The theory of evolution is battered and scarred. As I have explained already, it faced an existential crisis in the 1930’s from which it only just recovered through bluff. It faces another crisis today. Now let’s investigate some of the currently trending evolutionary arguments to see how well they match reality and how many assumptions they use to
Since the turn of the century, knowledge of the astronomical complexity of cellular biology and the genome has been exploding, and neo-Darwinian evolutionary theory is under threat once again. In order to save it, many new intellectual concepts are currently emerging that go under the umbrella term of the “Extended Evolutionary Synthesis“. This extended synthesis incorporates new ideas such as evo-devo, epigenetic inheritance, niche construction, junk DNA, Shannon’s Law and gene duplication. The final section of this essay will now deal with the supporting arguments for this emerging extended evolutionary synthesis, as well as some others traditionally used by leading human geneticists trying to keep evolutionary theory going in the face of mounting evidence to the contrary. As you read please be aware that Occam’s Razor takes a very dim view of theories with lots of built-in assumptions.
1. Junk DNA and Neutrality
Many geneticists (and blog sites) actually still cling to the now out-dated belief in junk DNA. We currently know that 80% of the human genome is functional and the more non-protein coding DNA an organism has, the more biologically advanced it is. By erroneously assuming most DNA is junk, many papers will then logically decide that most deleterious near-neutral and minor mutations are completely neutral in their biological effect, while all the rare but significant harmful mutations can be eliminated via natural selection. These false assumptions free geneticists to intellectually concentrate on how the one-in-a-hundred-thousand beneficial mutation can lead to upward evolution. This argument is slowly disappearing from educated commentary.
2. Evolution Now Complete
Alternatively the assumption is made that mutational evolution is now largely complete, so no new mutations are needed to increase genetic fitness. This is sometimes given as the reason why we do not see mutations leading to greater genetic complexity today, and why they are now more harmful than beneficial. Similarly, some geneticists will assume that adaptive mutations are now balanced with deleterious mutations, so we see little species advancement. In essence both are arguments justifying the absence of evidence and admissions of the non-existence of evolution.
3. Sexual recombination
This argument is also used as a solution to the problem of increasing mutational load. It assumes that, because the deleterious mutations become recessive, they eventually leave the genome due to mixing at reproduction. This was first popularised by Herman Muller. With the mutation rate now known to be over a thousand times higher than his feared upper limit, combined with the problem of linkage blocks, mutational near-neutrality and asexual duplication in our mitochondria and Y chromosomes, sexual re-combination is no longer a valid argument. At best it slows an inevitable decline to mutational meltdown and extinction. At worst it accelerates mutational load if the male is old.
4. Truncated Selection and Other Tricks
Many leading population geneticists will resort to the assumption that natural, and sometimes artificial (truncated) selection can eliminate all deleterious mutations faster than beneficial mutations build new genetic material. One recent research paper had to assume truncated selection, perfect heritability of all mutations, 10% beneficial mutations and zero biological noise to get around the problem of the high mutation rate in mammals. Another study facing the same problem had to assume to static genetic fitness regardless of increasing mutational load, that all mutations relative and therefore neutral, a static mutational rate and the total selectability of all deleterious mutations at the phenotype level. Unfortunately most of these tricks of the trade are largely lost on other scientists who accept the flawed logic of population geneticists without question. It is only when you step outside the closed-minded evolutionary paradigm that these artificial fudges become clear for what they are.
5. Shannon’s Law
This is commonly used excuse by evolutionists and their bloggers when refuting intelligent design. However, Shannon’s Law concerns potential information, not actual functional information. It is like looking at the letters in a scrabble box compared to this paragraph. Shannon information was not developed to address biological information but data transmission down wires and radio waves. Claude Shannon, the founder of information theory, even warned against applying it to biological systems. It is entirely unsuitable for biological systems because Shannon information can be achieved through an increase in randomness. An increase of randomness can easily be lethal to individual biological systems. Increasing informational randomness across a species (mutational load) eventually leads to extinction. Because mutations cause this increase in randomness, many evolutionists will appeal to Shannon’s Law for backing, mistakenly thinking mutations build new information.
6. The E. coli experiment
One of the oft-used arguments in favour of evolution is that it takes so long that you do not see it in a single generation, thus it cannot be subject to laboratory experiments.
