A Theory of Small Evolution

Small evolution would often be identified with micro-evolution, but there are some misunderstandings concerning the meaning of this term. Therefore, I would like to consider several possible definitions of small and large evolution and comment on each one.

The first possible definition is that the origin of new species is large evolution but evolution within a species is small evolution. This is what some biologists understand by macro and micro evolution. An obvious problem with this is that the origin of new species has been observed or can reasonably be inferred. So we reject this definition.

Another possible definition of small evolution is that almost all of the change between two species or sub-species is due to heredity (inheritance of existing traits or alleles in various combinations) rather than to mutations. It seems conceivable to me that this could even create new species if the gene pools of two populations became sufficiently different over time. Then we can define large evolution to mean that most change between two species is due to mutations, there must be a significant portion of the genome changed, and the resulting organism must be significantly different from the original.

One problem with this definition is that there could conceivably be change in between small and large evolution. However, that only illustrates that there is a continuum of possibilities. Also, some mutations have little or no effect, and we want to distinguish them from mutations having a large effect. Another issue is that from the fossil record, it is hard to know which is occurring without somehow looking at the genes. Even a long series of changes in body form could be due to small evolution as in the breeding of subspecies of dogs, for example. But large evolution would also be required for the standard theory of evolution, that is, the origin of all life from a common ancestor by ordinary physical processes. In order to demonstrate that large evolution had occurred, one would need to know the gene pool of the original and resulting species to demonstrate that there is new genetic material which could only have arisen through mutation. That would require many samples, difficult to obtain since the original species no longer exists. Another possibility is to examine the gene pools of species B and C, both known to have descended from A, and see if their gene pools are significantly different. But even this would not settle the question, unfortunately, since it could be that A had a large gene pool. A convincing transitional fossil sequence that could not be explained without many mutations might demonstrate that large evolution had occurred.

Though large evolution may be difficult to demonstrate, these definitions of large and small evolution have some analytical value. And I would say that no case of large evolution in this sense has yet been demonstrated, nor has any case of abiogenesis (development of cells from non-living matter through small replicating intermediaries). In this sense, evolution has not been demonstrated at all (a puff of smoke, as I said on talk.origins), though there are plausibility arguments that it did occur or could have occurred.

We want to clarify that recombinations (crossovers) are allowed in small evolution. These are very common, and often not harmful. A recombination (crossover) is when a chromosome derives partly from the father and partly from the mother. Since such mutations do not create new structure, but rather combine existing structure, it seems reasonable to include them in small evolution. These can also cause the copying or deletion of regions of DNA.

We can further specify these concepts by defining "large evolution" as evolution that is driven primarily by point mutations, which change one base pair in the genetic material. We define "small evolution" as evolution that is driven primarily by inheritance of existing traits, as well as recombinations, which recombine existing genetic material, sometimes with copyings. Now, even small evolution can lead to new species, as mentioned above, and I don't deny the generation of new species. My thesis is that all observed evolution can be classified as small evolution, that is, either the change is very small, possibly produced by one or two point mutations, or the change in the organism is large, but primarily the result of inheritance of existing traits and recombinations. It is difficult to know from the fossil record what kind of evolution was taking place, but one can have a considerable sequence of changes in bodily form due to small evolution. So I am proposing that the only kind of evolution that can take place is small evolution.

I do not try to define what the Biblical "kinds" are, as many creationists do. Instead, I propose a limitation of the processes that can contribute to evolution.

So these definitions of large and small evolution are about what we want, but are in need of elaboration, since not all point mutations have much of an effect on the organism. Now I try to give more precise definitions of large and small evolution than those just given. Recall that the purpose is to state an alternative to the theory of evolution which will permit the kind of evolution that has been observed, but without requiring that all of life have a common origin. The idea is that mutations have only a minor role in evolution, and that most change is caused by inheritance of existing traits. Since inheritance of existing traits (alleles) cannot change the essential structure of an organism beyond some limit, this puts bounds on what can be achieved by evolution, and argues against a common origin for all of life.

