Judaism – The Legal Case: Proof Beyond Doubt

Real Judaism could live with Evolution. It is basically irrelevant because it could have been one aspect of Creation. There are some valid and logical attempts at fitting mutation into every literal statement in Genesis, without changing the Torah account in any way. However the flaw is that this is a wasted effort as mutation is utterly impossible to accept from a strictly scientific and mathematical standpoint..

It is a convenient faith in the impossible to justify human behaviour. If we come from animals then obviously we must be expected to behave like them.

Every honest, intelligent and logical atheist should reject evolution as he rejects all faiths. Most leading scientists ultimately have reservations about it – but few dare to speak out.

So I am being purely vindictive and mischievous in laying bare the biggest scam of our age.

Mutation: The Blind Belief of Atheism

Yes, I am bashing Evolution because it is an excellent object lesson in how complete nonsense can so easily convince the world. This is unthinkable for you and you now know that I am a raving, drooling, wild-eyed lunatic. A fundamentalist killer. See how convinced you are? Have you checked into it? Well, for fun I did and it left me dumbfounded. And atheists will die on the sword to defend evolution whilst they reject all faithhead nonsense and all religion. Yet, they believe and will martyr themselves for a faith less supported than that in fairies.

I want to show how illogical man is when he needs to believe and find a vast, dinosaur-size get out clause. He thinks he came from apes – “But what a clever, civilized and clever ape I am!” Darwin strongly believed that he was one of the class of the ultimate elite, ruling beings. His last book – ‘The Descent of Man’ – lays this bare and shows his horrific and deeply disturbing inner being.

Social Darwinism equals Ethnic Cleansing.

It is really revealing actually to read the words of this self-confessed proto-Nazi. This was the philosophy behind evolution. The white man evolved – lower man did not. Read it and see if you can disagree with that analysis. Sweet, cuddly, white-bearded Saint Charles Darwin actually promotes – in so many words – the elimination of the lower classes of man, subjugation of women and much more. He was squeamish and recommended painless methods and eugenics. And we worship him and follow his creed!

Why was he an immediate success? Because, as we have mentioned, Darwin unwittingly gave the upper intelligentsia the silent mantra –“If I come from animals, no wonder I behave like one in my private life.” But that is step too far for you because you have been brainwashed that cuddly Uncle Charles was a latter day saint you gave us all a free card to everything we wanted to do. Just read huis words if you dare. Even insipid AI says:

“The Descent of Man” – Darwin’s last gift to mankind.

In The Descent of Man, Darwin observed that “civilised men” tend to preserve the “weak in body or mind” through institutions like asylums, poor-laws, and medical advancements, contrasting this with “savages” where the weak are “soon eliminated.” He argued that this preservation of the weak could be “highly injurious to the race of man,” drawing a parallel to the breeding of domestic animals where “hardly any one is so ignorant as to allow his worst animals to breed.”] This sentiment expressed a concern about the potential for the “degeneration of a domestic race” if care was “wrongly directed.

Darwin acknowledged a tension between the natural process of elimination and human sympathy. He stated that “we could not check our sympathy… without deterioration in the noblest part of our nature.” He believed that the expansion of human sympathy to the weakest members of society could, in theory, contradict the principles of natural selection by allowing the “unfit” to survive and reproduce.‘

Blind Belief in Mutation and Evolution

And you subscribe to that channel!!?? But, who cares, surely pure noble science proves evolution? No way. Just read on – and actually think independently. De-brainwash your brain..

Yet, still, how can any sane person question even are to accost this fair maiden of our life – Immaculate Mutation.? Well, firstly I am a raving, drooling …. … … and secondly, just examine the evidence provided by impeccable science. Also, evolutionists are always bashing religion – so I strike back in revenge.

And again, the Almighty could have created a world with evolution built in. It can be fitted in with Real Judaism’s cosmology. But it simply does not hold water.

The Blind Believer’s Manual

For over 150 years, Darwin’s On the Origin of Species by Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life (note that last part – ‘favoured races’!!??) has been presented as an unquestionable cornerstone of modern science. It is taken as a given and indeed often called ‘The Law of Evolution’. Yet, an increasing number of absolutely non-religious researchers, mathematicians, and physicists – the leading brains of our period – have argued that the mechanisms underpinning it, i.e. mutation and evolution are not merely fundamentally flawed; they are absolutely impossible.

First, its own science is clearly proven to be very unsteady and deeply flawed. We bring all the irrefutable evidence of this scam below in full scientific detail – just to bore everyone – except those scientists. Mind you none of them would deign to read a site like this – most think that they are too clever.

And again, remmeber, Darwin – a dilettante amateur and not at very bright – is absolutely palpably, plainly proven to be a Nazi, evil, elitist. Just read not only ‘The Descent of Man’ 1870 – his last book – and final message to his adoring followers. but also at the full, rarely-quoted title of ‘Origin of Species’ – the Preservation of Favoured Races in the Struggle for Life. ‘Favoured races’? Jawohl mein Herr. He was a grubby little man – who looked like and acted the white bearded saint – oh, yes, and despised women. That’s it, girls, dig him up and burn the remains.

The Proof Of “Mutation” Actually Disproves It

Even its strongest advocates have always shunned the simplest of questions – there is not one single example of any form of beneficial mutation from one species to another. The so-called ‘mutations’ of the Galapagos finches, fruit flies, guppy fish, and micro-mutations et al are all without exception either negative mutations destroying the ‘mutating’ life form – so ipso facto disprove the entire rational of evolution – or are clearly adaptions the engines of which were always present in the changing subject.

Throughout please remember that all these cases are of adaptation which is readily reversed after a few generations. There is not a hint of ‘mutation’ and certainly no new species magically becoming a dinosaur sparrow, or whatever. And please do remember also, my best friend the duck-billed platypus. He may be schizophrenic – and not too sure whether he is fish or fowl – but he disproves mutation at every wiggle of his tail.

The Detail: Debunking The So-called Scientific Evidence For Mutation

This section is packed with the scientific detail to prove that we are not merely making wild, emotional claims. The mutationalists’ own examples and experiments disprove their faith. This seems an astonishing claim so I am laying it all out in great, boring and confusing detail.

But to beat them, you have to show you can gobbledy gook as well as they do. And I therefore use their pseudo-scientific, extremely bad Latinisms and Greek terms with lots of signs and wonders just to show I can be as good a mountebank as they have been.

The Penicillin Ploy: Torturing a Poor Little Bacterium.

