they kill.”²⁸

There are “genetic flaws that make people fat…”²⁹ Werner’s syndrome results from a mutated site on human chromosome 8 that causes victims to “age prematurely fast and usually die before they reach 50.”³⁰ “Best’s macular dystrophy…destroys the part of the retina responsible for the sharpest vision ‘has been linked to mutations’ in the gene now called bestrophin.”³¹   Since 1990, “discoveries of heart-handicapping mutations have been pouring out of numerous labs at an ever-increasing rate, yielding more than 100 mutations in more than a dozen genes.”³²

Another genetic mutation “…causes children to die of old age…Children with Hutchinson-Gilford progeria syndrome age at a rate five to 10 times faster than normal.  They lose their hair, their skin wrinkles, and they die of arteriosclerosis, or hardening of the arteries, by their early teens.”  The defect is in “…a gene that controls the structure of the nucleus…”³³

“A genetic polymorphism called 11307K in either of…two APC genes doubles the risk of colon cancer.”³⁴ Spontaneous blood clots can form with the power to cause sudden death where a “patient with the disorder has inherited at least one defective gene encoding protein C.”³⁵ A mutated gene on chromosome 11 contributes to inherited hearing impairment.³⁶

Then there’s the unappetizing smorgasbord of birth defects caused by mutated genes: muscular dystrophy, spinabifida, cystic fibrosis, Huntington’s Disease, hermachromatosis, and Down’s Syndrome. Leukemia may result when a piece of chromosome translocates to another chromosome in the midst of cell division.

Regarding humans, researchers “calculated an unusually high rate of 4.2 mutations per generation, of which 1.6 diminish the fitness of the species…the species must survive in part because people who have accumulated dangerous mutations are least likely to successfully have children…the human reproductive strategy helps purge harmful mutations in batches…they mix their genes with another’s, and presumably some of the worst defects aren’t passed along. That wouldn’t happen if humans reproduced asexually.”³⁷

Fat Chance Odds 

“Genetic variation depends on the process of mutation, and mutations are rare events.  Any particular new DNA mutation will occur only once in about 100 million gametes.  Moreover, when a single mutation occurs in a single newborn, even if it is a favorable mutation, there is a fair probability that it will not be presented in the next generation because its single carrier may not, by chance, pass it on to its few offspring.”³⁸

Change in a single nucleotide would be the smallest possible modification of a genome.  One of neo-Darwinism’s architects guesstimated that as few as 500 mutations could evolve a new species.  Mathematic odds challenge the possibility.

“…It’s a matter of chance that a mutant survives.  It might spread through the population and take it over, but more likely it will just vanish…even good mutations are likely to disappear from the population” if it occurs just once. “The chance of 500 of these steps succeeding is 1/300,000 multiplied by itself 500 times.  The odds against that happening are about 3.6 x 10^2,738 to one, or the chance of it happening is about 2.7 x 10^-2,739…It’s more than 2,000 orders of magnitude smaller than …impossible.”³⁹

Impossible trumps improbable.

Computations of the likelihood for any single event beyond 10⁵⁰ chances qualifies as impossible unless absolutism is willing to concede the intrusion of a miracle.  No matter how many billions of chances and multi-millions of years allocated, the chance of those 500 “beneficial” mutation steps succeeding continues impossible ad infinitum.  Even an artfully loaded pair of dice will never roll a number higher than 12 no matter how many tosses.

Neo-Darwinism’s reliance on beneficial mutations conjured up by blind chance as natural selection’s raw material doesn’t compute.  Mathematic impossibility renders an already implausible theory extinct. Nothing remains but a Kerkut style assumption, lacking legs, heart or brains much less a rational intellectual life.

As to the tired cliché that mutations benefit bacteria by building immunity to antibiotics such as streptomycin, reality indicates “the mutation reduces the specificity of the ribosome protein, and that means losing genetic information” with “a loss of sensitivity.”  Despite some “selective value,” this mutation “decreases rather than increases genetic information.”⁴⁰

“…Antibiotic resistance is the result of loss of a protein, loss of the binding capacity of a protein, or the loss of a transporting system…It’s a loss of something…If you’re removing a transport protein to eliminate the bacteria’s sensitivity to antibiotics, then how is that explaining common descent by modification…?”⁴¹

