Catholic Apologetics

I just finished this book and had to write a quick synopsis.  It's good.

 

Not By Chance, by Dr. Lee Spetner, is an examination and critique of the neo-Darwinian model of evolution, called by Dr. E. Simon of Purdue's Biology Dept., "Certainly the most rational attack on evolution that I have ever read."

 

The author has a PhD in physics from MIT and a long career in science with focuses on information and communication theory.  The first part of the book is a mathematical examination of the alleged mechanism of evolution in the NDT: natural selection of random genetic mutations.  He shows, rather convincingly, that this theory actually can account for neither the necessary build up of the vast amounts of information in organisms' DNA nor the variety of phenotypical forms in nature.  (He is far from alone in coming to such a conclusion - many other biologists and other scientists have come to similar conclusions, though few go as far as to directly challenge the NDT hegemony.)

 

The second part of the book, where he advances a hypothesis of evolution he developed over several decades of research which he calls the "non-random evolutionary hypothesis", was most intriguing to me (as this was new territory for me).  Spetner asserts - and he developed this hypothesis solely due to the evidence, it seems - that evolution in species is driven by the environment inducing changes in either or both the genotype (DNA) or phenotype (physical form and traits) rather than by selection acting on random genetic variations.  

 

Here are some of the serious problems the NDT has with observed biology that his hypothesis explains quite well:

 

In the 1980s, Prof. Barry Hall at the University of Connecticut produced a strain of e coli that could not break down lactose; they lacked the gene encoding the first enzyme of an "array" of succession enzymes that processes lactose.  He grew these bacteria on another food but in the presence of lactose - and discovered two independent but closely related mutations in the bacteria.  The first was a before unknown "structural gene" and the second the "control gene" that enables it.  The first gene codes for an enzyme that breaks down - you guessed it - lactose, by a mechanism unrelated to e coli's normal lactose processing chain.  These bacteria were then able to live on lactose.  

 

A first important point is that each of these mutations is useless on its own: only together do they give the organism the ability to live on lactose.  And they are completely unrelated structurally in the genome (the genes being far apart physically, etc).  

 

And it's important to note that both these genes were already present in the bacteria's genome - of course there's no way such complex information could have "evolved" in this short time (if at all).  

 

So far there is nothing earth-shattering here or even fundamentally surprising - because we haven't talked about the math.  What are the odds of both of these mutations arising and taking hold in this population in a relatively small number of generations?  The odds of both mutations appearing in one bacterium were calculated at 10(-18) - enormously small odds.  Of course, bacteria populations are very large and they replicate very quickly.  But this doesn't help: the expected time for the mutation to occur a single time in Hall's population, randomly, was 100,000 years!  Yet Hall found at least 40 such occurrences within several days.  Any statistician will tell you this is absolute proof that these mutations did not occur randomly.

 

This throws the neo-Darwin model on its back immediately: the model insists that variation arises from random mutation (there are several mechanisms for this, of course) and that selection of these mutations is the process of evolution.  Here we have a clear example of the environment directly influencing genetic change in an organism.  (I'll get into how a bit later.)

 

This experiment was not an isolated occurrence.  Hall did a similar experiment with salicin (another potential food source) with similar results (mutations defying mathematical odds).  In 1988, John Cairns at Harvard performed another experiment in the same vein using another species of bacteria and saw behavior of the same sort.  He concluded, "The cells may have a mechanism for choosing which mutations will occur... Bacteria apparently have an extensive armory of such 'cryptic' genes that can be called upon for the metabolism of unusual substrates." (Emphasis is mine.)

 

You might imagine that a series of experiment so upsetting the Darwinian apple cart would prompt certain people to find explanations that could leave the existing model unharmed: you'd be right.  Spetner discusses some of these experiments.  It seems that most, such as those of Foster at Boston University (1992), Sniegowski & Lenski (1995), Foster and Trimarchi (1994), Rosenberg et al (1994), Galitski & Roth (1995), and others, have bolstered rather than contradicted Hall and Cairn.  (Spetner's book was written in 1998, and admittedly I don't know what's gone on on this front since.)

 

Spetner next discusses evolutionary change that doesn't involve any change to the genome.  Does such a thing even makes sense?  Before, I'd read this book, I'd surely have answered "no", but I realize now that this is only due to bias or misunderstanding brought on by decades of exposure to the NDT.  I make that latter statement because upon thinking about it I realized that I've always been aware that certain organisms adapt themselves to their environment - goldfish and other fish and animals that regulate body size, plants that regulate the number of seeds they produce depending upon how many of their kind are nearby, etc.  Well, if such changes became permanent  due to relatively permanent changes in the environment, they look like evolution.  Examples below will make this clear.

 

The first mechanism is extremely well-known and well-documented: the development of an embryo.  It is known that such development occurs under the direction of both the animal's genome and the environment; as Spetner says, "The same genome under different environmental conditions will often produce a different phenotype.  Signals originating in the environment are no less influential in the developing embryo than are the signals originating with the organism itself.  Indeed, one cannot entirely separate the two because they act only together... The developmental pathway of the entire embryo would be different if some of the environmental signals were different."

 

Spetner discusses biologists who claim that the distinction between inherited and acquired characteristics is not "operationally valid".  For example, consider that bone and muscle systems are influenced to a large extent in how they are used by the growing animal.  This can be especially relevant  in areas such as the jaw, and the teeth.