Antibiotic Resistance in Bacteria (e.g., MRSA)

• Point mutations in penA or gyrA [sorry these are their names] genes are claimed to confer resistance to penicillin or other antibiotics. Observed in real-time these actually are not mutations at all.; e.g., MRSA evolved via SCCmec cassette insertion – changing the existing traits. These ‘new’ strains were always present and merely are uniquely resistant to that penicillin and survive all the other strains – reproducing exponentially as their competition dies off.
• Evidence: Each and every lab evolution experiments and global spread tracking since 1960s has failed to find one provably original – ‘mutated’ penicillin-resistant strain.
• Now you are forearmed, look at the following simple, proven facts about our little bacterium and penicillin. They are really baffling. If I used parallel examples to prove Judaism, atheists would have me roasting over a fire on a toasting fork in a jiffy. Mind you, they probably would do even without such provocation.
• The claim is that ‘brand new alleles’ – genes – that improve survival chances are ‘produced’ through evolutionary mutation. More amazingly, organisms build on these to create ab initio ‘new metabolic pathways’ – a whole new body of new genetic information. It is demonstrably self-evident that this is never seen in nature and that constant artificial reproduction of adapted organisms is parallel to interbreeding cattle that give richer milk, or dogs to create Chihuahuas.
• These entirely new genes are most-famously claimed, as above, for bacteria previously controllable by antibiotics such as penicillin. These have ‘mutated’ to become resistant to almost all of them. This is so obvious that the experts merely repeat that the bacteria have ‘become more drug-resistant’. We have explained however that no one looks into the detail, which they themselves publish, that reveals the simple truth. The nasty little things die in their trillions except for a few which were always – always – resistant. These survive as the ‘Fittest’ and thrive in the absence of competition. They did not mutate. They survived because they were different to begin with. Now there was no one left to pinch their favourite food, so they exploded in numbers.
• Yes, they have metabolic pathways and other tricks that allow them so to conform themselves as to survive. This is nothing new. They have always had them. Their dead cousins did not. Yes, they now use these new pathways they always had, in order to survive. They absolutely have never ever, ever, ever, ever, ever have been found to ‘mutate’ as in Darwin. And despite those five ‘evers’, you just will not believe me so I must give a little more detail.
• In 1967 the first Penicillin-resistant Streptococcus pneumoniae was observed; then Tetracycline resistance exploded to 80% in the 1990s and then Kanamycin became clinically useless. This clearly indicates a rapid growth of antibiotic resistant bacteria; but let us understand how antibiotics work.
• When patients are given, say, Streptomyces antibiotics these cunningly stop ribosomes (protein synthesis thingies) in their target-disease cells from using protein. These cells ‘starve’. Surrounding human cells are immune to the antibiotic and carry on chomping. The nasty bug dies off.
• Penicillin antibiotics work slightly differently in brutally making the targets’ cell walls burst. The nasty bug explodes. Again our human cell walls are immune to this.
• However, a tiny number of disease bacteria always have had, (since Creation!), attributes which can neutralise various antibiotic SWAT team attacks. Billions of their close cousins die, but they simply smile and survive. How? Some literally pump out the antibiotic; some have protective proteins to change the bacteria’s conformation; some enzymes actually modify the antibiotic. But all these defence techniques have been there from the beginning. There is absolutely no mutation whatsoever. None. These naturally-resistant immune bugs survive. They find all their neighbours have been killed by the antibiotics. Suddenly there is no competition for food and they go crazy. They have street parties, go wild and reproduce exponentially in their billions. And they are really mega-nasty. They are the antibiotic-resistant bacteria.
• Further, it has always been possible for them to transfer their rare resistance genes to other bacteria, because ‘lateral gene transfer’ has always been a unique favourite party trick of bacteria. By this method, an antibiotic-resistant bacterium can transfer its resistance to a friend. This is how they show affection. There is absolutely no beneficial, permanent mutation whatsoever. None.
• There are claims of some magic trick by which it is ‘estimated’ that an unspecified ‘proportion’ of the bacteria – before being killed – mutate and develop resistance. This is insane speculation. First, they must do this quickly before the antibiotic gets to them. Impossible. Secondly, this has never been observed – merely presumed. Impossible. Thirdly, this imaginary mutation would not be beneficial as it would compromise survival in a normal environment. Impossible.
• Proper micro-biologists all agree however that fatal mutations – like cancers – do occur and can confer resistance by chance to an antibiotic. Indeed, bacteria do suffer from these. Ultimately, as in all forms of life, this leads to extinction. However, as in all forms of life, these negative mutations can temporarily have surprising benefits. Below we deal with the sick deception over sickle cell anaemia. In humans, we have this boringly-unintelligent repetition of claims that sickle cell anaemia confers an immunity to various malaria.
• Yes, in a minute number of bacteria, a fatal mutation could possibly create immunity. The ‘stricken’ but newly resistant bacteria would not die from the antibiotic but from the mutation, which will have made them more susceptible to other antibiotics, unable to function competitively or otherwise fatally compromised. There is absolutely no beneficial, permanent mutation whatsoever. None.
• But, once a strain of bacteria has achieved resistance, it explodes in number – usually through human activity – because we keep on killing off its competitors by flooding the population with our increasingly ineffective antibiotics. This will have tragic consequences but do not blame Mother Mutation. For once, I can be on her side.
• Not one little bacterium has mutated. The immune strains are not new mutations which did not exist twenty years ago. They are also twenty years old – or whatever. They are the descendants of old, tiny irrelevant strains that always historically survived our onslaughts but were insignificant in their survival, until the competition was wiped out by a new drug, to which they resistant and then they began to explode in population.

The Lederberg Experiments

• This was emphatically proven by Esther and John Lederberg in 1952 when they found this. Identical groups of various strains of bacteria were replicated. Half were left untouched. Of the others, different sets of the colonies were exposed to antibiotics and the surviving immune colonies noted. They were exposed again and again survived the antibiotics. The researchers presumed that mutation had occurred to allow some to survive.
• However the Lederbergs then, amusingly, absolutely disproved the presumption of mutation. They simply washed the original plate of untouched colonies with the same antibiotic and only the same type of presumably ‘mutated’ colonies survived. Note, these, of course, had never been exposed to the antibiotics and thus had not ‘mutated’ in order to survive. They were proven to be naturally immune without mutation.
• So the penicillin-resistant bacteria were there in the population before they encountered penicillin. They did not mutate and evolve resistance in response to exposure to the antibiotic.
• Thus the fact is that bacteria are pre-set with a set of tricks to defeat their natural competition with other bacteria. Some of these include resisting antibiotics – which are simply competitor bacteria artificially-introduced by doctors. Bacteria have always done this quietly even before little men in white coats started poking them and making them squeal.
• As to the plethora of experiments on these poor tiny organisms, the adaptations at this micro-level are beneficial to the micro-organisms themselves only within the false environment created to force them to happen. They are nearly always lethal to any corpus that is comprised of billions of such micro-organisms – such as a palaeontologist or dinosaur.
• The experiments are obviously incredibly artificial and rely on relentless, carefully-orchestrated repetitions under stringent and specialised conditions. If adaptation at this level is detected, it can scarcely be stated to be random or the result of natural selection.
• The amount of effort and time taken to achieve any sign of adaptation in these experiments actually prove that, as we discussed earlier, there has not been enough time in our universe even to change a skin cell into a hair cell.
• Having dealt with the most popular myth of mutating bacteria and resistance to antibiotics above, let us look really closely at some of the other bacteria claimed to have ‘mutated’:

Algae: green footprints.

