SOTT FOCUS: Natural Selection – The Jesus of Evolution

4 horned goat evolution

Two horns weren’t good enough for survival, so natural selection made two more. Twice as many horns = twice as many offspring. However, a competing, equally ridiculous theory says these were a gift from Satan, whom these goats worship.

Listening to promoters of evolution, like Richard Dawkins, you get the feeling that natural selection is something utterly amazing, on par with Jesus. It’s this magical thing that sorts through random mutations, separates the good ones from the bad ones, lets the bad ones disappear, and ‘selects for’ the good ones, and we get cool new life forms. Whatever living things exist, and many are amazing, to be sure, we’re told that natural selection ‘made’ them. It gave us giraffes and birds and chameleons. But of course, this only makes sense if you don’t actually think about it for a few minutes.

Can natural selection (NS) really make things? How would it do that? What power does it really possess? Let’s reduce it to the simplest question – what really is natural selection?

“If something manages to reproduce, it passes on its genes to the next generation. Otherwise, not.”

That. That’s it. That’s all of natural selection. It’s not a force of any kind. It doesn’t “do” anything. It’s a passive process, or rather, a commentary on something that has happened. Basically all it says is that whatever survives, survives. Well, no shit, Sherlock. We kinda knew that.

So while it’s often talked about as if it was the Jesus of Evolution, it’s really nothing much. It doesn’t do anything; it doesn’t make anything. It just sits on the sidelines and says things like, “Oh look, this guy with the new mutation just had a baby. Oh, that other guy without the mutation also just had a baby. Weird.” There’s no ‘select for’ button. (Though if you read Dawkins’s books, you might well think there is.)

So how did NS get its almost godly status? Well, the theory that stupid, dead atoms just randomly assemble into better and better things couldn’t fool anyone for long, so something godly had to be introduced. Random mutations are random and thus follow the rules of entropy and make things worse, so the only other candidate was NS. I mean, we see all these amazing things around us, and we’ve decided that they have evolved from less amazing things, and any intelligent input is strictly forbidden, so it must be NS doing that. That’s the general idea.

NS turned out to be a great tool because most people can’t really imagine what it is, so evolutionists use it as a personification of a godlike force that can do just about anything, and for most people the concept is too vague to find any particular flaws with it. So it was established that NS gets rid of all these deleterious mutations, of which there are plenty, and that it ‘selects for’ the occasional, rare, beneficial ones. Make sense? If you said yes, then you haven’t really thought about it.

Turtle theory of evolution

This turtle evolved spikes to prevent other animals from sitting on it, which was always slowing it down. Its offspring production has skyrocketed since. Other kinds of turtles apparently never had this problem.

In order to determine how these mutations can affect the whole species, we need to understand the nature of mutations better. Firstly, the deleterious ones outnumber the beneficial ones thousands to one, so mostly we get the negative ones, pretty much all the time. If they kill the organism before it reproduces, the mutations are stopped dead in their tracks. And that’s about the only time anything significant happens according to the rules of NS. The mutated gene was bad, creature died, mutated gene’s gone, species continues as it was.

So what if a beneficial one appears? Well, first of all, we need to understand that any mutation is so small that its effects, especially the positive ones, are unlikely to even be visible. The negative ones can be, because one little bad change can screw up everything. One wrong nucleotide can result in a nonfunctional protein, which then fails to perform a function necessary for life, and the organisms dies. In fact, most so-called “positive” mutations are actually ones that break an existing gene, which ends up having an unanticipated positive effect, kind of like your passenger car seat falling out the side door, resulting in better gas mileage.

But what can one positive mutation really do, one that actually improves on an existing function? Even some bacteria have millions of nucleotides. Humans have three billion. So imagine an aeroplane that has millions of parts. You can guess that breaking one vital part can be deadly. But how could one small modification of one part out of millions make the whole noticeably better? If you make one tiny change to a plane, will anyone be able to tell that this plane is better than the other ones? Will the passengers say, “Oh, the flight was great today. This plane is much better than the one I flew with last time”?