However, Richard Lenski is currently conducting a long-term experiment in “bacterial evolution” that has been going since 1988. He proudly boasts that it has become a “50,000 generation salute to Charles Darwin”. However, E. coli has 4.7 million nucleotides to a mere 13,000 in an RNA virus, a ratio of 360:1. Because each E. coli is only a single cell, it takes about 1,000 generations for a mutation to occur. The E. coli in the experiment have only had enough time to accumulate a few hundred mutations since 1988. During that same timeframe, an RNA virus would have been mutating a thousand times faster. Having said this, the E. coli experiment is already actually showing the first signs of biological decay. All “evolutionary” adaptation to the artificial test-tube environment touted by Lenski has so far involved either loss of regulation or loss of function. In addition, half of the E. coli’s genome involves functions completely irrelevant to the artificial test tube environment they now live in. Thus half the increasing mutational load is invisible to selection and to human observation. So the mutational load is actually increasing twice as fast as is being measured. Thus these “evolving” strains of E. coli are slowly degenerating to the point where they will only be able to live in a test-tube. If this experiment goes for several hundred years longer, it will show signs of significant genetic entropy, not advancement.
7. Gene Duplication
Duplications can be any copying mistake, from a single nucleotide, right through to whole chromosomes and genomes. Gene duplication is often cited as a new saviour for evolutionary progress and as a means of generating ‘new’ information. The theory states that the original gene continues to function as normal while the duplicate is free to create substantial new biological information, thus “fast-forwarding” the evolutionary process.
However, there are many assumptions and therefore problems with this recent poster-child scheme for evolutionary progress. Because of the ENCODE program we now know that DNA codes for both the construction of proteins and the regulation of all biological systems within an organism. Any disruption to these functions is detrimental to the future of that organism. Gene duplications, by their very definition, are a genetic disruption, confusing the functionality of the whole organism. In addition, they only duplicate existing information and always disrupt these existing exquisitely fine-tuned information pathways. This is why duplication of chromosome 21 is the cause of Downs Syndrome in humans. Genetic duplications are also the cause of many developmental birth defects as embryonic development is highly sensitive to correct levels of protein construction.
In the real world we know that gene duplication will also copy all the accumulated mutations in the original block of information. After the duplication, mutational degeneration will then continue in both genes at roughly the same rate. Reverse duplication could also cross-contaminate both genes again at any time in the future, further destroying the original code. In addition, the organism must now waste much more energy reading both sets of genes. The physiology of the organism is severely compromised as correct gene expression and regulation depends on exact DNA counts and copy numbers. Because of epistasis, gene expression at other sites near to the duplicated code is also compromised. The duplicated gene will always be less stable than the original, and natural selection is actually now less effective as there are two copies of the gene. All of these consequences will accelerate degeneration, not advancement.
Like most ideas in the evolutionary universe, the possibility of gene duplication giving rise to new functions is conceptually possible but vanishingly unlikely, and becomes more unlikely with each degree of complexity required for the development of new functions. How likely is new information to arise via the duplication of a letter, word, paragraph or page in this essay? Belief in gene duplication is biologically naive, but now firmly entrenched in evolutionary circles as it gives hope that the theory is correct.
8. The Sleeping Gene
In another “just so” evolutionary mechanism, a gene is duplicated, then turned off via another mutation, mutated over time, turned on again through a different mutation, and, voilà, a new function has arisen. This is not an argument from evidence, but from desperate necessity due to the emerging field of epigenetics.
Invariably, the people who use this as an argument never tell us the rate of duplication necessary, how many duplicated but silenced genes we would expect to see in a given genome, the needed rate of turning on and off, the likelihood of a new function arising in the silenced gene, how this new function will be integrated into the already complex genome of the organism in the future, or the rate at which the now silenced DNA would be expected to be lost at through natural selection. These numbers are not friendly to evolutionary theory. Why would anyone assume a deactivated gene would hang around for a million years or more while an unlikely new function develops? And in that million years or so multitudes of deleterious mutations have severely degraded the original gene.
9. The Persistence of Life
This argument goes something like this: If genetic entropy is true, then why are we still here, with little evidence of genetic entropy around us? Species such as mice, bacteria and viruses should have gone extinct long ago.
However, given the strict naturalistic rules of neo-Darwinian evolution, which is limited to mutations and natural selection, the extinction of all species on earth is absolutely inevitable! Mutations add no significant genetic information (let alone a whole genome), are almost universally deleterious, recessive, locked inside linkage blocks, almost universally invisible to selection, occurring at an astronomical rate and expanding in a linear fashion. On the other side of the coin, natural selection cannot see individual nucleotides, works on the phenotype rather than genotype, is disrupted by epistasis, epigenetics, environmental noise and homeostasis, and is always and at all times a loss of genetic information. Mutations and natural selection did not create the genome and are powerless to stop its continuous degeneration. The whole purpose of this essay is to blow the lid on the secrecy surrounding this fact, one increasingly acknowledged by the world’s leading geneticists no less.