• Chlamydomonas have chlamy feet. They are minute green slimy things – algae. Unsurprisingly they enjoy spring sunlight. We all do. But ‘they are somewhat capable of growing in the dark by using acetate as a carbon source.’ Now you and I may not regard that as fun, but they do. These poor things were grown for 600 generation in the dark. And, surprise, surprise, the ones that survived in the dark – survived in the dark. My laser sharp intellect was fully taxed to appreciate that otherwise they would not have survived. It was after all dark. Further, we are told that lots of their babies kept in the dark survived – with no enthusiasm – but they survived.
  This apparently proves ‘new, beneficial mutations are capable of adapting an organism that almost required light for survival…’. Sorry, my CV may, most misleadingly, suggest some modest achievement, but that one just went miles over my head. Some could anyway grow in the dark before the experiment – they ‘almost’ required light. They were put in the dark. Some grew in the dark. Lots didn’t develop in the dark. They deceased. Only those that did not die – well – survived. They had babies. They did not mutate – they survived. They used a trait previously in them. The magic word ‘adapting’ is actually used. Perhaps I missed something?
  Unproven. Case dismissed.
  Chlamydomonas not only have clammy feet, they can have big feet. By sieving them in their millions through a fine sieve, the bigger Chlamydomonas were isolated and then kept together. After forty generations, one ended up with – what a surprise – bigger Chlamydomonas. Where is the mutation? At best, this is artificial selection again using an inherent trait – as in chihuahuas. So, woof to that.
  Unproven. Case dismissed.
• Beer Yeast
  Apparently, beer yeast is Darwinian. Another fact about yeast is that chomps phosphate. It lives off the stuff. So, being nasty scientists, they made it go on a starvation diet. Very un-Christian; well – they are atheists. After 800 generations in a phosphate-limited environment, there were a series of pronounced improvements in its surviving on different food. These occurred because of ‘an extremely important mechanism in evolutionary history’. This was the ‘mutation’ of the permeable molecule (allowing permeation of the food through its cell wall), and separately the ‘mutation’ of the phosphatase (the phosphate chomping bit). Strangely, in the repeated repetitions of this experiment, these mutations occurred in different orders. So they did not actually rely one on the other. Sorry to be boring – but ‘Where is the mutation? At best, this may be selection again using an inherent trait.’ Yeast absorbs phosphate. It has mechanisms to do this. Under extreme conditions, it has mechanisms to survive, inherently within its genetic script.
  Even my metabolism will adapt if I fast or eat only doughnuts or only lean steak: my entire internal body chemistry changes. This does not mean that I am mutating into becoming a doughnut eater from a primal hunter and gatherer. Show me food and I will do anything necessary to live on it. In fact, show me food and I will do anything necessary to get my hands on it. In this, I am very like a bacterium.
  No novelty appeared. The yeast did not become a different strain of yeast.
  Unproven. Case dismissed.
  E. coli
• Now drew the short straw. More vivisection. For decades, this unfortunate bacterium has been subjected to incessant battering. It ticks many boxes for any researcher, the most important being its astounding rate of reproduction. Without question, researchers have shown that it has the ability to lose and gain, at a molecular level, certain traits. This then improves dramatically its ability to survive in highly artificial environments. But those very adaptations, involving survival mechanisms, spell death in any other than such environments. In a natural, random environment such bacteria would not have a chance. Further, the ‘mutations’ widely quoted are always inherent traits or mechanisms which have been previously used in another micro-biological process within the bacterium in question.
  In this series of experiments E coli was, rather like the yeast, forced to survive on unnatural and second choice nutrition. Here, its ability to survive on citrate was tested. Again no new strain appeared. The old strain simply adapted. Similar results were obtained as with the beer yeast and phosphates.
  Unproven. Case dismissed.
   
  Innumerable similar tests on starvation diets for bacteria – this time of lactose or glucose – produced identical results. Yes, we can wonder at the versatility created within these organisms and it is a well-known fact that the certain bacteria can switch between gobbling up lactose or glucose. But they only do this if no glucose is put into their baby-bottles and in fact, it would be an ultimately fatal mutation for a larger organism. Such non-beneficial adaptation – or the loss of a useful trait – is uncontroversial.
  Dr Richard Lenski is the leading and evidently very persistent researcher whose work is most often quoted on E.coli. He has produced trillions of bacteria. Careful research of his results prove his brilliance and persistence but one could not find one example of anything that could not be simply inherent adaptive capacity within the DNA of his subjects.
  So, yes, as above, micro-biologists have found survival of the fittest or adaptation and called it ‘mutations’. They adapt – not mutate – rapidly to become resilient to ridiculously artificial nutritional regimes or drugs. Many do not adapt but die leaving naturally resilient strains to survive and reproduce.
  They need to prove beneficial, irrefutable, progressional mutation happening in nature by pure chance. What do they do? They quote from reactions to the most highly-artificial interference imaginable –progressively trying chemically to exterminate an organism – which eventually, screaming in pain – ADAPTS. Yes, this is palpably not the mutation Darwin espouses. They are literally scraping the microscope slide for examples. This is so far from mutation that even a bacterium could see the difference. Even I can see the difference.
  These tiny creatures bravely step up and prove that Darwin has far, far less than a balance of probabilities on his side – never mind proof beyond any reasonable doubt – and forget scientific evidence. And yet the atheists insist on scientific proof from the faith-head-blockheads and roar with laughter at us. Here is ocular proof that their own faith relies on fantastic nonsense. Yes, we must admire them as a men of truth and scrupulous research but also faith. They have indeed absolute faith in immaculate mutation.
  
  

Lactase Persistence in Humans – Moo, moo, moo. (No, stop laughing. They are being serious.)

• The claim is that drinking milk after weaning is unnatural and therefore cow’s milk is unnatural for adult humans and man was originally lactose intolerant. We are told that the ability to drink milk without ill effects arose some 7,500 years ago via mutation and this tolerance spread through natural selection in dairy cultures.
• Single nucleotide polymorphism (SNP) in MCM6 gene enhancer (-13910*T allele) allows adult lactose digestion. This little unpronounceable mouthful is at the centre of this scam.
• The claim is that we mutated and kept this mouthful gene enhancer so we could go milking. Even if it is true – which not proven – we always had this thing as babies. ADAPTATION. Ever heard of it?
• This is sheer insanity – mad cow disease bigly – this is obviously adaption and described as such. The entire argument is that as infants we are tolerant and then we become intolerant after weaning. So an innate tolerance has been switched off, as it were. Then, in dairy cultures, adult men developed tolerance once again even after weaning and continued the lactose tolerance, but now to cow’s milk. So the entire process is palpably the use of an inherent trait. An adaption. Further note the easy slide between human milk and cow’s milk. Also, sheep and goat milks were consumed for eons before the dairy cow era.
• The mutationalists are actually openly using a non-mutation to prove – mutation. Huh? Now had we all mutated into calves – then I may accept the theory – possibly. But this does not seem to have happened.
• Further, much of today’s USA middle class lactose intolerance is described as hype. Yes, of course it really exists. Yes, globally, perhaps over half of population groups in non-dairy cultures can be affected, but not uniformly. It’s rare in Northern Europeans, common elsewhere. In the US, it’s significant but affects specific groups who do not live the dream and swallow great glasses of milk and milk shakes. The hype level is moderate to high in pop culture. It has become very cachet indeed amongst celebrats and their clade and admirers. Many self-diagnosed cases are overstated or misattributed, fueling unnecessary dairy avoidance. If you suspect it, get tested—most can handle some dairy, and lactase supplements work well.
• Dairy-based cultures however of course do test this propensity in their populations and strongly challenge them to adapt and tolerate milk – and so large numbers do adapt and continue to be tolerant after infancy. Even if we thus adapted – not mutated – to be able to drink our Neolithic milkshakes, the single nucleotide polymorphism (SNP) in MCM6 gene enhancer (-13910*T allele) has always been present in our systems and merely was called into use as we suddenly began keeping cows. In ‘non-dairy’ cultures, there was no need to adapt – note that little word – ‘adapt’.