It is my impression that organisms have a loosely constrained part, consisting of characteristics like skin color that are easily modified without many effects on the remainder of the organism. There is also a tightly constrained part consisting of many elements that are tightly interconnected, and one cannot change anything without significant effects on many other things. For example, many proteins that have to interact with each other would be tightly constrained, because a major change to any one of them would prevent its interaction with the others. And, it is difficult for such groups of genes to evolve because of the many interactions. It may be possible, however, to modify some of the amino acids in such a protein without much effect on its function. This would be a minor change to the highly constrained part of the organism, and I am willing to consider such mutations as part of "small evolution." However, major mutations to the tightly constrained "kernel" of an organism would be "large evolution" if there were a significant number of them.

Thus we have two parts of the genome, the loosely constrained part and the tightly constrained part, or kernel. We also have two kinds of mutations, those that have little effect (minor mutations) and those that have a significant effect (major mutations). Small evolution asserts that there can only be a small number of major mutations in the tightly constrained part of an organism.

We consider the probability that a mutation to the highly constrained part of the organism will be beneficial or fatal. Kimure (cited in ReMine, The Biotic Message, page 246) estimates that mutations which alter amino acids are ten times more likely to be harmful than neutral or beneficial. It would be a simple matter to run laboratory tests to see how often a point mutation causes a major change in the shape of a typical protein. I suspect that over half of the mutations that cause an amino acid substitution would be major mutations, and that these would almost always be fatal. If the shape of a protein changes drastically, the chance that the protein will still have a useful function in the cell is extremely small. Thus the ratio of harmful or fatal mutations to beneficial ones (ignoring neutral mutations) would be very high. A major mutations to the highly constrained part (kernel) of the organism would almost always be fatal. Also, changes to the shape of a protein probably occur in large jumps or small increments, because of how proteins fold. If the folding of a protein is changed due to a point mutation, its shape will significantly change. Otherwise, the shape will not change appreciably. Thus there are gaps even in the structure of proteins.

Here is a quotation from Introduction to Evolutionary Biology at the talk.origins archive:

"Most mutations that have any phenotypic effect are deleterious. Mutations that result in amino acid substitutions can change the shape of a protein, potentially changing or eliminating its function. This can lead to inadequacies in biochemical pathways or interfere with the process of development"

We can say yet more about which mutations are major mutations and which are minor mutations. The amino acids found in proteins can be grouped according to their chemical properties. Some have side chains that attract oil, and some have side chains that attract water. Of those that attract water, some have positively charged side chains, and some have negatively charged side chains. Some are partially positively charged, and some are partially negatively charged. This gives five groups of amino acids. There are also other properties that can influence shape, such as the length of the side chain. In fact, each amino acid has different chemical properties. These facts are discussed near the end of Behe's book. A much more thorough discussion of the structure of proteins entitled Principles of Protein Structure Using the Internet may be found on the internet. The substitution of an amino acid by another one in the same group would be a minor mutation, and would probably have at most a minor effect on the organism. The substitution of an amino acid by one in a different group would probably change the shape and function of a protein significantly. This would be a major mutation. Since there are several groups, one would expect that most point mutations would produce an amino acid in a different group, so that most point mutations in the coding region of the DNA would be major mutations. Almost all of these mutations in the kernel of the organism would be fatal. Other kinds of mutations include copyings, deletions, and inversion. In general, a mutation that changes many bases of the DNA would be a major mutations, except for recombinations and some copyings.

Note that by examining genetic material, we can estimate whether two organisms could have evolved from a common source by small evolution. This would be so if their essential genes could be obtained from one another by minor mutations (with perhaps a small number of exceptions). Such a test could only be done for genes having only one allele, but even this could give some information. This could also be useful in defining the Biblical kinds, although that is not our main motivation.