In biology, the selection is supposed to be determined by survival rate. So the organisms with the mutation must survive a lot more than the others, on average, so that the mutation can spread in the population. But again, while a single mistake can have the power to kill off the whole organism, can a single small improvement to one part out of millions make the organism survive significantly more often that those without the mutation? In case of the plane, how could we modify one single part of the plane in a simple manner so that it functions significantly better than the other planes, to the point that the company can notice this and decide to make these new planes and not the old ones anymore?

You can probably imagine that this would be rather difficult. Even if a small improvement is made, the old planes still work like they always have. Now, planes don’t reproduce, but there’s a reasonable analogy here. For a mutation to become widespread, the mutants have to survive much more easily than the non-mutants, or the non-mutants have to start dying out for some reason. If a plane is slightly improved, we could theoretically dump the old planes and start making new ones, but the cost of dumping functional planes would be so high that obviously they’ll keep flying for a long time, basically as long as they can. And just like a replacement of a plane won’t happen quickly, it won’t with organisms either. Just like the old planes still perform the job just fine, so do the non-mutant organisms, and so they survive at about the same rate as the mutants.

Add to this the fact that the first mutant, despite some very small advantage, is just as prone to all kinds of dangers, from accidents to predators, that it may well die before the new gene even gets passed on at all. Just because this mutation is beneficial doesn’t mean the organism has to survive. As long as there are only a few of the mutants, they’re much more susceptible to being wiped out by a random disaster than the more numerous general population without the mutation. A beneficial mutation doesn’t prevent an organism from dying by any number of means. NS cannot ‘do’ anything. It’s not something that can take action. It’s something that just ‘happens’.

And this was the best case scenario – a mutation that’s beneficial and at least slightly visible. Most aren’t visible.

distribution of mutations

Above is a graph of a realistic distribution of mutations. Deleterious ones are on the left, beneficial ones on the right. As you can see, the beneficials are rare, and they’re actually exaggerated many times in the graph. The small triangle to the right of “0” should really be so small that you wouldn’t even see it, but then… you couldn’t see it, so it’s magnified. The mutations at “0” are neutral, i.e. they don’t affect the organism in any way. (If you’re curious how this is possible, consider that usually several codons code for the same amino acid. For example, CCU, CCC, CCA, and CCG all code for Proline. So the last of the three nucleotides can mutate into any of the 3 other letters without affecting the outcome. And this is just one example of a neutral mutation.)

So we can see that most mutations are on the negative side, close to being neutral. We call them near-neutral mutations. They don’t improve anything and cause very slight and/or occasional damage, but it’s not significant enough to affect the organism’s survival rate. People survive and reproduce even with pretty bad genetic defects, which can involve many mutations, so one small mutation that does a little damage somewhere won’t be visible on the level of the whole organism. It may just cause the production of certain chemicals to be slow.

If you’re wondering about how such things would affect you, think about cases such as you getting out of breath a bit quicker than others while running, or having a bit of a trouble falling asleep, or handling cold weather worse than others, or bruising more easily, or being unable to digest certain proteins, or being bad at mathematics because your neurons fire less efficiently, and so on. It’s clear that these things are detrimental and make you ‘worse’ rather than ‘better’, but you can just as easily see that none of this even remotely prevents you from surviving or having children.

This means that while you – and all the rest of us – are suffering from any number of small defects, NS is blind to them because you still survive and have children, and your slightly defective genes get passed on to the next generation. Such mutations are in the ‘No Selection Zone’ in the picture. This is a zone where the mutations aren’t significant enough to change your survival rate compared to others around you. And the zone works just as well for the beneficial mutations.

Think of the people who are somehow slightly ‘better’ than the rest of us in some way. The fastest runners, best fighters, smartest scientists, and so on. Does NS ‘select for them’ and over time create a population of fast runners and smart scientists? Clearly not. The incidence of such people in the population over time is still about the same. These characteristics give them some advantage, but don’t make them reproduce more than the rest of the population. So we can see that even fairly significant advantages have little to no impact on survival and reproduction. Plus a smart scientist can be fat and lazy and sick, and the fastest runner can be totally dumb, which gets us to another point.