Citrate Utilization in E. coli (Lenski Long-Term Experiment) Back to poor old e-coli.

• After ~31,000 generations, a mutation duet (promoter duplication + gene activation in citT) allowed aerobic citrate digestion— but this not proven as a new trait. It was probably always inherent.
• The ‘evidence’ is drawn from frozen fossils theoretically ‘replayed’ which allow potentiating mutations. That, in English, means that in the thorough and actually brilliant research of Blount et al., described in 2008, 2015 in Nature and eLife, scientists could (in theory) “thaw” or ‘revive’ ancient DNA from fossils preserved in ice or permafrost, then “replay” evolution by letting those ancient organisms live and evolve again in a lab—like rewinding and re-running an old movie of life’s history.
• Before that replay could happen, certain key mutations would have to occur first. These “potentiating” (enabling or priming) mutations are the ones that set the stage, making later big evolutionary changes possible.
• If we could restart evolution from ancient, frozen life forms, the genetic changes that open the door to new traits would need to happen before the more dramatic shifts we see in the fossil record. But are not ‘dramatic shifts’ – only mis-read as such. They all are simply different species whioch never mutated nowhere, ever, honest Injun.
• But most tellingly, it would appear that, subject to specific confirmation, it seems Blount et al. did brilliantly show how to “replay” evolution using lab-preserved living fossils, but they did not actually work on actual DNA from the relevant periods. They recreated laboratory produced DNA. This seems to have zero connection to reviving ancient DNA from ice or permafrost. The reader should research this, but as far as I could establish, as yet, they have not actually managed to conduct direct research on this. Confusion likely stems from the term “fossil record” in the LTEE (frozen samples), which is a metaphor—not literal geological fossils.
• Blount et al.’s work is a masterpiece of controlled, modern experimental evolution using revivable lab archives—but has no link to ancient fossils. True ancient evolution if found would have to be studied using the structure, function, evolution, mapping, and editing of genomes – the complete set of an organism’s DNA (or RNA in some viruses), including all of its genes and non-coding sequences. We have only suggestions from a plastic model in a sense. So actually, we are still without a scintilla of proof.

Nylon-Eating Bacteria (Flavobacterium)

• Frameshift mutation was loudly claimed for the nylonase gene (nylB) created enzyme digesting nylon-6 byproducts. Arose post-1935 (nylon invention).
• The evidence was hopelessly flawed. But of course no-one whispered about that. ‘Grasp any straw’ is the normal standard of transparency.
• The detail again is utterly damning. I bring it here absolutely to crush not the research but its inappropriate use as proof.
• Overview of the Nylonase Case
• The nylonase enzyme (specifically the 6-aminohexanoate-dimer hydrolase, EII, encoded by nylB on plasmid pOAD2 in Flavobacterium sp. KI72, now often reclassified under Pseudomonas or related genera) is frequently cited in evolutionary biology as evidence for frameshift mutations generating novel metabolic functions. Nylon-6 manufacturing began in 1935, and byproducts like 6-aminohexanoate cyclic dimers accumulate in wastewater. The strain was isolated in the 1970s from such wastewater, and the enzyme hydrolyzes these dimers (not linear nylon-6 oligomers efficiently).
• The key claim (e.g., from Ohno, 1984) is that a frameshift mutation in a duplicated nylB’ (altered form of nylB) relative to an ancestral gene created a new reading frame, yielding a protein with nylon-digesting activity that did not exist before. Evidence includes:
• Plasmid transfer: Conjugative transfer of pOAD2 confers activity to other bacteria (Ohno, 1984; Negoro et al., 1980s–2000s).
• Specificity: EII prefers cyclic dimers over linear ones; kinetic studies confirm activity (e.g., Negoro et al., 1983, 2007; K_m ~0.5 mM for dimers).
• However, this is not a valid example of a de novo frameshift creating a novel enzyme, unless you have a very urgent need to mislead. Below are the main weaknesses in the proofs, substantiated by sequence data, functional analyses, and evolutionary interpretations.
• 1. No Actual Frameshift Mutation Occurred in nylB (EII)
• Core Issue: Ohno (1984) proposed a frameshift in nylB’ (encoding EII’) based on aligning it to a putative ancestral sequence, claiming it shifted the reading frame to produce nylonase activity. However, genome sequencing shows nylB and nylB’ are separate genes from an ancient duplication event, not frameshifted versions of each other.
  • nylB (EII): 1,176 bp, 392 aa protein with high activity.
  • nylB’ (EII’): 1,176 bp, but 99% identical at nucleotide level, differing by ~4–6 silent/substitutions; protein identity ~88–95% (depending on strain).
  • No insertion/deletion (indel) creates a frameshift; both are in-frame from the duplication.
• Evidence Against Frameshift:
  • Full plasmid sequencing (e.g., Kato et al., 1994; GenBank accessions) reveals no indels disrupting the frame.
  • Homology: Both align to carboxylesterases (e.g., nylA on same plasmid encodes EI for linear oligomers). The “shift” was an artifact of Ohno’s manual alignment ignoring codon boundaries.
  • Modern analyses (e.g., Prijambadi et al., 2008; Yasuhira et al., 2010) confirm duplication predates nylon, with divergence via point mutations, not frameshifts.
• Implication: The mutation is gene duplication + point mutations, not a frameshift generating novelty. Frameshift claims are debunked.
• 2. The Enzyme Is Not Truly Novel; It Evolved from Pre-Existing Promiscuous Activity
• Ancestral Function: nylB descends from beta-lactamases/esterases with broad substrate promiscuity. Ancestral reconstruction (e.g., Ohno’s own lab later; Negoro et al., 2007) shows the pre-duplication enzyme had weak activity on nylon dimers (10⁻³ to 10⁻⁴ relative to EII).
  • EII specificity arose via 2–5 amino acid substitutions (e.g., Thr267Ala, His266Asn in substrate-binding pocket; Yasuhira et al., 2010, site-directed mutagenesis studies).
  • No need for frameshift; activity amplified from latent promiscuity (common in enzymes; Khersonsky & Tawfik, 2010).
• Non-Specificity Critique: EII hydrolyzes esters generally, not just nylon byproducts. It acts on penicillin analogs and non-nylon substrates (Kinoshita et al., 1981). “Nylon-eating” is overstated—it’s wastewater-adapted, not de novo.
• Timeline Weakness: Duplication likely pre-1935 (possibly millions of years ago, given divergence). Selection post-1935 refined it, but the core scaffold existed.
• 3. Experimental and Interpretive Flaws in Key Papers
• Ohno (1984): Relied on partial sequences and hypothetical alignments. Claimed frameshift without indel evidence; ignored that nylB and nylB’ are co-expressed and both active (EII’ has ~1% activity of EII).
  • Later retracted implicitly by Negoro/Ohno collaborators (e.g., Okada et al., 1983; Negoro et al., 1992).
• Plasmid Transfer (Valid but Limited): Confirms plasmid encodes activity (Negoro et al., 1980), but doesn’t prove mutational mechanism. Transfer to E.367 coli yields active enzyme, but no frameshift demonstrated—sequence is intact.
• Specificity Studies (Negoro 2000s): Use purified EII; confirm k_cat/K_m ~10⁵ M⁻¹s⁻¹ for dimers. But:
  • No comparison to true ancestral (pre-duplication) enzyme under identical conditions.
  • Mutagenesis shows single swaps (e.g., Gly to Asp at 181) boost activity 100-fold without frameshifts.
• 4. Broader Evolutionary Critiques
• Not De Novo Creation: Maximum novelty is tuning promiscuity via 2–5 point mutations post-duplication. Frameshift would likely produce non-functional protein (99% of random frameshifts are deleterious; Eyre-Walker & Keightley, 2007).
• Population Genetics: Strain from pond with ~10⁹ bacteria/mL; rare duplication + mutations plausible in large populations, but not evidence for frameshifts driving innovation.
• Alternative Explanations: Horizontal transfer of plasmid (common in Pseudomonas); activity may predate nylon in natural ester-rich environments.