“There aren’t any known, clear, examples of a mutation that has added information.” Instead, mutations lead “to a loss of sensitivity to the drug…the effect is heritable, and a whole strain of resistant bacteria can arise from the mutation…A change in one of its proteins is then likely to degrade the organism…Information cannot be built up by mutations that lose it.”⁴²

“For information to build up in living organisms, it must be created somewhere…Although in some special cases a loss of information can lead to an advantage for the organism, the large-scale evolution for which the NDT [neo-Darwinian Theory] is supposed  to account cannot be based on such muations.”⁴³

As to the neck of an 18 foot-tall giraffe with a heart 2 ½  feet long, mutations contribute nothing more to the explanation of its origin than do fictitious gemmules.  The heart powerful enough to pump blood up the extended neck to the brain is also powerful enough “to burst the blood vessels of its brain” when it reaches down for a drink of water.  But when the giraffe bends down, “a protective mechanism” kicks in causing “valves in the arteries in its neck” to begin to close.⁴⁴

“…Most mutations which cause changes in the amino acid sequence of proteins tend to damage function to a greater or lesser degree…most of the amino acids in the centre of the protein cannot be changed without having drastic deleterious effects on the stability and function of the molecule.”⁴⁵

“There’s no mutation that gives them [evolutionists] what is necessary for common descent with modifications.  There are all kinds of mutations that eliminate proteins.  They may eliminate transport protein, an enzyme, the action of an enzyme, or regulatory systems.”  Mutations are “…not making new transport proteins!  They’re not making new regulatory systems!  Antibiotic resistance is an example...Every time you read about antibiotic resistance…they’re going to talk about this as…an absolute example of evolution.” One of Darwin’s false assumptions “…was that natural selection had a building or creating capacity, and it doesn’t…”  It removes information.⁴⁶

“…Every molecular example of a mutation we currently have fails to provide a mechanism that can account for the origin of any genetic activity or function.”⁴⁷

Natural selection functions but it doesn’t power evolution.

Marcel Schutzenberger sees odds of 10-1000 “against improving meaningful information by random changes…The astronomers Fred Hoyle and Chandra Wickramasinghe placed the probability that life would originate from non-life as 10-40,000 and the probability of added complexity arising by mutations and natural selection very near this figure.”⁴⁸

Limits to Change

Mutations can’t breach genomic barriers to change.

Microbiologist Michael Denton agrees. “…The degree of change that can be experimentally induced in a wide variety of organisms, from bacteria to mammals, even under the most intensive selection pressures, is always limited by a distinct barrier beyond which further change is impossible.”⁴⁹

Wheat, corn, chickens, strawberries, and dogs can be bred to size, shape, and color by shuffling the gene cards. But genetic codes define limits to change unless something like gene splicing (guided by intelligence) introduces new information into the genome. Even then, modified products continue as selected strains of wheat, corn, chickens, strawberries, and dogs.

Luther Burbank made the case alluding to what he defined as Reversion to the Average.  “…I can develop a plum half an inch long or one 2½ inches long, with every possible length in between, but I am willing to admit that it is hopeless to try to get a plum the size of a small pea, or one as big as a grapefruit …there are limits to the development possible, and these limits follow a law.”⁵⁰

Plant breeders were able to increase sugar content in sugar beets from 6% to 17%.⁵¹ Apple growers managed to convert the Hawkeye, “a round, blushed yellow apple of surpassing sweetness,” discovered in 1880 in a Madison County, Iowa orchard, into Washington’s once popular Red Delicious, with unique points at its base. “Breeders and nurseries patented and propagated the most rubied mutations” altering the color, shape, flavor, skin and juiciness.⁵²

Natural selection occurs, but it doesn’t power evolution.  

Crowds of thousands, seated on the grass just west of a nation’s Capitol steps, respond with goose bumps and cheers to the National Symphony’s rendition of John Phillip Sousa’s Stars and Stripes Forever.  Nearby, at the MCI Center, “The Three Irish Tenors” inspire standing ovations while rhythmic beats created on the Kennedy Center stage cover the waterfront of melody. All these tunes and arrangements share the identical octave of musical notes!  The piano keyboard’s five black keys offer intermediate sounds inviting creative innovation. 

Different sequences of half-notes, quarter notes, or wholes laced with syncopated beats; the pace of the rhythm generating a march or the swing of a waltz; and arrangements featuring an artsy mix of instruments---thousands of melodies all built within the limits of music’s octave scale.