Since detrimental near-neutrals are the most common and invisible, they keep accumulating in the genome over time. So when you actually get a beneficial mutation, you already have hundreds or thousands of detrimental near-neutrals in your genes. So any improvement comes along with a baggage of detriments. Mutation happens at the level of nucleotides; NS happens at the level of the whole organism. There’s no way to let only a part of your genome survive. And along with the near-neutrals, you may easily pick up a few not so neutral ones.

For example you may be a really smart scientist, maybe a Nobel Prize scientific material, but have a serious genetic disease that complicates your life somehow. So what will happen with regard to NS? Well, either you have children and pass on both the benefits and problems, or you don’t. There’s no way to separate one from the other. And if you pass on both, then over time, things only tend to get worse because negative mutations always accumulate much faster.

So any slow accumulation of beneficial mutations will always be accompanied by a rather fast accumulation of detrimental ones. Whatever benefit you acquire may easily get ‘broken’ in the future, but any damage you acquire is very unlikely to get fixed. So if you get one plus and one minus and pass them on, the future generations are thousands of times more likely to lose the plus than get rid of the minus. This is entirely logical if you think about entropy.

spider theory of evolution

Millions of years ago: “Oh what the hell?! What is this sticky thing suddenly coming out of my butt? Am I evolving again? Jesus Christ, what am I supposed to do with this?” (…Because first you get a mutation for producing the material and only millions of years later you get another one for knowing how to make a web.)

It should be becoming clear that even when beneficial mutations appear now and then, the genome tends to degrade overall anyway, and natural selection can’t reverse that. It has no power, no means to change that outcome. When you look at the distribution of mutations again, you see that the vast majority of all mutations are a) detrimental AND b) invisible to NS. This means that every organism keeps acquiring these all the time. The damage is slowly increasing in small steps, which is perfectly in line with entropy, but perfectly opposed to the idea of evolution. Things do not get progressively better. They actually tend to get progressively worse. The main effect of NS is not ‘selecting for’ anything, but eliminating the really bad damage, in the sense that whatever mutations kill the organism before reproductive age are prevented from propagating.

So where did anyone even get the idea that NS can create something good? Save for the delusional fantasies of Richard Dawkins, this notion mainly comes from what we see in very small organisms like bacteria. A bacterium is infecting humans, humans make a drug to kill the bacteria, bacteria are dying until one of them develops resistance to the drug through mutations, mutants survive while non-mutants die, and the bacterium has ‘evolved’ through NS (if you can call a man-made drug natural, which is debatable). Now, this does happen, but it’s opening a can of worms, so we need to slow down and look closely at what’s really going on here and why.

Probably the most important element we need to notice here is the environmental factor. The mutants live while the non-mutants die. Why? I said before that NS would have no power to ‘select for’ the mutants. The difference here is that the environment had changed. We’re not talking about bacteria living their usual life. We’re talking about bacteria in crisis, dying off because of a drug. So the thing that causes the huge difference in survival rate between the mutants and non-mutants is a new external factor, a drug that’s literally killing off the non-mutants. And this is about the only condition under which such a separation can happen. (And again, this drug is not a natural occurrence but a product of design, something supposedly nonexistent until the appearance of humans.)

If a certain fox develops a small beneficial mutation, normally it won’t make any difference for all the other foxes, and NS will have nothing to do. Only when a changed condition starts killing off the non-mutant foxes will there be a significant difference in survival rates. So it’s important to realise that this whole idea of NS ‘selecting for’ something comes from a case where external conditions had drastically changed (by design, with the actual intention of eradicating the bacteria) and is extrapolated to apply in general, which is highly unreasonable for reasons explained. This kind of mutation could only have an impact on larger animals during some widespread plagues. Under normal conditions, a small improvement in a mutant will have no impact on anything. So we could almost say that evolution by natural selection only works under unnatural conditions.

Toad evolution

Spikeless ancestors of frogs couldn’t compete with the evolved spiked frogs, so they died out. Wait, no, they didn’t… What the hell?

For evolution by NS to be true, trillions of mutations would have had to occur in the course of history. But for each of them to spread efficiently in the population, there would have to be a significant crisis for the non-mutants, so history would have to consist of one disaster after another, on a scale difficult to even imagine, never mind supported by any evidence. The ‘selective pressure’ that evolutionists like to talk about so much doesn’t exist 99.99% of the time. And even when it does, it is extremely unlikely that a single mutation will make a huge difference in an organism much larger than one cell.

