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Dr. Spetner tried to convince Dr. Max of some errors in his pap

I am, to put it mildly, less than impressed with Spetner's arguments. Here's something I wrote and posted the last time he came up on this forum:

He [Spetner] spent the academic year 1962-63 on a fellowship in the Department of Biophysics at the Johns Hopkins University. During that time he became interested in evolution and published several papers investigating information buildup in evolution. (more)"
I note that 1962-3 is *way* out of date for any rapidly advancing technical field, but again, the man's bio is irrelevant either way. His arguments will stand or fall on their own technical merit no matter what his background.
As to the British peppered moths (p. 67):
Although it may be an example of natural selection, it is not an example of random variation. It turns out that when the soot began to cover the lichens, the light-moth population didn't have to wait for a mutation to turn dark. The dark moth was already in the population.
...because of RANDOM VARIATION. Spetner apparently is unclear on the distinction between "variation" and "mutation".
It was living as a small minority among the light moths [Bishop and Cook 1975]. Where the tree trunks are light, most of the moths are light colored. Where the tree trunks are sooty, most of the moths are dark.
Correct, but nothing new here.
There was no random (emphasis here and in all subsequent instances in the original) variation. Both types of moths have been living side by side in both environments.
Again, Spetner reveals amazing ignorance of the meaning of the words that he himself chooses to use. He admits that the moths varied in color, and then incredibly claims that "there was no" variation. Of course there was. They varied in color. Spetner is just rambling like an old fool.
Here we have an example of microevolution that is not an example.
Now *you're* rambling. From where did you pull *that* silly conclusion? There was indeed variation among the moths, as even Spetner admits (although he boneheadedly doesn't want to call it that), and there was selection among the various colored moths in various colored environments. That's microevolution.
It gets more interesting.
I certainly hope so, becaue it's pretty tedious so far.
Page 138:
All point mutations that have been studied on the molecular level turn out to reduce the genetic information and not to increase it.
Spetner is, in a word, wrong.
Spetner can only make this silly claim by creating his *own*, idiosyncratic *personal* definition of "information", which sharply varies from the way that all other scientists and mathematicians measure information content. His defintion is stacked in a way as to be a self-fulfilling prophecy. Furthermore, some of his examples even violate his own definition.
But before we go on, let's examine his amazing claim above, that "All point mutations that have been studied on the molecular level turn out to reduce the genetic information and not to increase it". The fallacy in this claim should be obvious even to the layman -- a "point mutation" is a single DNA base pair being replaced by some different base pair. In computer terms, it's equivalent to a "flipped bit" in a bit sequence like "101011010101110", or a single altered character in a character string like "KEIJBIESSE".
By any *accepted* definition of "information", a single bit/character/DNA-basepair substitution neither adds or removes information, it simply alters the constant amount of information that's already there. A 12-bit string contains, not surprisingly, 12 bits worth of information. Flipping one of the bits doesn't change that. Likewise for a character string of a given length, or a DNA strand.
So how does Spetner manage to "see" increasing or decreasing information in a single "flip"? By eccentrically "redefining" information as "specificity". Specificity of/to *what*, you may ask? Well, to/of whatever Spetner wants it to mean for any particular case he's looking at... It's like the subjective definition of "pornography", being "I know it when I see it".
Even worse, Spetner's personal definition of "losing information" often correlates to *increasing* complexity of function, which most people would intuitively consider to be an *increase* in genetic information. For example, a mutation which causes a cellular mechanism to perform *two* functions when originally it performed a single function would count as a "decrease of information" in Spetner's eyes, because the mechanism became "less specific". And yet, most people would see the ability of the mechanism to juggle two jobs instead of one to be an increase in complexity, and thus an *increase* in genetic information content.
Let's examine what's known about the resistance of bacteria to antibiotics . . .
Page 139:
Scientists have studied how streptomycin and other mycin drugs keep bacteria from growing, and how a point mutation makes bacteria resistant to the drug [Davies et al. 1971, Davies and Nomura 1972]. They found that a molecule of the drug attaches to a matching site on a ribosome of the bacterium and interferes with its making of protein, as shown in Fig. 5.3. With the drug molecule attached, the ribosome is unable to put the right amino acids together when it makes protein. It makes the wrong proteins. It makes proteins that don't work. The bacterium then can't grow, can't divide, and can't propagate.
The ribosomes of mammals don't have the site at which the mycin drugs can attach, so the drugs can't harm them. Because the mycins can stop bacterial growth without harming the host, they make useful antibiotics.
So far so good. But then he gets whacky:A point mutation makes the bacterium resistant to streptomycin by losing information. . . We see then that the mutation reduces the specificity of the ribosome protein, and that means losing genetic information. This loss of information leads to a loss of sensitivity to the drug an hence to resistance. Since the information loss is in the gene, the effect is heritable, and a whole strain of resistant bacteria can arise from the mutation.
Oh, man, where do I start?
First, note that Spetner openly admits that when he says "information", what he really means is "specificity" (sentence #2 in the above passage). What he "forgets" to mention is that he's the *only* person using the word in that fashion. Quite bluntly, this makes him rather a crank.
Second, if he wants to argue that decreased "specificity" is somehow a significant observation, he should stick with that word and not try to muddle the issue by idiosyncratically calling it "information".
Third, he later tries to argue that since the few mutations he has examined appear to lose "information" (by *his* definition) that therefore it's not possible for evolution to accumulate significant amounts of "information" (by the *ordinary* definition). This is a classic "fallacy of equivocation", whereby a word is used with one meaning in one place of an argument and used with another meaning elsewhere to falsely link things together. The classic example is, "brussel sprouts are better than nothing, nothing is better than a juicy steak, therefore brussel sprouts are better than steak" -- the shifting use of the word "nothing" makes the conclusion unsupportable.
Fourth, even Spetner himself admits that there's more to the measure of "information" in an enzyme than just specificity. He writes (emphasis mine):
The information content of the genome is difficult to evaluate with any precision. Fortunately, for my purposes, I need only consider the change in the information in an enzyme caused by a mutation. The information content of an enzyme is the sum of many parts, among which are:
Level of catalytic activity
Specificity with respect to the substrate
Strength of binding to cell structure
Specificity of binding to cell structure
Specificity of the amino-acid sequence devoted to specifying the enzyme for degradation
These are all difficult to evaluate, but the easiest to get a handle on is the information in the substrate specificity.
To estimate the information in an enzyme I shall assume that the information content of the enzyme itself is at least the maximum information gained in transforming the substrate distribution into the product distribution. (I think this assumption is reasonable, but to be rigorous it should really be proved.)
Good lord... Spetner admits that it's "difficult to evaluate" the information content, admits that there are *multiple* components of an enzyme's information content (and then uses only *one*), admits that this is his "assumption", admits that his measure hasn't yet been "proved"... And then makes firm conclusions about whether a given mutation has gained or lost "information" based on his fuzzy "assumptions".
Need we even go on?
Another critique of Spetner's work