Sickle-Cell Trait and Malaria Resistance. A sickly stunt.

• Point mutation in hemoglobin beta gene (Glu6Val) causes sickling but heterozygotes resist Plasmodium. (English translation – sickle cell anaemia kills you – but you may not catch malaria if any is around before you die.)
• Evidence: Population genetics in Africa; balanced polymorphism (Allison, 1954).
• Now the true perspective:
• We know that one type of mutation does occur frequently throughout practically all life forms. It is the fatal destruction of the template by cell mutation as in carcinomas and other diseases. This is often misquoted or distorted into ‘beneficial’ mutation.
• The favourite scam is this sickle cell anaemia. This is a disease with severe symptoms that would mean death by starvation in a hunter gatherer world. Within the sufferer’s DNA, mutations occur transforming healthy cells into deadly sickle cells. This causes blood-clotting, pain and weakness. Carriers do not have the disease but can pass it on. This in itself jeopardises their line’s survival in evolutionary terms.
• At this stage the reports become bizarre. The claim is that there is a powerful and wonderful ‘beneficial’ effect. This is that sufferers and carriers are not susceptible to malaria. The guy is dying of sickle cell anaemia or will pass it on to his children and you are congratulating him that if he were to be bitten by an infected mosquito, they would still die of sickle cell anaemia not malaria. Mazel Tov!
• Wow. So, a mutation that makes you dysfunctional and threatens your offspring has a side effect which means you won’t be killed by malaria if you live long enough. And do we find huge populations of people with this mutation surviving in malaria ridden areas? Are they the fittest – surviving and grinning as they watch the funerals around them? No way. They are all long dead and do not reproduce. And you call that a beneficial mutation? Mutation schmutation. Yes, I know, if we could capture that mutation and harness it we could immunise the world. But that is irrelevant to our discussion.

CCR5-Δ32 Mutation and HIV Resistance – sorry another drenching in pseudo-‘aren’t we clever’ jargon.

• This is a negative mutation of a particular gene which seemed to confer immunity to smallpox and perhaps, HIV.
• The only evidence is functional studies centred on smallpox historically (Galvani & Slatkin, 2003).

Now the truth in the necessary detail:

While CCR5-Δ32 is a perhaps example of a recent human adaption under selection, several limitations weaken its use as proof, particularly for smallpox-driven selection. These stem from incomplete evidence, alternative explanations, and biological nuances:

Thus, attaching an evolution tag is ridiculous. Proving the claim that “mutation arose and spread due to advantage” requires ruling out all other more likely explanations such as drift/admixture; statistical power is limited by sparse aDNA.

Lack of Direct Evidence for Smallpox Protection:

Galvani & Slatkin (2003) used mathematical modelling to show that a lethal pathogen like smallpox could drive Δ32 to observed frequencies if it conferred ~10-20% survival advantage per epidemic. However, this is complete speculation – indirect—no historical records, archaeological DNA, or experimental data confirm any role in respect to the causative agent of smallpox (now eradicated) or how the virus infects a human host, replicates, spreads within the body, and causes disease

CCR5 is not a known causative agent; smallpox enters via other pathways (e.g., unknown mechanisms or possibly EGFR). In vitro studies show small pox causation can infect CCR5-deficient cells, and no epidemiological data link Δ32 homozygotes to smallpox survival in outbreaks (e.g., 18th-19th century Europe).

Galvani & Slatkin (2003) used mathematical modeling to show that a lethal pathogen like smallpox, yes, theoretically, could drive Δ32 to observed frequencies if it conferred ~10-20% survival advantage per epidemic. However, this is indirect— there are no historical records, archaeological DNA, or experimental data confirm CCR5’s role in variola pathogenesis.

Alternative Selective Pressures:

Other pathogens: Evidence suggests protection against other poxviruses (e.g., monkeypox in modern cases) or bacteria (e.g., Chlamydia or Yersinia pestis in plague models). A 2018 study (Weinberg et al., J. Infect. Dis.) found Δ32 associated with reduced West Nile virus severity, hinting at broader antiviral roles.

Non-pathogen factors: Genetic drift in small founder populations (e.g., post-Black Death bottlenecks) or linkage to nearby beneficial alleles could explain spread without strong selection. The mutation’s clinal distribution (high in North Europe, low in South/Asia/Africa) aligns with drift as much as selection.

Weakness: Smallpox is a “just-so story”—plausible but untestable without time-machine evidence. HIV resistance is modern (HIV emerged ~1900s), post-dating the mutation’s fixation.

Incomplete HIV Resistance:

HIV resistance is a “free lunch” today – actually irrelevant historically— and indeed undermines using it as primary proof of past benefit. All it does is simply demonstrate balancing selection (benefits vs. costs) rather than unidirectional advantage or any process such as mutation..

Dating and Demographic Confounds:

This small pox resistant trait is deemed to have developed about 700 years, or ~25-30 generations ago but its actual effectiveness against smallpox is in no way proven and a mere suggestion. Population migrations, plague and many unrecorded factors could have accounted for smallpox variations.

The Finches – At Last The Faithless Finches Fix

Darwin’s lack of perception and limitations are clearly illustrated by those so famous Galapagos finches. I deal later with the other animals claimed to prove mutation and show how they actually absolutely disprove it. Indeed I call them as witnesses and allow you to cross examine them and see how speculation and faith have perjured their testimony.