But that’s not the only thing that separates bacteria from large organisms. There are several reasons why this kind of thing will be thousands of times more efficient in bacteria or viruses than in anything else. First of all, single-celled organisms mutate orders of magnitude faster than large organisms. This is logical. Short generation spans mean that instead of once every few years, you get a new generation with new mutations several times a day, plus there are far more specimens of bacteria than of larger organisms. Bacteria go through as many mutations in a few decades as many mammals have gone in their whole existence on Earth. So it’s not reasonable to expect that what we see in the bacteria’s resistance to drugs is even applicable to pines or bears. If it takes a few weeks for the bacteria to hit upon the right mutation to resist the drug (meaning hundreds to thousands of generations), it would take bears hundreds to thousands of years. But by that time, any plague would long have killed them off and be gone.

This is an important point. Bacteria is where most of any useful effects of mutations and selection have been observed, but it is also where the mechanism has thousands of times greater power than anywhere else. Extrapolating that this is how all species evolve is irrational.

There is a second important point here as well, though. Not only do bacteria mutate much faster, but the mutations also have a far stronger effect than in larger organisms. The drug resistance often results from only a single mutation. Now think about the difference between a single mutation in a bacterium and in a bear. In the bacterium, one nucleotide out of maybe a million has changed and has only one cell to affect. In a bear, one nucleotide out of maybe a billion has changed and has a creature of trillions of cells to affect.

The effect of a single mutation will be the strongest in the smallest of organisms, namely viruses and bacteria. In a larger organism, the mutation is likely to affect only a certain type of cells, like red blood cells or kidney cells. In bacteria, it affects the only cell there is, which is the whole organism. If a thousand cells die because of a mutation in a bear, the bear is probably fine. If one cell dies in a bacterium, the bacterium is dead. So mutations affect bacteria not only much faster, but also much more strongly. And again, biologists extrapolate from what they see in bacteria to all organisms, not taking into consideration that there’s a completely different context.

It’s true that the logic of “what happens in bacteria in days can still happen in bears in centuries, and evolution is slow” makes sense to some extent. But all creatures live in (more or less) the same environment, here on Earth. So think of it this way: The fast-mutating bacteria are fighting slowly-adapting human scientists. The slowly-mutating bears are likely to be fighting those fast-adapting bacteria and viruses. So not only do the bears need a lot more time, but they’re actually fighting something that’s a million times faster than them at adapting. So we cannot just say that if the bacteria can do something in a week, bears could do it in a century. There is a different context for each of them.

Keep in mind that we haven’t observed any kind of evolution directly in anything other than the smallest of organisms, which, as I have explained, are actually much more likely to undergo such changes than any other organisms, even considering prolonged time scales for the large organisms. So how reasonable is it to judge how large animals evolve from what we see in bacteria? Let’s recapitulate:

  1. New mutations can spread efficiently only when an external agent is killing off the non-mutants en masse.
  2. Single-celled organisms mutate thousands or millions of times faster than larger ones.
  3. Single-celled organisms are likely to be affected much more strongly than larger ones by small mutations.
  4. Environmental factors have more or less the same speed for everyone, so while bacteria will likely come across a useful mutation in time, larger organisms will likely die long before any such mutation occurs.

These points show that mutations and selection do have fairly strong effects in bacteria and viruses, but they also show that it’s because those are single-celled organisms that things actually work this well. It is very short-sighted to suggest that all organisms have evolved by this same mechanism. There is no reason to expect this to work on a large scale.

planthopper gears

If you can explain how natural selection ‘made’ the Planthopper’s gears from one random mutation at a time, over millions of years, please tell us.

Another very important thing worth noting is that these small organisms have never ‘evolved’ anything complex or really new. No new genes, no new organs, they never change from single-celled to multi-celled, and their basic structure is still exactly the same, even after millions of generations with billions of specimens. Most of the mutations that we’ve seen make a difference are single mutations, and at best we see two or three mutations working together. Which is about as much as we can expect when we do the math. With increasing complexity, the probability of success drops exponentially.

