Header 1

Our future, our universe, and other weighty topics


Sunday, November 13, 2016

Epigenetics Cannot Fix the “Too-Slow Mutations” Problem

Recently in Aeon magazine there was an article entitled “Unified Theory of Evolution” by biologist Michael Skinner. The article starts out by pointing some problems in Neo-Darwinism, the idea that natural selection and random mutations explain changes in species or the origin of species. The article says this:

One problem with Darwin’s theory is that, while species do evolve more adaptive traits (called phenotypes by biologists), the rate of random DNA sequence mutation turns out to be too slow to explain many of the changes observed...Genetic mutation rates for complex organisms such as humans are dramatically lower than the frequency of change for a host of traits, from adjustments in metabolism to resistance to disease. The rapid emergence of trait variety is difficult to explain just through classic genetics and neo-Darwinian theory.... And the problems with Darwin’s theory extend out of evolutionary science into other areas of biology and biomedicine. For instance, if genetic inheritance determines our traits, then why do identical twins with the same genes generally have different types of diseases? And why do just a low percentage (often less than 1 per cent) of those with many specific diseases share a common genetic mutation? If the rate of mutation is random and steady, then why have many diseases increased more than 10-fold in frequency in only a couple decades? How is it that hundreds of environmental contaminants can alter disease onset, but not DNA sequences? In evolution and biomedicine, the rates of phenotypic trait divergence is far more rapid than the rate of genetic variation and mutation – but why?

As interesting as these examples are, they are merely the tip of the iceberg if you are talking about cases in which biological functionality arises or appears too quickly to be accounted for by assuming random mutations. The main case of such a thing is the Cambrian Explosion, where we see a sudden explosion of fossils in the fossil record about 550 million years ago, with a large fraction of the existing phyla suddenly appearing. Instead of seeing some slow gradual progression in which we very gradually see more complex things appearing over a span of hundreds of millions of years, we see in the fossil record many dramatic new types of animals suddenly appearing.

The other main case of functionality appearing too quickly to be accounted for by random mutations is the relatively sudden appearance of the human intellect. The human population about 1 million years years ago was very small. This article tells us that 1.2 million years ago there were less than 30,000 in the population. The predicted number of mutations is inversely proportional to the population size, which means the smaller the population, the lower the number of mutations in the population. So when you have a very small population size, the predicted mutation rate is very low. But suddenly humanity about 100,000 or 200,000 years ago seems to have got some dramatic increase in brain power and intellectual functionality. Such a thing is hard to plausibly explain by mutations, given the very low number of mutations that should have occurred in such a small population.

But Skinner tries to suggest there is something that might help fix this “too-slow mutations” problem in Neo-Darwinism. The thing he suggests is epigenetics. But this suggestion is mainly misguided. Epigenetics cannot do the job, because it is merely a kind of “thumbs up or thumbs down” type of system relating to existing functionality, not something for originating new functionality.

Skinner defines epigenetics as “the molecular factors that regulate how DNA functions and what genes are turned on or off, independent of the DNA sequence itself.” One of the things he mentions is DNA methylation, “in which molecular components called methyl groups (made of methane) attach to DNA, turning genes on or off, and regulating the level of gene expression.” Gene expression means whether or not a particular gene is used in the body.

The problem, however, with epigenetics is that it does not consist of detailed instructions or even structural information. Epigenetics is basically just a bunch of “on/off” switches relating to information in DNA.

Here is an analogy. Imagine there is a shelf of library books at a public library. A librarian might use colored stickers to encourage readers to read some books, and avoid other books. So she might put a little “green check” sticker on the spines of some books, and a little “red X” sticker on the spines of other books. The “green check” sticker would recommend a particular book, while the “red X” sticker would recommend that you avoid it.


Perhaps such stickers would have a great effect on which books were taken out by library patrons. Such stickers are similar to what is going on with epigenetics. Just as the “red X” sticker would instruct a reader to avoid a particular book, an epigenetic molecule or molecules may act like a flag telling the body not to use a particular gene.

But these little “green check” and “red X” markers would not explain any sudden burst of information that seemed to appear in too-short a time. For example, suppose there was a big earthquake at 10:00 AM, and then at 11:00 AM there appeared a book on the library shelf telling all about this earthquake, describing every detail of it and its effects. We could not at all explain this “information too fast” paradox by giving any type of explanation involving these little “green check” and “red X” stickers.

Similarly, epigenetics may explain why functionality that appeared too fast is or is not used by a species, but does nothing to explain how that functionality appeared too fast. Epigenetics is making some valuable and interesting additions to our biological knowledge, but it does nothing to solve the problem of biological information appearing way too quickly to be accounted for by assuming random mutations.

Another analogy we can use for epigenetics is what programmers call “commenting out code.” Given some software system such as a smartphone app, it is often easy for a programmer to turn off particular features. You can do what programmers call “commenting out” to turn off particular parts of the software. So the following is a quite plausible conversation between a manager and a programmer:

Manager: Wow, the app looks much different now. Some of the buttons that used to be there are no longer there, and two of the tabs have disappeared. How did you do that so quickly?
Programmer: It was easy. I just “commented out” some of the code.

Such “commenting out” of features is similar to gene expression modification produced by epigenetics, in which there's a “let's not use this gene” type of thing going on. But the following is a conversation that would never happen.

Manager: Wow, the app looks much different now. I see there's now some buttons that lead you to new pages the app never had before, which do stuff that the app could never do before. How did you do that so fast?
Programmer: It was easy. I just “commented out” some of the code.

The programmer would be lying if he said this, because you cannot produce new functionality by commenting out code. Similarly, some new biological functionality cannot be explained merely by postulating some epigenetic switch that causes some existing gene not to be expressed. That's like commenting out code, which subtracts functionality rather than adding it.

I can give Skinner credit for raising some interesting questions, but he does little to answer them. The problem remains that biological information has appeared way too rapidly for us to plausibly explain it by random mutations.

For every case in which random mutations produce a beneficial effect, there are many cases in which they produce a harmful effect. Long experiments on exposing fruit flies to high levels of mutation-causing radiation have not produced any new species or viable structural benefits, but produce only harm. We have so far zero cases of species that have been proven to have arisen from random mutations, and we also have zero cases of major biological systems or appendages that have been proven to have arisen from random mutations. So why do our scientists keep telling us that 1001 wonderful biological innovations were produced by random mutations?

It's rather like this. Imagine Rob Jones and his family get wonderful surprise gifts on their doorstep every Christmas, left by an anonymous giver. Now suppose there is someone on their street named Mr. Random. Mr. Random behaves like this: (1) if you invite him into your home, he makes random keystrokes on whatever computer document you were writing; (2) if you eat at his house, he'll give you probably-harmful soup made from random stuff he got from random spots in his house and backyard, including his bathroom and garage; (3) if you knock on his door, and ask Mr. Random for a cup of sugar, he'll give you some random white substance, maybe sugar or maybe plaster powder or rat poison. Now imagine how silly it would be if Rob Jones were to look on those fine Christmas gifts on his doorstep, and say to himself: Let me guess who left these – it must have been Mr. Random!