However I mention the finches here because, even whilst they disprove mutation – yes, you read that correctly – see just below – these little birds show how the Darwin machine began rolling. The propaganda states that ‘Darwin’s Finches’ clearly ‘proved’ mutation by allegedly mutating into different species with differing beaks. The problem is that the world’s greatest experts, Peter and Mary Grant, devout Darwinists, who lived on the Galapagos for years working on these birds, have proven absolutely that this is fiction and the exact opposite of the truth. They remained precisely the same species with temporary adaptations.

Darwin noticed differences between the mocking birds of South America and three Galapagos Islands. This led him to think about adaptation. He did not notice the finches particularly. He collected what he thought were different species of bird and when these were shown to experts in London they told him that many were all one species – finches. Their beaks had adapted to different food types.

He concluded from others’ observations that these were adaptations within one species. They were not ‘Darwin’s Finches’. This whole idea was invented decades later as part of the proof that new species evolve. Darwin himself clearly stated that in finches there was absolutely no evidence of mutation into another species at all. He wrote in his journals:

 … these variations are ‘utterly inexplicable in the ordinary view of the independent creation of each species but are explicable on the view of the colonization from the nearest and readiest source, together with the modification and better adaptation of the colonists to their new homes …’

Now that statement itself is very strange. Why, if you recognise creation, is it ‘utterly inexplicable’ that two different finches with diverse beaks could not be created? And if you reject creation – which Darwin did not – we note his acceptance of ‘modification and adaptation’.

It is relevant to state very clearly that today we know that these famous, fake-news finches are – not – not – different ‘species’. Fact: species means inter alia a group that breeds only within itself – if it means anything at all. These little birds can, do and always did interbreed with one another regardless of their home island, food type or beak shape.

Yes, when living in isolation, they married and settled down with the girl next door on that island – and both had the same beak. Yes, they seemed to have adapted their beaks to different foods on different islands. But the Grants – quoted in ‘Nature’ in ‘Speciation Undone’ – clearly state that the finches had always readily interbreed and indeed individual types on some islands are disappearing because of hybridization. Some have become extinct, 30% of the others are on that path and new hybrids are appearing.

Spotted the problem – that’s right – species are defined as creatures that cannot breed together. Huh? If by chance they can – the offspring are infertile like the mule.

So although constantly using the term ‘species’ for the different islands’ finches, the Grants repeatedly discuss hybridisation between them. Their different ‘species’ inter-breed successfully. And remember that their whole raison d’etre is proving the truth of Darwin’s observations.

So, think of mules whenever you hear someone using ‘Darwin’s Finches’ as proof.

Lizard Brains of Pod Mrcaru

Consider the ‘Lizards of Pod Mrcaru’ experiment. No, this is not a sequel to a Harry Potter book or even an offshoot from Tolkein et al.

We know that mutationists desperately needed rapid mutation or they were sunk and these lizards were claimed to have exhibited rapid mutation. The lizards themselves emphatically disagreed but they did not have the book rights, nor under European legislation, any Human Rights. After all, it was correctly argued, they were lizards not evolutionists. We meet this again and again with finches, fruit flies, mice, moths, guppies, whales, bacteria. Each has proved our mantras and that mutation is a myth and in every single case, reversible adaptation. Yet each is blindly used to ‘prove’ mutation.

But let us cross-examine these late, badly-used lizards and lay to rest the myth of ‘rapid’ mutation.

Italian wall lizards, Podarcis sicula, were moved from one island to another in an experiment. The first island was barren. The lizards survived there by eating mainly insects. This was pretty intelligent of them because there was very little vegetation – or even pizza. But extremely importantly, they did eat a small quantity of vegetation when they could find it.

In contrast, the second island had plenty of vegetation (but still no pizza.) You can guess the rest of the yarn. In less than 40 years, those lizards moved to the second island developed features which assisted in the eating and digestion of vegetation. They had different, stronger jaws – all the better for crunching fibrous plants with – and a slight adaptation in their guts – nominal cecal valves – all the better for digesting fibrous plants with.

And then? Repeat the mantras and then answer the question. Mutation is a myth. All of its claims are better explained by completely non-Darwinian, common-sense causes – all organisms have always had the innate ability to adapt and adapt back – within strict boundaries. This is adaptation not mutation.

Obviously, these lizards had no need of such features on their first island. But, most significantly, they did eat some vegetation on that first island. Thus, we are certain that their template allowed for vegetation-consuming features. These simply developed and adapted with their new diet and environment within their physiological template. The better veggie chompers were the stronger and had more kids. Note the word – ‘adapted’. Note the absence of the word – ‘mutated’. Difficult stuff this.

Proof # 1 – they remained exactly the same species – DNA proves this.

# 2 – when returned to the first island, they interbred with their old flames from back home on the first island.

# 3 – as above – their template allowed for vegetation-consuming features. They used to chomp veggies back home.

Proof 4 – they lost these ‘mutated’ features as soon as they were plonked back on the first island.

Proof 5 – we have no knowledge of the original 5 pairs of lizards transplanted. The population which descended from them certainly will have passed down their idiosyncratic features. These will have been greatly exaggerated through inbreeding. Perhaps two or three of the progenitors had bigger jaws and funny guts (sorry – nominal cecal valves).

As an insight into this, and as a comparison and parallel tale, consider the not inconsiderable Northern Elephant seal. It was on the verge of extinction from the greed of the greatest scourge ever to hit planet Earth – blubber hungry Homo Sapiens Avarus. All the world’s surviving stock disappeared except for 20 survivors on one Mexican island about 100 years ago. The Mexicans extremely sensibly simply shot poachers. All our elephant seals in the Northern hemisphere are their descendants and have therefore converging DNA and accentuated idiosyncrasies. This would be greatly exaggerated with only five original pairs of lizards.

Proof 6 – Further, the whole bigger jaw story seems strange – as many slim-jawed species of lizards eat only vegetation without mutating into mini-Tyrannosauri Regi. How come the original population of the second island did not have super jaws?

Proof 7 – A slightly different type of lizard already living on the second island did not, as above, have these ‘new’ features. This leads us to another question. These guys, the original inhabitants, had been there for ever and a day. They had been chomping vegetation for ever and a day. Why had they not developed the jaws and guts of the ‘mutating’ interlopers? Answer – simple. Their template did not have such features scripted. So they did not develop them. And to illustrate this particularly painfully, the old population of the second island were eliminated by the new population with the adaptive template.

Let us dissect this extremely carefully. The second island’s origin population of lizards – who had never adapted – were exterminated by the new-comers who did adapt. In other words, as is so often true, this example absolutely disproves mutation. Why did the second island’s indigenous population not mutate. They had a billion years so to do – or at least much longer than 40 years. The cost of not adapting was annihilation. Surely, they had every reason to adapt. They could not – so they did not. Dead lizards do tell tales.

Again, over-eager, bright-eyed faith-head mutationists have cooked their own goose – or lizard – and taken mutation down with them.

The Abuse Of a Pygmy People – Typical Darwinian White Supremacy.

