(Read parts 1 and 2 in the series)

The heart of the neo-Darwinian synthesis is that evolution advances via the process of natural selection working on random mutations (RM+NS).  Natural selection itself lacks any creative power – it only eliminates what doesn’t work.  Eliminating the unfit, however, does nothing to “explain the origin of the fit”![1]  The burden falls entirely on RM to create the biological novelties required by Darwinism to drive evolution forward.  It must be asked, then, whether RM has the creative power required by Darwin’s theory.  Can RM produce the new biological information necessary to drive evolution forward and explain the diversification of all life?  What exactly can RM do? 

When the neo-Darwinian synthesis was set forth some 70 years ago, answers to these questions could not be ascertained.  While the theory was plausible on a conceptual level, there was no real way of testing its biological plausibility.  Over the last 30 years, however, we have been able to observe both the power and limits of RM+NS at the biological level.  What have we discovered?  We discovered that while RM can produce variability within an organism, it is not capable of producing the kind of changes required by Darwin’s theory.  RM is severely limited in what it can accomplish. 

The best way to gauge the power of RM is by observing microbial life such as bacteria, parasites, and viruses because their populations are so numerous and their generation times so short.  When it comes to evolvability, the most important factors are mutation rates, population sizes, and reproduction rates, not time.  At an optimal reproduction rate of 30 minutes, a single E. coli bacterium can generate a population size of more than 7 quadrillion organisms (7,000,000,000,000,000) in just 24 hours.  Over the course of one year it can spawn 17,520 generations[2].  That’s a lot of room for evolutionary advancement!  Mammals cannot come close to such astronomical population sizes and generations, and thus we can learn what RM can do in mammals over a long period of time by observing what it can do in microbial life over a relatively short period of time (“short” from a mammalian perspective). 


Richard Lenski has been culturing E. coli for more than 44,000 generations, which is equivalent to approximately 800,000 years of human evolution.[3]  What has RM been observed to produce?  Nothing much.  No new biological systems have developed.  According the Lenski, “the most profound change” he has observed is the ability some E. coli evolved to digest citrate.  While this is a bona fide positive change, it is not all that remarkable when you consider the following:

  1. E. coli can normally digest citrate in anaerobic (absence of oxygen) conditions.
  2. The E. coli already possessed the enzymes necessary to metabolize citrate.  They only lacked a way of getting citrate through their membrane in the presence of oxygen.[5]  The situation is analogous to a fox living on a chicken farm.  While he possesses the ability to digest those chickens, he does not do so because he is separated from them by an impenetrable fence.  Once that fence is breached, however, that fox can and will eat his heart out!
  3. It took 32,000 generations to produce this tiny change. At this rate of evolutionary improvement, it would take billions of years for complex organisms like mammals to change from one species to another (since our population sizes and reproduction rates are orders of magnitude smaller than bacteria), but Darwinism requires that it happen in 10s, 100s, or 1000s of years.  
  4. Why should it take so long for E. coli to develop this transport mechanism, when they’ve been swimming in citrate for so long?
  5. If E. coli could only evolve one major biological improvement in the equivalent of ~500,000 years of human evolution, why think all other animals have evolved thousands, if not millions of improvements during the same timeframe?
  6. This beneficial change was not achieved by increasing the information content of the E. coli’s genome, but by degrading the genome.  Evolutionary advancement, however, requires that new genetic information be added to the cell, not that it be lost.  While losing genetic information can be beneficial to survival at times, macroevolution cannot be achieved by constantly giving up biological information.  Eventually such a progression will lead to extinction, not advanced evolution.

All of the observed changes in Lenski’s E. coli are examples of microevolution, not macroevolution.  The population began as E. coli, and millions of mutations and thousands of generations later, they remain E. coli.  In fact, rather than gaining complexity and fitness, some of the E. coli populations have been observed to be in a state of devolution.  Some have lost their ability to repair DNA during transcription, resulting in a mutation rate that is 70 times that of normal E. coli.  As a result, they are losing genetic information, not gaining it; devolving, not evolving.[6]


Humans have been battling malaria for thousands of years.  The advent of modern medicine provided us with a weapon to finally beat this ravaging parasite once and for all.  Or so we thought.  Unfortunately for us, malaria has been able to develop immunity to every drug we’ve thrown at it.  For example, malaria quickly developed resistance to Atovaquone.  All that was required to circumvent the effectiveness of this drug was a single point mutation at position 268 in a single malarial gene.  The odds of developing this particular mutation are one in a trillion (1012).  While those odds would be difficult to overcome for most organisms such as human beings or beetles, they are a cinch for malaria due to their staggering population sizes and reproduction rates.  One trillion malarial parasites reside in each infected person, so odds are that at least one malarial parasite will develop resistance to Atovaquone in each and every infected person who takes the drug.  Luckily for us, malaria is not always so lucky.  Resistance to Atovaquone only develops in one out of three infected persons treated with the drug.