So there’s a paradox here: If there is environmental pressure, then what we get is quick hacks and a net loss of genetic information, rather than anything new and complex, and if there isn’t any environmental pressure, then there is no opportunity to evolve new things.

When we put together all the single-celled organisms on this planet, they have undergone more mutations just in our lifetime than humans or any other mammals have in all of their existence. But none of them have evolved into a multi-celled organism, none of them have produced a single new gene from scratch, and none have changed into a different species. Yet supposedly mammals, in whom mutations would have a much smaller effect, have transformed from one species into another? What reason is there to believe that?

The number of generations and specimens involved in the supposed evolution from monkeys to humans occurs in bacteria on the order of decades, yet they have zero new genes to show for it. So if we were to extrapolate from bacteria’s evolutionary achievements to mammals based on science and not fantasy, the conclusion would have to be that any significant evolution is extremely unlikely at best, even with 100 billion years.

Kangaroo evolution

The kangaroo’s pocket evolved very slowly. First it was so small that the kangaroo could only carry little items like a pen or a lighter. After millions of years, it evolved to carry little kangaroos, which was vital for their survival. How they survived before they had pockets is unclear.

Yet another fact is that even most of those mutations that create drug resistance or somehow increase survival in similar situations are still detrimental in a genetic sense (as opposed to in the sense of survival). Most of these adaptations actually happen by breaking genes, rather than by evolving something new or at least being genetically neutral. Often the bacterium gains an immediate advantage by throwing away something that would have been beneficial in the long run.

So not only does NS have little if any power in selecting, but it is also extremely short-sighted. Whatever quick hack will ensure survival right now is what will be passed on to the next generation. NS doesn’t care if other things get broken, as long as immediate survival is ensured. And that’s what usually happens – something specific is changed to ensure survival at the cost of breaking something else.

For example a bacterium may be able to metabolise different kinds of sugars. While getting a mutation that induces drug resistance, the gene for metabolising one sugar may be broken. As long as another sugar is available, NS doesn’t care that the organism has lost a useful ability. But in the long run, a part of the genome has been lost for a single mutation that happened to provide drug resistance, and it will never come back. The genome again degrades over time. Calling this evolution is somewhat misleading, to say the least.

So instead of saying, “If bacteria can do this in 30 years, surely fish can evolve into bears in 500 million years”, we should be asking ourselves, “If bacteria can only come up with 2-3 mutations together at most and never evolve anything complex while breaking many functional things, why would we expect that more complicated organisms would do any better?” The results are rather poor in single-celled organisms when looking at the big picture, and NS has far less power in larger organisms. And it should be noted that for anything significant to ‘evolve’, thousands of improbable mutations would have to pile up in a useful manner, and we’ve seen that it is difficult for even one to be established in the population.

Panda theory of evolution

“Hi, I am Panda. I have evolved to spend half of each day munching on bamboo because it helps me produce lots of little pandas. That’s why you see them everywhere.”

Let us look realistically at the idea that the giraffe’s neck has evolved by NS (for which there is zero evidence). The theory is that this happened one mutation at a time. But by how much can one mutation make the neck longer? Enough so that it increases survival rate? Will a giraffe with a 10 cm longer neck survive where another one will die? Hardly, given that 10 cm is well within the natural variation among specimens.

So what, one mutation made the neck half a metre longer? That certainly seems ridiculous, but this amount of difference would also need at least some of those changes in the giraffe’s blood circulation that ensure that its head doesn’t explode every time it drinks. And this illustrates the ever-present problem of evolution – a change too small has no visible effect and is unselectable, and a change too large cannot happen by a single mutation and is thus impossible.

How large a change actually affects survival and reproduction? This simple question, when explored even superficially, shows the lack of realism in evolutionary explanations regarding NS. It is easy to see that differences between two individuals involving hundreds of changes have no impact on survival rate. The natural variation of characteristics in many species is quite large. Size differences of 30% are not uncommon. And since they’re not disappearing, they clearly don’t affect survival rate.

A missing finger (or an extra finger) doesn’t affect survival rate, but that’s a larger change than the vast majority of mutations can produce. Even one eye missing is nowhere near ensuring that such a specimen won’t be able to reproduce. Animals with a cut-off tail have generally no trouble surviving, but according to the evolutionists, this tail could only have evolved under selective ‘pressure’, meaning the animals without it couldn’t survive next to the ones with it. It shouldn’t be hard to see that this doesn’t make any sense.