A parallel example is that of the extinct Palau People. These pygmy inhabitants of a west-Pacific island group have been the subject of much speculation ranging from the insane to the hilarious. A cave of fossilised bones on Palau has borne a mass of theories of yet more ‘hobbits’ – Bilbo’s relatives some of whom also apparently inhabited Flores, an Indonesian island. The Palau were said to prove all things that the bright and beautiful have pronounced upon in relation to rapid mutation. The scientists muttered in awed whispers the tantalising probability that they had ‘mutated’ in just a century or so into very, very short, massively-built, long-toothed pre-humans from moderately short massively-built, long-toothed pre-humans. They changed certain attributes in nano-seconds – in mutational time – rather parallel to the lizards. So, we find ‘incredibly’ rapid mutation being used to support the theory of mutation.

However later studies (no, not by the Baggins family) decided this was a load of nonsense. The Palau were simply a group that either were normal pygmies but perhaps a little smaller in height, or had adapted – note the word – adapted to their island or had a large number of shorter but dominant males amongst them. But they were after all small, long dead and good material for a yarn – so no one actually stated that it is patently not ‘rapid’ mutation. And, more importantly, although abandoned on their island, they again failed to show any purported mutation over millions of years, a fact unsurprisingly ignored. That they are another piece of disproven, fantastic speculation is also amazingly not mentioned. Again, whatever the consequences or contradictions, mutation must be right.

Mickey Rock Pocket Mouse

Even smaller than ‘Palau Man’ is the incredibly bullied, poor little Rock Pocket Mouse. This brave creature disproves mutation quite clearly – but because it is so small and helpless, it has been forced to give false witness in favour of the god. We are assured that Rock Pocket mice have been snuffling around for as long as man has. For some reason however they were suddenly noticed in 2003. The story is precisely that of the lizards, guppies, pepper moths, fruit flies and other ridiculous examples.

I actually deeply understand the interest because I am rather fond of mice. I had a pet one as a boy – until I realised that this would involve cleaning its cage, taking it on walks in the park and training it to retrieve sticks etc. But perhaps my memory is confused.

The very sweet Rock Pocket mice are just about 3 inches long and skip about the desert rocks in southwest USA. They have a simple life, living within desert areas. Unfortunately this simple life includes birds of prey – mainly owls. Their only defence is to dive into the nearest crevice or burrow or rely on the camouflage their colour provides as they are a sandy colour. It was soon noticed (by zoologists and owls) that those on very dark basalt lava flows were not sandy. They were all dark – like the rocks beneath them. This set the mutationist mind thinking. Uh – The two populations – uh – blonds and brunettes – uh – lived separately on their – uh – respective dark or light rocks.

Now being zoologists and not owls they soon saw how this, like everything in the universe – proved evolution. And, bingo, this was not just mutation; this was rapid mutation. These guys changed their hair pigment as easily as having a colour rinse. Further, not only had these mice ‘mutated’ to fit in to their environment but also the DNA within each colour group had actually ‘mutated’ to reflect this. Sure, and mice fly. But, of course, hey presto, some brilliant research proved this so. The melanocortin-1 receptor gene responsible for pigment was different in each population. Even more amazingly, different isolated populations on different ‘islands’ of dark rock and light sand had independently gone to the local salon to change their DNA.

Unfortunately their Mexican cousins across the border did not show the same DNA results at all. But that little problem was brushed aside by saying it was ‘convergent’ mutation. This imaginary genie is a useful magical cure often shaken out of its bottle when evolutionists are in a tight spot. Two or more species exhibit a similar useful trait, for example flight in birds, bats and insects. They must have evolved. Right? They all fly. Right? They did not mutate their pre-wing limbs into wings similarly. Right? So they must have gone to different plastic surgeons for the same sort of job. Right? They all decided independently to solve their problems with a parallel mutation.

Thus the Mexican Rock Pocket mice had simply used a different means, agreed to by the drug cartels, to achieve the same colour changing result(!) Thus we have it all – mass, rapid, multiple and ‘convergent’ mutation!

Now had I been a mouse, I would be mighty impressed. But, I needed to have a few questions answered by the researchers.

The undisputed facts are:

The colour-changing thingy (agouti signalling peptide) indeed makes the mouse’s pigment change from dark to light by forcing the melanocortin-1 receptor gene itself to change. The gene is auto-set to change, was auto-set to change and will always be auto-set to change – as below. This how the thing works in all creatures – great and small.

Conversely, when this peptide is not active and the ‘default’ thingy – melanocyte-stimulating hormone – is dominant – the gene does not ‘mutate’ and the hair grows its default dark brown or black. This happens in almost every mammal exhibiting colour of skin or hair, including you.

That which prompts the (blond) agouti signalling peptide to become active remains a mystery. It seems, in human populations, however perhaps to be a response to dietary needs and vitamin deficiencies.

This has been going on since the beginning of time. It is not ‘mutation’ as in Darwin. It is simply that a single gene is switched one way in light mice from its equivalent in dark mice. Kill all the light mice and the resulting population – with the melanocyte-stimulating hormone – will have the dark characteristic.

On sand, darker mice are visible and eaten.

On basalt, lighter mice are visible and eaten.

They meet and marry dark and light mice without apartheid.

However, they do not marry dead mice, and the number of easily-seen surviving mice in their locality will be very small. Thus the survivors of the owls, who pair up will tend to be of the camouflage colour.

Generally, only favourably-coloured offspring will not be eaten.

The dark mice exhibit and pass on the ‘dark ordinary’ gene characteristic.

The light mice exhibit and pass on the peptide that forces a sandy colour.

If you move 1000 dark mice on to light sand and put up chicken wire to keep off the predators and evolutionists and isolate them from light mice – they do not change.

If you move 1000 light mice on to dark rock and put up chicken wire to keep off the predators and evolutionists and isolate them from dark mice – they do not change.

They have not had the guts to try the last suggestions. I challenge them to try. Get some chicken wire, dark mice and a hammer and nails. How long can it take? Unmolested the mice will not change; molested they will be eaten and only the other colour survive to breed.

In other words, the mice are not ending up mutating. They are ending up inside owls. Only the camouflaged mice stay outside owls. One of two gene ‘choices’ which have always been there within their DNA ensures the survival of the flittest. The population is adapting to predation by the survival of those with the flipped or non-flipped gene. Those owls are simply killing off the visible mice and this is no different from breeding by selection resulting in brindle Great Danes and sandy Great Danes. Men select dogs and owls – mice. We see this also in so-called micro-mutation just below.

So, we should not be surprised that the very examples put forward ‘proving’ rapid evolution, actually disprove it. Together with Palau-an Man, Italian lizards and Rock Pocket mice, we must soberly conclude that rapid mutation is a derisory piece of fantasy – but can always be relied to keep the sinking ship of mutation afloat a little longer.

That dick-billed platypus … talk about magic! No I’ll leave that creature to your imagination.

In addition to the inadequacy of all the above ‘evidence’ we must remember what all leading minds agree. Mutation is a miracle when viewed from a realistic balanced assessment of its possibility.

Everyone agrees that immutable laws of science and mathematics “utterly destroy” the concept of mutation. They, the atheist scientists, shake their wise heads and mutter, ‘It really is like a miracle. But we are here. And this is the only story available – to an atheist libertarian world.’ The following sections briefly outline how, indeed, probability, thermodynamics, and radiometric time constraints render Darwinian mutation completely untenable.