 

It is well-known that rats, for example, spread food preference "culturally": a small number of rats will "sample" new foods, and if it passes muster somehow communicate this so that soon all rats in a colony will eat the new food.  The choice of food can drastically affect how the rats' jaws develop: hard food or large food will produce rats will very different characteristics than very different food types.  These are changes that can be seen in fossils and would typically automatically be attributed to changes in the genome arising from Darwinian processes - when in fact they are nothing of the kind.  

 

On that note, G. Fryers of Windemere Laboratory in Wales criticized the conclusions of Harvard paleontologist Peter Williamson who attributed changes in snails' shell structure in 400 vertical meters of fossils to Darwinian evolution; it could just as easily (and in fact more likely) have been caused by "changes in the phenotype brought about solely by changes in the environment".  "One can't help wondering how much of the fossil record might be the results of the direct influence of environment on the phenotype without any changes in the genotype", Spetner notes.  In fact, a great many examples could be given of genetic change (not to mention natural selection) being merely assumed or inferred.

 

Spetner notes documented lack of correlation between changes in genotype and phenotype - another very serious difficulty for the NDT.  For example, there are species of frog nearly identical but with radical differences in their genomes, and mammals with radically different phenotypes but great genetic similarity.

 

Although there is not a single documented example of a mutation adding information to a genome (despite the fact that such a mechanism is completely core to the NDT), there are many documented examples of environmentally-triggered changes to phenotype - some entailing DNA changes and some not.  These are nonrandom changes - the same cue results in the same change, predictably.  An organism's ability to change with cues from its environment is known as phenotypic plasticity.

 

Spetner discusses how plants and animals (despite the Darwinian/Malthusian myth) very rarely exhaust their resources: instead, they tend to reduce or stop their rate of reproduction.  Another example given is that of snails that are preyed upon by crabs - when there are no crabs in the area the snails' shells grow much thinner; when crabs are about they grow thick enough that the crabs cannot eat them.  (Again, imagine the inferences made if such fossils were found in subsequent strata somewhere.)  Other similar examples are given.

 

A couple more examples of environmentally-induced changes - and these are the best ones.  In 1967 100 finches were brought from Laysan Island in the Pacific three hundred miles to Southeast Island, one of a group of four small islands within a ten-mile radius.  The birds spread to all four islands quickly.  They were examined in 1984, after only a few generations, and found already to be visibly different from the original finches - and from their local neighbors on other islands!  They differed mainly in bill shape, with each island having a sub-species (I'm assuming they could still interbreed and remained a single species - Spetner doesn't say) with a bill "tuned" to local food sources.  It goes without saying that there is absolutely no possibility of such changes arises from random genetic mutations acted upon by natural selection in so short a time.  Furthermore, if the variations existed already (in the phenotype) of the original population, why have they never been observed on Laysan Island?  

 

Speaking of finches reminds one immediately of Darwin's birds on Galapagos, doesn't it?  Of course, Darwin observed finches there unique from what were known previously.  A main (possibly the main) differentiator among these finches is indeed their bill size and shape and that of the muscles attached to them.  Darwin, of course, suggested, and this is still the view of mainstream evolutionary biologists today, that the Galapagos finches evolved from a small population that somehow travelled there in times long past.  However, there have been those who thought differently: 

 

"It stretches credulity to imagine, for example, that the woodpecker first got a long beak from some random mutation followed by other random mutations that made it go in search of grubs in the bark of trees." (Ho & Saunders)

 

Indeed it does.  It stretches credulity much farther when one has actually studied the mathematics of evolution.

 

Another example is given in the text regarding the phenotypical changes of guppies induced by the presence of predators.  In a study conducted by David Reznick of the University of California major changes in behavior were recorded in a span of two years; the evolutionary rate calculated was approximately 10 millions times the rate suggested by observations of the fossil record.

 

Finally, the author offers some very intriguing observations concerning "convergence" - that mystery of evolution whereby all kinds of different animals end up evolving in extremely similar ways even though they bear no genetic kinship.  Examples: short limbs in cold climates, lighter skins in cooler, dryer regions, number of vertebrae in fish varying with water temperature.  Is it more likely or sensible that these convergences are all the result of natural selection on random variation or that they represent the same type of plasticity in disparate species?

 

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Spetner's hypothesis is one that postulates that evolution occurs at the individual level rather than that of the species.  What he is suggesting is that individuals in a species carry with them, lying in dormant genes, all the information necessary to adapt to changes in their environment.  Of course, this carries with it the overt suggestion of design: Someone had to have had the set of 'possible' environments and conditions in mind ahead of time.

 

His model handles something else very nicely: it offers a very plausible explanation for the large amount of "useless" DNA that has been thought to exist.  I won't go into details on this (largely because they're hazy to me now), but I know there have been many examples functionality (information) being found in so-called "useless" DNA segments.  How many dormant genes might there be, waiting for a single point mutation to activate them?

 

It also seems that, as he claims, Spetner's rough model accounts for the data much better than does the NDT, based on randomness.  (The NDT departs from Darwin on this critical point, by the way - Darwin recanted his original claim that natural selection was somehow based on operation on random changes.)

 

As he points out, the NDT has an agenda behind it: a completely natural explanation for the origin of life.  But, of course, the NDT doesn't actually even attempt that, as it offers no model whatsoever for the initial origin of life.  The NDT's agenda, and its philosophical implications, certainly have much relation to the ferocity with which it is defended.