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Is Evolution Random? Answering a Common Challenge

Ann Gauger


Evolutionists often challenge us for referring to Darwinian evolution as “random.” They point to the fact that natural selection, the force that supposedly drives the train, always selects more “fit” organisms, and so is not random. That is only part of the story, though, and to understand why evolution can indeed be called random, the rest needs to be told.

Evolution can be considered to be composed of four parts. The first part, the grist for the mill, is the process by which mutations are generated. Generally this is thought to be a random process, with some qualifications. Single base changes occur more or less randomly, but there is some skewing as to which bases are substituted for which. Other kinds of mutations, like deletions or rearrangements or recombinations (where DNA is exchanged between chromosomes), often occur in hotspots, but not always. The net effect is that mutations occur without regard for what the organism requires, but higgledy-piggledy. In that sense mutation is random

The next part, random drift, is like a roll of the dice that decides which changes are preserved and which are lost. As the name implies, this process is also random, the result of accidental events, and without regard for the benefit of the organism. Most mutations get lost in the mix, especially when newly emerging, just because their host organisms fail to reproduce, or die from causes unrelated to genetics. It can also happen that new mutations are combined with other mutations that are harmful, and so get eliminated.

The random effects of drift are large enough to overwhelm natural selection in organisms with small breeding populations, less than a million, say. New mutations are not born fast enough to escape loss due to drift. There is a fractional threshold in the population that must be crossed before a new mutation can become “fixed,” that is, universally present in every individual. A new mutation generally is lost to drift before that population threshold is crossed.

The third part, natural selection, is not random. It acts to preserve beneficial change and eliminate harmful ones. It can be said to be directional. But there are several caveats. Beneficial mutations are rare, and usually only weakly beneficial, so the effects of natural selection are not usually all that strong. Most changes provide only a slight advantage.

In addition, it can happen, and often does, that a “beneficial” mutation involves breaking something, meaning a loss of information, and a loss of potential improvement. This breaking can be irreversible for all intents and purposes. The premiere example in human evolution is that of sickle cell disease. Sickle cell disease is caused by a mutation to the hemoglobin gene that makes red blood cells resistant to the malarial parasite. In one copy the broken gene is beneficial (it increases resistance to malaria), but when two copies are present (both chromosomes carry the mutation), the red blood cells are deformed and cause painful debilitation. The broken gene is actually functionally worse than its normal version, except where malaria is present.

This brings out an important point. Natural selection does not always select the same mutations. The environment determines which mutations are favored. For example, natural selection acts to favor individuals carrying one copy of the sickle cell trait where malaria is present, but acts against the sickle cell gene where malaria is absent. So in this context, selection meanders over a fluctuating landscape of varying criteria for what is beneficial and what is not. Now it is beneficial to carry the sickle cell trait, now it is not. Different populations get favored at different times. In this sense one might say selection has a random component too, because only rarely is selection strong and unidirectional, always favoring the same mutation.

We see this variation in selection with another example, the evolution of finch beaks on the Gal�pagos Islands. In drought, large beaks are favored, in wet years, small beaks. The weather fluctuates, and so do the beak sizes.

Subpopulations may acquire traits, but because of environmental variation the traits do not become universal. For example, lactose intolerance — we do not all carry the version of the gene that allows us to digest lactose as adults. Unless suddenly everyone in the world has to eat cheese as a major part of their diet, lactose intolerance won’t disappear from our population.

There is a special way evolution can occur — a sudden bottleneck in the population will tend to fix the traits that predominate in that population. Suppose a nuclear holocaust wiped out everyone except Swedes. The lactose-digesting gene would almost certainly become fixed, as would blond hair, blue eyes, and other Scandinavian traits, provided they ate cheese and lived at high latitudes. Until new mutations in new environments occurred, that would remain the case.

Now you know more about the population genetics of evolution than you imagined could be true. The sum of all these factors is what is responsible for evolution, or change over time. Mutation, drift, selection, and environmental change all play a role. Three out of these four forces are random, without regard for the needs of the organism. Even selection can be random in its direction, depending on the environment.

So tell me. Is evolution random? Most of the processes at work definitely are. Certainly evolution won’t make steady progress in one direction without some other factor at work. What that factor might be remains to be seen. I personally do not think a material explanation will be found, because any process to guide evolution in a purposeful way will require a purposeful designer to create it.

Image credit: David Adam Kess (Own work) [CC BY-SA 3.0], via Wikimedia Commons.

Ann Gauger

Senior Fellow, Center for Science and Culture
Dr. Ann Gauger is Director of Science Communication and a Senior Fellow at the Discovery Institute Center for Science and Culture, and Senior Research Scientist at the Biologic Institute in Seattle, Washington. She received her Bachelor's degree from MIT and her Ph.D. from the University of Washington Department of Zoology. She held a postdoctoral fellowship at Harvard University, where her work was on the molecular motor kinesin.