The Law of Probability

The Impossibility of Existence

Mathematically, the chance of life arising or different life forms developing from random mutation is impossibly low— millions of times less likely than you personally having walked on the moon. The odds of a functional organism or new species emerging through mutation are estimated at 1 in a trillion billion, making the event effectively impossible. Did you walk on the moon? What is the likelihood of you coming up with ‘That’s one small step for man, one giant leap for someone stuck in this spacesuit’. You had about a one in half a billion chance. Don’t fret – one cannot achieve everything.

Linked Sequential Events

Mutation depends on a precise sequence of beneficial changes. Because each step depends on the previous one, probability multiplies exponentially. For example, drawing three aces in a row from a pack of 52 cards has odds of 52 x 51 x 50 – just 1 in 132,600. Mutation involves trillions of such linked events—rendering the total probability zero for all practical purposes.

The Eye Paradox

Calculations suggest that the human eye would take 94.5 billion years to evolve through random mutation, while the universe is only 13–15 billion years old. A mere blink of the impossible eye.  Mutation, therefore, runs out of time before it can even begin! 

Cosmic Improbability

Physicist Roger Penrose—a Nobel prize scientist and mathematician and an honest genius who famously worked with Hawkins -—calculated the fine-tuning of the universe as requiring precision to one part in 10^10^123, acknowledging the absurd improbability of life arising by sheer chance. All the greatest unbiased scientists agree – but they keep silent. Why lose a good pension?

The Second Law of Thermodynamics: Entropy vs. Evolution

Einstein’s Second Law dictates that all systems naturally move toward disorder (entropy). Evolution, however, requires increasing order and complexity—a direct contradiction.

• Life’s Contradiction: Living organisms demand increasing order while the universe tends toward chaos.
• Chemical Impossibility: Under normal physical conditions, complex organic molecules disintegrate rather than form spontaneously. Mutation theory depends on “non-ordinary” conditions never observed in nature.

Who would you trust – Charlie Darwin – an upper class dilettante and failed-doctor who just managed to qualify as a clergyman or Einstein, who, one must admit, was pretty bright? And, by the way, Charlie was a complete plagiarist – stealing all his ideas from previous fantasists – including his own father. Again, see below the simple facts about this woman-hating, racialist, eugenics promoting amateur in our section on his ‘final advice to mankind’, the despicable book ‘The Descent of Man’.

Time Constraints and Radiometric Dating Problems

Running Out of Time

Even under conventional dating methods, life began around 4 billion years ago—insufficient for the trillions of beneficial mutations required for gradual Darwinian evolution.

The Cambrian Explosion

The “Cambrian Explosion,” where complex organisms appeared within 25 million years, is inconsistent with Darwin’s slow mutation. Critics call this “rapid mutation” theory “suicidal insanity” for Darwinian models.

Inconstant Constants

Radiometric dating depends on fixed physical constants. Yet if constants like the fine-structure constant (alpha) vary—as some evidence suggests—then all dating methods, and by extension mutation timelines, collapse completely! However if they do not fail – paradoxically they still  annihilate evolution.

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Logical and Observational Refutations of Mutation

The Single Relevant Fact: There is not one Observed Beneficial Mutation

The most damning argument against mutation is empirical:

“There has never ever been found one single beneficial mutation in any gene of any living organism.”

As fully proven above, while harmful mutations (e.g., cancer) are common, no proven beneficial mutation has ever been observed. The few examples touted are pathetic cries of double-speak or perfectly acceptable adaptations – not mutations – as below.

Adaptation, Not Mutation

Observable biological changes are adaptations within a genetic framework—not evidence of new species.

Examples of Reversible Adaptation – remember –

• Darwin’s Finches: Beak variations revert as conditions change. There is no speciation.
  
• Italian Wall Lizards: Developed digestive changes within decades, yet remain the same species.
  
• Antibiotic Resistance: Resistant bacteria pre-exist, they simply outsurvive weaker strains.
  

All examples show micro-adaptation, not macro- or micro-mutation.

Fraudulent or Misleading Evolutionary Icons

Fossil Misinterpretations

• Coelacanth: Declared a missing link—later found alive and unchanged.
  
• Tiktaalik: Fossilized footprints older than Tiktaalik disprove its “ancestor” status.
  
• Rodhocetus: Whale ancestor drawings based on speculation, not fossils.
  

Anthropological Hoaxes

• Piltdown Man: A complete forgery.
  
• Orce Man: A donkey skull misclassified as human.
  
• Ardi: A composite of 36 skeletons—no evidence of bipedalism.
  

Vestigial Organs and Natural Selection

The concept of “vestigial” organs—useless leftovers of evolution—is self-defeating.
Natural selection by definition should have removed useless traits, not preserve them for millions of years.
When functionality is found (e.g., whale pelvic bones support reproduction), the vestigial argument collapses entirely.

The Species Definition Problem

Darwin himself admitted:

“I was much struck how entirely vague and arbitrary is the distinction between species and varieties.”

If scientists cannot define “species” consistently, then the concept of “speciation through mutation” lacks a coherent foundation.

Darwin’s Own Words: The Nazi Manifesto

Beyond the scientific critique lies a sickening moral and philosophical one. We just need to scrutinize Darwin through his own words. There is one usually hidden work, The Descent of Man (1870) that truly showcases his bigotry. Rooted in elitism, misogyny, and racial hierarchy, you truly start to understand how evil and amoral he was. This is why the Germans embraced it.

Racial Hierarchy and Extermination

Darwin wrote:

“At some future period… the civilized races of man will almost certainly exterminate and replace the savage races throughout the world.”

He deemed this to be a healthy outcome!! This establishes a hierarchy where “civilized” Caucasians dominate “savage” races—a worldview identical with Nazi Germany and right-wing fascists.

Eugenics and the Rejection of Compassion

Darwin lamented that civilized societies protect the weak, arguing it was “highly injurious to the race of man.”
He hoped that the “weak and inferior” would refrain from marriage—an explicit endorsement of eugenic ideology.

Morality as Self-Interest

Darwin reduced wider altruism to merely the misdirection of the “instinct of sympathy” reserved for one’s own immediate ‘tribe’ who of course in reciprocity preserve you. This is all serving evolutionary advantage rather than genuine compassion. According to the book, this transforms morality into elitist self-preservation—ethics without empathy.

Darwin’s Admission of Adaptation, Not Mutation

Much has been credited to Darwin that he did not actually deduce. He had a sense of common sense modern mutationalists lack. Even Darwin conceded that finch variations were adaptations, not evidence of new species. He wrote of “modification and better adaptation” rather than mutation—confirming that all observed changes remain within the template of existing species.  This is carefully hidden from your average Joe.

Conclusion: Mutation, the Collapse of a Myth

From mathematical probability to thermodynamic law, from fossil evidence to Darwin’s own words, the mutation theory collapses under scrutiny. But the moral parameters of your lifestyle are based upon it. It was a failed, illogical fantasy which became instantly popular as soon as people realized that they could behave like animals if they in fact came from animals.

This is all proven beyond any doubt in ‘Mutation: Schmutation’.