This leaves the issue of time. Evolutionary theory assumes deep time. There are multiple lines of real world observations that suggest this is not a foregone conclusion. In the biological world mice go through hundreds of life cycles to every human generation, subjecting them to more efficient selection, but genetic entropy is still visible. Bacteria go through a thousand or more such selection cycles for every human life cycle and every cell is subject to selection individually. These facts lead to slower genetic entropy the smaller the species. Actually, humans should go extinct before most other species on earth as we have long lead times before reproduction and very few offspring. The only scientific reason why we are not extinct is the lack of time to go extinct.
Given the 100 to 1,000 mutations building up every generation in humans, we can easily calculate a maximum longevity clock for our species, going both backwards and forward. It should follow an exponential decay curve, and according to ancient Jewish records it is. Our genetic fitness levels are now only one-fifth what they were a mere 6,000 years ago. Extrapolating our linear mutation rate backwards brings us to perfect genome fidelity some 4,000BC. We now have over 10,000 genetically caused diseases and it is rare for a family on earth to be free of them. Some secular geneticists are now predicting future male fertility rates at 1% of today’s levels in another 100,000 years due to the current mutation rate in the male Y chromosome alone. There’s a word for that; extinction. Michael Lynch sees major deterioration in the human genome in just the next few hundred years. Extinction will occur in thousands, not millions of years. This is a fact, and one the human race does not want to acknowledge as it overturns all of its arrogant pride in independent self-advancement.
10. Evolutionary Development Biology (evo-devo)
This very popular theory suggests that a tool-kit of very ancient and conserved “homeobox” genes have suffered little degeneration over hundreds of millions of years inside most genomes. They act on gene expression at a fundamental level, cascading all the way through to physical development of the adult organism. They can thus create major changes in function originating from a tiny mutation at the nucleotide level. Evo-devo thus creates a mechanism by which individual nucleotides can create major leaps forward in evolution. An extra set of wings or a leg on the back of a grasshopper are often cited as examples of evo-devo.
However, evo-devo assumptions contradict the assumptions built into the primary axiom which says evolution can only undergo tiny and incremental changes while climbing Mt Improbable. It is in effect suggesting that a stumble can take you 1,000 metres further uphill, when we know from real world evidence that a genetic “stumble” on Mt Improbable can be lethal. It also assumes the genome as a bag of individual nucleotides that can have direct impact on phenotype, something population geneticists know is so rare it is nigh impossible. Assuming millions of years of evolution, evo-devo completely ignores the continued and rapid rise in genetic load for the genome in all other locations, leading to eventual extinction. All physical evo-devo changes are also subject to severe fitness valleys so would rarely if ever make it to a second generation.
Evo-devo, if taken to its logical conclusion would assumes we can get a new species from a few well-placed and timed mutations that replace and wipe out millions of nucleotides and old functions. This is like improving a book by adding words and removing chapters. Finally, study of homeobox genes demonstrates similarity between many species. Therefore, evolutionary time-frames assume they must have been immune from mutations for hundreds of millions of years. Because we now know how rapid and consistent mutational rates are across species, we know this to be a false assumption.
11. Mutation Count Mechanism (MCM) & Synergistic Epistasis
At least this argument acknowledges the danger that mutation load is to all populations, yet it still attempts to find a solution around it. It assumes mutations build up unequally across a population and when those individuals with a high mutational load are eliminated, natural selection has taken place at less cost to the population as a whole. Mutational load is thus contained. It is an argument of control not advance. This argument also places emphasis on the number of mutations while completely ignoring their severity. As we now know, only rare catastrophic mutations effect selection. MCM also ignores all observational data that the number of mutations varies little between individuals unless they are part of a very small population. In large populations genetic drift is not an issue. Mutation Count is incompatible with reality.
Another defensive argument, synergistic epistasis, assumes deleterious mutations may build up over time and synergistically amplify each other’s effects, causing the accelerated selection and elimination of the individual carrying those mutations. These events can indeed happen, but are exceedingly rare. All geneticists agree that mutations normally act linearly, not exponentially. If it does happen, synergistic epistasis simply accelerates mutational load, fitness valleys and extinction. It can do nothing more.
Given what you now know about the absence of evolutionary genetics and the iron-clad law of genetic entropy, the final part of this essay take you to the only logical conclusion available to us.