It is interesting that the cytochrome C sequences for all members of a species are identical. This implies that none of the point mutations are neutral, else more variants would persist. This means that even minor mutations have a significant effect on the function of a protein. The other possibility is that life has only existed for a short time. It would be interesting to test in a laboratory whether there are point mutations that do not affect the chemical properties of cytochrome C. If so, this would seem to invalidate the theory of large evolution. It is also possible that in a small population, differences in genetic material become eliminated over time. This could explain the observed uniformity in some cases. However, we would expect that at least some species would have existed for hundreds of millions of years, according to the standard evolutionary view, with huge populations. At least, many species persist for long periods in the fossil record with few changes; this would imply a large population lasting for a long period of time. Examples with especially large populations and small generation times might be bacteria and protozoans. We should expect to find some such species with substantial variation in their cytochrome C and non-functional DNA within the species.

Another interesting fact is that all the variants of cytochrome C known in all organisms all have the same three-dimensional shape (tertiary structure). All the known preserved mutations substitute amino acids, but do not change the essential shape of the protein. I believe that this is also true for other commonly shared genes. I doubt that there are even any preserved mutations that add amino acids to the end of the polypeptide chains. On the large scale, we see many differences between organisms, but at the level of their shared proteins, there seems to be no essential change at all. For example, consider the following quotation from the introduction to the HSSP database:

"Homologues are very likely to have the same 3D structure as the PDB protein to which they have been aligned."

... pairs of natural proteins differing in up to 70% of their amino acid sequences virtually always fold up into the same general 3D structure.

A friend mentioned to me some material from Michael Denton's book, Evolution: A Theory in Crisis, where he discusses "junk" sequences in various organisms. He points out that the expected evolutionary pattern is not found. All major classes of animals are equidistant from each other. Sometimes it even goes the wrong way, i.e., cytochrome C in humans is a closer match to certain bacteria (65 % divergence) than some strains of yeast are (72 % divergence). But according to evolution, yeast is not far removed from bacteria, whereas humans presumably are. This pattern applies to "junk" sequences as well as functional ones.

If yeast developed early, then one should expect many species of yeast to have developed that are very different from one another in their junk DNA sequences, since mutations would have caused a divergence. (We would expect non-functional DNA to mutate at a constant rate.) But all species of yeast, apparently, have junk DNA sequences and cytochrome C sequences that are very similar. Bacteria and protozoans also should have junk DNA sequences that vary widely, because the different species should have had plenty of time to diverge. Species (such as man, or even the primates) that developed later should have much less between-species divergence in their junk DNA and functional DNA sequences. However, I believe that bacteria, protozoans, yeast, and primates all have junk DNA sequences and protein sequences that are very similar (within each respective group). From an evolutionary view, this could imply that the so-called "junk" DNA really has a function. From a creationist viewpoint, perhaps the different versions of cytochrome C really have slightly different functions, appropriate for different organisms. Or perhaps the diversity of proteins makes it more difficult for a common disease to sweep through many different kinds of plants and animals.

Here is an example of the differences in cytochrome C between organisms; this was posted on talk.origins:

"Nearly every living thing on earth has as part of its makeup a protein called cytochrome C. This protein is made up of about 100 amino acid molecules arranged in a long chain.

In a yeast cell ony 50 of these amino acids are the same as man's.
In a kernel of wheat 43 are different.
In a silkworm's body 31 are different
In a tuna fish's body 21 are different.
In a frog's body 18 are different.
In a snake's body only 14 are different.
In a dog's only 11 are different.
And in a rhesus monkey's body only 1 amino acid out of 100 in the chain of cytochrome c is different."

"When methods were developed in the 1950's to determine the sequences of proteins, it became possible to compare the sequence of one protein with another. A question that was immediately asked was whether analogous proteins in different species, like human hemoglobin and horse hemoglobin, had the same amino acid sequence. The answer was intriguing: horse and human hemoglobin were very similar, but not identical. Their amino acids were the same in 129 out of 146 positions in one of the protein chains of hemoglobin, but different in the remaining positions. When the sequences of the hemoglobins of monkey, chicken, frog, and others became available, their sequences could be compared with human hemoglobin and with each other. Monkey hemoglobin had 5 differences with that of humans; chickens had 26 differences; and frogs had 46 differences. These similarities were highly suggestive. Many researchers concluded that similar sequences strongly suggested common descent."