A living genome provides analogous potential for variety! 

Sharing similar genes does not equate a genetic link nor prove common ancestry any more than different songs, derived from the same octave of sounds, establish musical relationship. The genetic mix, sequences, and formulas vary radically, just as songs fashioned from the same sound options, produce radically different musical compositions!

Then there is the atom, invisible to the naked eye, with its positively charged nucleus encircled by an array of electrons---the smallest unit of any element charted in the classic periodic table displayed in High School classrooms.  Inorganic matter is so reliably constant in its identifiable properties that elements can be combined pursuant to chemical recipes producing results readily replicated ad infinitum.

From the microscopic minutiae to the cosmic; from the inorganic to the living; natural world science exemplifies precision!!!! The glaring exception to this universal commonality of the science of order and the mathematically real is evolutionism’s mutant “science” of origins where the logic of the measurable equation is thrown to the winds in favor of assumptive myth.

Evolutionism ignores the real and postulates the unreal.  Empty rhetoric poses as substance once all hype, bells, and whistles are removed. Slick diagrams, catchy slogans and colorful imagination can’t guarantee scientific respectability.  Against impossible odds, evolutionism attracts minds to the obscenity that an ancient, grand pappy fish accidentally spawned all humanity.

Truth stands tall and unassailable in three dimensions; it needs no defense. Falsehood collapses on itself, melting to nothingness  under the relentless scrutiny of the morning sun.  “Evolutionism is a fairy tale for grown‑ups. This theory has helped nothing in the progress of science.  It is useless.”⁵³

Realistic evolutionists accept reality: mutations are deleterious, with rare exceptions.  So what about those rare exceptions, the so-called “good” mutations?  Again reality steps in: mutated bacteria remain bacteria; fruit fly descendants, however deformed, continue as fruit flies; and of course, those Galapagos finches still fly the skies as finches, generation after generation after…………!  Even “good” mutations are incapable of delivering the “raw material”  natural selection needs to achieve evolutionism’s goals.

Evolutionist Stephen J. Gould, undercut the core essence of neo-Darwinism with cold-eyed logic.  “You don’t make new species by mutating the species…A mutation is not the cause of evolutionary change.”⁵⁴

So where does that leave neo-Darwinism’s iconic lynchpin?

Warren L. Johns, Esq.
Editor, CreationDigest.com

1---Lee Spetner, Not by Chance: Shattering the Modern Theory of Evolution (Brooklyn: Judaica Press, 1997) 160.

2---Ian Taylor, In the Minds of Men, 160, 161.

3---Byron C. Nelson, After Its Kind (Minneapolis, Augsburg Publishing House, 1927) 98, 99.

4---Nelson, 101, referencing Alfred Russel Wallace, Letters and Reminiscences, 340.

5--Jonathan Wells, Icons of Evolution (Washington, D.C.: Regnery Publishing, Inc., 2000) 180.  

6---Nelson, 101, quoting Wallace from Letters and Reminiscences, 95.

7---Alfred Russel Wallace, “The Present Position of Darwinism,” Contemporary Review, August, 1908.

8---Nelson, 101, citing Theory of Evolution, 163.

9---Nelson, 99,101 citing Smithsonian Institute Report, 1916, 343.

10---Nelson, After Its Kind, 101, 102, citing Science Progress, January, 1925.

11---Albert Fleischmann, "The Doctrine of Organic Evolution in the Light of Modern Research," Journal of the Transactions of the Victoria Institute 65 (1933): pp. 194-95, 205-6, 208-9.

12---Wells, 181. 

13---Michael Denton, Evolution: A Theory in Crisis (Bethesda, Maryland: Adler & Adler, Publishers, inc., 1986)  75 citing Julian Huxley, Evolution After Darwin ed. Sol Tax, vol. 3 (Chicago: University of Chicago Press, 1960) pp. 1-21, see 1. 

14---Albert Fleischmann, University of Erlangen Zoologist.  See John Fred Meldau, ed., Witnesses Against Evolution (Denver: Christian Victory Publishing, 1968), 13.

15---Henry M. Morris, “The Microwave of Evolution,” Back to Genesis, August, 2001, a.

16---Pierre-Paul Grassé, The Evolution of Living Organisms, (New York: Academic Press, 1977) 88, 103.