What exactly are those mutations that are so small that you can’t see them but so significant that those who don’t have them die much faster than those who do? Can anyone show me such mutations in multi-celled organisms? Can anyone show me a mutation of one nucleotide in an animal that visibly increases the survival rate of the mutants compared to the non-mutants? When I put the question like that, does anyone actually believe such a thing exists?

caterpillar evolution

Whatever’s going on here is absolutely essential for survival (or helps produce more offspring). Otherwise it couldn’t have evolved.

So what can and what can not happen as a result of natural selection? The key appears to be the difference between changes in existing variation and appearance of new features. Small modifications of what already exists are certainly possible. Creation of completely new structures (new organs, new genes) is still undocumented and unobserved, after 160 years of searching and bragging about how awesome evolution is. Dog breeding shows selection (by design) from existing variation, with clearly observable limits to how far these changes can go. But evolution would need to go way beyond these limits, way beyond changes in existing variation. It would have to produce variation that didn’t exist before.

For all the variation that we see around us to appear in the first place, some kind of consistent massive input of information over the course of billions of years is needed. An input that NS cannot provide, and neither can random mutations. Random mutations won’t produce a new organ any more than glitches in a computer will produce a new program. And if random mutations don’t produce the raw material, NS has nothing to build from, even if it had the ability.

But there’s much more that speaks against NS being an effective evolutionary tool. For example, lots of organisms have a complex social structure where the survival of individuals is tightly connected to the survival of the whole group. So if one individual has a new mutation, NS can’t do anything about it if the group acts as a whole. How would one ant have a better survival chance than the other ants? What about animals that hunt in groups? One catches prey, and they all eat. Where’s the selection?

If a whale swallows ten thousand shrimp in one bite, did the slightly genetically improved shrimp escape? If a tornado destroys everything in its path, do the most genetically fit animals survive? If a river gets poisoned, how are the animals drinking from it selected for survival based on mutations? If an area becomes devoid of food, it is no good that a specific individual is ‘evolving’ better lungs, even if that was possible in the first place (which, judging by the evidence, it isn’t). It is extremely difficult for any efficient ‘selection’ to occur, and many environmental and other factors affect everyone the same, ignoring genetics.

And then there’s of course the case of humans, the ultimate species to prove that NS is almost completely impotent. Even the stupidest, slowest, laziest, and most incompetent of humans are perfectly capable of having sex and producing offspring. In fact, because they’re stupid, they often do a lot of that, because they don’t really know how to do much else, which was so nicely depicted in the movie Idiocracy.

Black rooster evolution

This animal failed to evolve appropriate camouflage, so instead it has evolved a stare that turns you to stone.

It is also interesting to reflect on how the idea of NS has led to many stupid ideologies, culminating with Hitler’s Nazism. What’s really interesting about it is that these ideologies were meant to ‘help’ natural selection because it was observed that NS wasn’t really working. Hitler decided that Aryans were cool and Jews were lame, and because NS wasn’t taking care of it, he created the other NS, National Socialism, to ‘fix’ that problem.

But it wasn’t only Jews that some parts of the society wanted to get rid of at various points. It was also people like cripples. You know, the people who, if NS worked properly, should have been eliminated naturally. But clearly that wasn’t happening. In the end, both Darwin’s NS and Hitler’s NS turned out to be failures in terms of achieving the required goals.

Just like the Biblical Jesus is based on a real person (or several) but is largely made up, so natural selection, as seen by Darwinists, is based on a real process but largely made up. Macroevolution by natural selection is a story, just like Jesus walking on water. Neither walking on water nor evolution of a new organ has ever been observed, and both violate established scientific principles. Based on our real-life experience, gravity or entropy don’t just disappear when we wish so. Natural selection exists, but just like Jesus, it can’t ‘perform miracles’, which is what’s required for the Darwinian model to be true.

So the next time you hear some smartass tell you that natural selection has created this or that amazing creature, demand a realistic explanation of how exactly that happened, as opposed to the implied “natural selection waved its magic wand, and there it was”.