(Darwin's Black Box, p. 174)

If these different versions of proteins really have identical functions, then there is a problem with the theory of evolution, as mentioned above, because we should see more diversity within each species. However, if not, then the fact that similar organisms have similar protein sequences does not necessarily indicate anything about common descent or rates of evolution, but rather that similar proteins are best suited to similar organisms.

There is another argument that seems problematical for the theory of evolution, and this is that parallel evolution or convergence occurs also at the molecular level, as noted by ReMine, The Biotic Message, page 400:

The theorsists' attempts to construct phylogeny were frustrated by convergence --- this time at the molecular level.

According to the theory of evolution, the tightly constrained kernel of the organism has to change in order for an organism to evolve into something significantly different, and this probably has to happen by mutations. This is the kind of thing I am referring to by large evolution.

What I am trying to do is not only to present a theory more compatible with creationism, but also to make it clear exactly what has been demonstrated so far in the theory of evolution and what has not. My impression is that the evolution that has been observed directly or in fossils is small evolution, and I think it is likely that this is the only kind that can occur. This implies that many organisms had to have been designed, and not evolved from a single celled ancestor.

We will later develop techniques for estimating rates of mutations based on some of the ideas presented above. For now we just sketch some of the ideas. I suspect that it is not too difficult for beneficial mutations to the loosely constrained part of an organism to occur. So we might have, say, 10 percent beneficial mutations to this part of the organism. For the tightly constained part, we might have one in a thousand or one in a million beneficial mutations. For the non-coding (so-called junk) DNA, most mutations have no effect. Assuming that about half of the coding DNA is tightly constrained seems to be plausible for estimating mutation rates. The non-coding DNA (which may have some function after all) is thought to be about 90 percent or 95 percent of the human genome, which has about 3 billion base pairs.

So, how many generations are needed per mutation for the tightly constrained part of an organism (I realize that this is a somewhat vague term)? A beneficial mutation would have to spread to 1000 or a million individuals to have a significant chance of another beneficial mutation. So we can assume that it would take probably 10 or 20 generations for this mutation to increase its frequency by a factor of a thousand or a million. Thus we can assume say one favorable mutation to the tightly constrained part of an organism per 10 or 20 generations. Of course, these figures can be refined as more is learned about the structure of the gene.

Another point to consider is that changes to a highly organized structure often must be made in a very constrained order. Certain changes are not beneficial until others have been made. If we were to try to change a fish into a reptile, for example, we would have to plan very carefully a sequence of modifications. So this ordering requirement also tends to make the probability of such a transition low and require more time (if it can occur at all).

By considering the size of the genome of various organisms and the allowed time to evolve, one can estimate whether there would have been enough time for evolution to have occurred, assuming the standard geologic timetable. One can count the number of generations and the number of changes to the genome that must have taken place. Later we will consider these points in much more depth.

If the shape of a protein changes, the protein will likely have no function in the organism. The protein will continue to have no function until enough mutations have accumulated that it again has a function in the cell. All of these intermediate mutations will be neutral ones. In order to obtain the new functional protein, all of the combinations of neutral mutations have to be generated, since evolution has no way to distinguish between them on the basis of fitness. Thus evolution has to do a blind search in this case, which is very inefficient.