We humans would not be outdone by malaria, so we concocted a new drug – Chloroquine – to help us defeat our microscopic enemy.  To develop resistance to this drug, malaria would have to randomly experience two simultaneous and specific point mutations in a single protein.  While single point mutations are fairly common (1 per 100,000,000 nucleotides per the life of an organism), double-point mutations are extremely rare.[7]  The odds of developing a double-point mutation like the one malaria would need to develop if it hoped to survive its battle with Chloroquine are 1:1020 (one in a hundred billion billion).  If malaria populations were “small”—say 1,000,000 parasites per infected person—it would take one million years for malaria to meet those odds, but because there are so many malarial parasites (1 trillion per 1 billion people affected = 1,000,000,000,000,000,000,000 malaria parasites living in humans) they can, and have beat the odds.  By chance alone one malarial parasite in every billionth infected person will gain resistance to Chloroquine.  Once that resistant strand of malaria reproduces and spreads to other humans, it undermines the general effectiveness of Chloroquine. 

How long would it take mammals to develop a similar mutation by chance?  Given our tiny population sizes and long generation times, it would take us twenty billion years!  Not only is that 15 billion years more than the age of Earth, but 6 billion years more than the age of the universe itself!  And what would we get for our long wait?  A transformation from one species into another?  No.  A new biological system to help advance us toward the next stage of evolution?  No.  A new protein?  No.  We would simply get our existing cellular machinery broken in a manner that is fortuitously advantageous (micro-evolution of the devolution sort).  This is the biological equivalent of using a TV to plug a hole in a dam.  It may be a functionally acceptable solution to stave off immediate disaster, but it does nothing to build a new and improved dam.

Microbiologist Allen Orr wrote, “Given realistically low mutation rates, double mutants will be so rare that adaptation is essentially constrained to surveying—and substituting—one-mutational step neighbors.  Thus if a double-mutant sequence is favorable but all single amino acid mutants are deleterious, adaptation will generally not proceed.”[8]  In other words, if a certain evolutionary change requires a double point mutation, we can be almost certain the organism will not evolve.  The fact of the matter is that many features of advanced life would require double point mutations and greater, and thus we can be reasonably certain that macroevolution via random mutation is impossible.

In the next post we will explore what viruses have revealed about the power of RM to wrap up this topic.  

[1]George Sim Johnston, “An Evening With Darwin in New York”, Crisis magazine, April 2006, pp. 32-37; available from http://www.discovery.org/scripts/viewDB/filesDB-download.php?command=download&id=745; Internet; accessed 05 April 2006.
[2]It would take humans approximately 300,000 years to experience the same number of generations, and yet after all that time we wouldn’t come within a hair’s breadth close to the population size of malaria.  More malarial cells have existed in just the last 50 years than all mammals combined over the entire course of mammalian evolution (250,000,000 years).
[3]The replication rates of his E. coli are only seven times per day.
[4]New Scientist, available from http://www.newscientist.com/channel/life/dn14094-bacteria-make-major-evolutionary-shift-in-the-lab.html.
[5]New Scientist, available from http://www.newscientist.com/channel/life/dn14094-bacteria-make-major-evolutionary-shift-in-the-lab.html
[6]Michael Behe, “New Work by Richard Lenski,” available from http://www.evolutionnews.org/2009/10/new_work_by_richard_lenski.html; Internet; accessed 22 October 2009.  Reported on at http://www.scientificamerican.com/blog/post.cfm?id=evolution-details-revealed-through-2009-10-18.
[7]That’s why malaria quickly developed a resistance to Atovaquone, because all that is required is a single point mutation at position 268 in a single malarial protein.  The odds of doing so are 1 in a trillion (1012).  Since 1 trillion malarial parasites reside in an infected person, the odds are that malaria will develop a resistance to Atovaquone in each and every infected person.  Usually, however, it occurs in every 3rd person.
[8]Allen Orr, “A minimum on the mean number of steps taken in adaptive walks”; Journal of Theoretical Biology. 220:241-47, as quoted in Michael Behe, The Edge of Evolution: The Search for the Limits of Darwinism (New York, NY: Free Press, 2007), 106.