17---Henry M. Morris, "What They Say," Back to Genesis (March 1999) a.

18---Morris, b.

19--Bert Thompson, The Scientific Case for Creation (Montgomery, Alabama: Apologetic Press, Inc., 2002) 124.

20---Noble, et. al, Parasitology, sixth edition, “Evolution of Parasitism,” Lea and Febiger, 1989, 516, as cited by Frank Sherwin, Origins Issues, “Natural Selection’s Role in the Real World.”  

21---Colin Patterson, “Cladistics,” The Listener (1982) 106:390.   

22---Søren Løvtrup, Darwinism: The Refutation of a Myth (London: Croom Helm,1987) 352.

23---Charles Siebert, “Unintelligent Design,” Discover, March, 2005, 35.

24--- Siebert, 34. 

25---Richard Milton, Shattering the Myths of Darwinism (Rochester, Vt.: Park Street Press, 1997) 169, 170.

26---See Tim Friend, "Gene Defect is Linked to Parkinson's," USA Today (June 27, 1997) and USA Today, January 17 (180, 2005.

27---Josie Glausiusz, "The Genes of 1996," Discover (January 1997) 36.

28--David A. Demick, "The Blind Gunman," Impact (El Cajon, Calif.: Institute for Creation Research, February, 1999) iv.

29---The Star, Ventura, California, June 24, 1997.

30---The Star, June 24, 1997.

31---Elizabeth Pennsi, "New Gene Found for Inherited Macular Degeneration," Science 281 (July 3, 1998) 31.

32---Marcia Barinaga, "Tracking Down Mutations That Can Stop the Heart," Science 281 (July 3, 1998) 32.

33---Reuters, “Genetic Error Causes Rapid-Aging Syndrome,” The Washington Post, Thursday, April 17, 2003, A6.

34---Rick Weiss, "Defect Tied to Doubling of Risk for Colon Cancer," The Washington Post, August 26, 1997.

35---Daniel C. Weaver, "The River of Life," Discover (November 1997) 55. 

36---Karen P. Steel and Steve D. M. Brown, "More Deafness Genes." Science 280 (May 29, 1998) 1403.

37---Rob Stein, "Sex May Rid Us of DNA Flaws," The Washington Post (February 1, 1999) A9.

38---Morris, c, citing Richard Lewontin, The Triple Helix (Cambridge, Massachusetts: Harvard University Press, 2000) 91.

39---Spetner,  97-103.

40---Spetner, 139, 141.

41---Kevin Anderson, “Radio Interview with Dr. Kevin Anderson,” Creation Matters, No. 4 July/August 2004, 1. 

42---Spetner, 131, 141, 143.

43---Spetner, 181, 198. 

44---See Jobe Martin, The Evolution of a Creationist (Rockwall, Texas: Biblical Discipleship Publishers, 2002) 131, 132.

45---Denton, 322.

46---Anderson, 1. 

47---Anderson, “Definition of Evolution,” Anderson@nsric.ars.usda.gov, 9-4-2002.

48---Lane P. Lester and Raymond G. Bohlin, The Natural Limits to Biological Change (Dallas: Probe Books, 1989) 85, citing Fred Hoyle and N. A. Wickramasinghe, Evolution From Space (London: Dent, 1981).

49---Denton, 91. 

50---Norman Macbeth, Darwin Retried, 36, citing Wilbur Hall, Partner of Nature (Appleton-Century, 1939).

51---Lane P. Lester & Raymond G. Bohlin, The Natural Limits to Biological Change (Dallas: Probe books, 1989) 95. 

52---Adrian Higgins, “Why the Red Delicious No Longer Is,” The Washington Post National Weekly Edition, August 15-21, 2005, 19. 

53---Louis Bounoure The Advocate, 8 March 1984 , 17, quoted in The Revised Quote Book,  5.  Bounoure has served as director of the Strasbourg Zoological Museum, and research director at the French National Center of Scientific Research. 

54---Stephen J. Gould, Speech at Hobart College, February 14, 1980, cited by Luther Sunderland, Darwin’s Enigma (El Cajon, California: Master Books, 1984), 106 (emphasis in original) cited by Bert Thompson and Brad Harrub, “National Geographic Shoots Itself in the Foot Again,” (Apologetics Press.Org online report, 2004) 36.

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