Typical polypeptide chains have from 50 to 3000 amino acids, so their genes have from 150 to 9000 base pairs. Often several polypeptide chains fit together in a protein, and their shapes have to match very carefully for this to occur. Once a gene has mutated, it will probably take a number of further mutations until it again has a function in the cell. For purposes of illustration, let's start with a gene having 100 base pairs and suppose that at least 5 point mutations are needed until it again has a function in the cell. Now, the more mutations that occur, the more random the gene will become, so we would expect that the density of useful genes decreases with increasing numbers of mutations. Therefore, the most efficient way to discover a new useful gene is to generate all possible combinations of mutations in order of the number of mutations. How many combinations of 5 point mutations are there? This would be 3 ⁵ (100*99*98*97*96)/(1*2*3*4*5) since there are 3 point mutations at each locus. This is about 18 billion. We need to have at least 18 billion individuals, then, with different alleles, to be able to generate all of these. (We might find a useful gene before all of the combinations were generated, though. This could reduce the number 5 to somewhere near 4.) Anyway, this requires at least 18 billion mutations in a region of 100 base pairs, or about 180 million mutations per base pair. The genome probably has at least 10 million base pairs, so we would need about 2 * 10 ¹⁵ mutations altogether. This might be feasible in a million years in a population of a billion with about a mutation per year per individual.

But only 5 point mutations to get a new shape of a functional protein seems very small when there are 150 to 9000 base pairs. If there are 10 mutations, the same calculations lead to about 10 ¹⁸ combinations, which is about 10 ¹⁶ mutations per base pair, for a total of 10 ²³ mutations in the population if the genome has about 10 ⁷ base pairs. A billion individuals for a billion years would give 10 ¹⁸ mutations with one mutation per individual per year, so we would need a trillion individuals for 100 billion years, or a higher mutation rate.

Of course, even 10 point mutations is quite small, and many genes have many more than 100 base pairs. One would expect many more than 10 point mutations to an allele before it again has a (new) function in the cell. So the numbers soon become astronomical and completely infeasible. In addition, we need to consider that some genes work together with others, so we might need to generate 3 or 4 genes at the same time, making the task even much more difficult. (This corresponds to Behe's "irreducibility." Note that this does not prevent evolution, but makes it astronomically more difficult, if irreducibility can be demonstrated.) For several polypeptide chains that fit together, it would be very hard to imagine how the whole complex could change shape gradually except by very large steps, which we have shown to be impossible. Another problem is that neutral mutations tend to die out of the population, so it may not be possible to generate all these alleles even in a vast amount of time unless the population is even more astronomically large to generate the combinations of neutral mutations rapidly in a single line of individuals.

According to the talk.origins archive, neutral mutations are eliminated from a population on the average in 2(Ne/N)ln(2N) generations (if I understand the matter correctly), where Ne is the effective population size, N is the population size, and ln is natural logarithm. Note that Ne/N is at most 1. For a population of a billion, this would be about 44 generations. For a population of a trillion, it would be about 56 generations. The chance to accumulate a significant number (even 2) of neutral mutations to a gene within 44 to 56 generations is negligible. (Recall that the neutral mutation will not be increasing its frequency in the population on the average.) The chance that a neutral mutation will fix (reach a frequency near 1 in the population) is proportional to its frequency. If such fixing did happen, it would not help the case, since what we need is a large number of alleles to have a hope of generating a new functional gene. So it really seems impossible for such shape changes to take place by blind search, since it would require the accumulation of at least several neutral mutations in the same gene in many different ways.

This argument constitutes a fairly strong objection to evolution; it shows that the task of random evolution is much like the task of writing a book by generating letters at random, when one considers such changes to the shape of proteins. Evolutionists argue that long time periods and many individuals generate enough combinations for evolution to occur. However, experience in exhaustive search algorithms shows that the search spaces are often so huge that even trillions and trillions of trials are often not enough to generate anything interesting. The only way I can see to overcome this objection is to say that there is some easily generated subspace of the sets of mutations that happens to be rich in useful genes. It remains to be shown what this subspace is. Another possible way out is to show that even when the shapes of proteins change, they still retain some residual function which can guide their evolution. Of course, this is not true at least some of the time, because many point mutations completely inactivate a protein. At least, a change of shape will severely degrade the function of a protein, and the chance that it will acquire a new, beneficial function is astronomically small. Anyway, from now on we will mostly ignore this argument about the improbability of shape changes in evolution, and will consider the likelihood of evolution under a variety of other assumptions about occurrences of beneficial mutations.

Back to home page.