>>"not only does your link go nowhere but neither do the arguments offered."<<

Sorry about the link, but it is the same as the one in my earlier post. I don't know why this copy failed. Here it is again:

www.talkorigins.org/faqs/fit...tner.html

As far as the arguments offered, here is more on that subject:

Below is a good discussion of Lee Spetner and his flawed use and understanding of information theory:

www.talkorigins.org/faqs/inf...tner.html

Some quotes from the above link:

“In this review I will consider if Spetner's metrics can be validly applied to biology, and how Spetner actually applies them to real world examples. Although his arguments are superficially plausible, a closer look with some knowledge of biochemistry shows significant flaws. I will first briefly describe Spetner's metric of information, I will then show that 1) Spetner's metrics depend on a binding mechanism that does not occur in nature, 2) that Spetner's metrics require that substances bind to enzymes in an all or nothing fashion, whereas real substrates do not bind in this way. Furthermore, I will show that Spetner himself is inconsistent in his application of his metrics. In his Xylitol example he does not actually use the measure he develops, and in the streptomycin example he swaps to a different metric, when his original metric would show increased information. Finally, I will show that his "directed evolution" model is based on a misunderstanding of one form of random mutation.”

“Conclusion:

So to summarize, although Spetner's arguments are superficially plausible, a deeper look with some knowledge of biochemistry shows massive flaws. Spetner is wrong in the details of the biology, ligand specificity is not directly governed by binding string length as required by Spetner's theory, and ligand binding is not an "all or nothing affair". This invalidates his analyses. Even then, Spetner's own examples do not support his claims. Furthermore, when using his metrics Spetner swaps metrics when one shows inconvenient changes.”

Here is a good discussion of one good example of a mutation where “information” is clearly gained and Dan’s favorite creationist website’s continuing, silly attempts to deny that this has been demonstrated and accepted by the scientific community:

www.talkorigins.org/faqs/inf...tein.html

Some quotes from this article:

“In the 1980's a small Italian community was found to have a mutant version of a protein, called Apolipoprotein AI (Apo-AI), which is associated with a decreased risk of arteriosclerosis (clogged arteries), heart attack, and stroke (1). The reduction in risk in these people has been attributed to the mutant protein (known as the Apolipoprotein AI Milano allele, henceforth referred to as Apo-AIM), and Apo-AIM has often been used as an example of a beneficial mutation.”…

“AiG uses another definition of "information," equating it with "specificity." This was originally coined by Dr . L. Spetner, and is related to the number of substrates an enzyme binds (the fewer substrates, the more specific the enzyme is and the more "information" it has (14)). Applying this measure to non-enzymes is not entirely straightforward. With this measure, it is claimed that random mutations do not increase "information" in a protein. In the case of Apo-AIM, AiG claims that the mutant apolipoprotein has lost specificity as it has lost (or restricted) the ability to form HDL particles, and the antioxidant ability of Apo-AIM is "non-specific". We have seen that in fact Apo-AIM has not lost the ability to form HDL particles, and that these HDL particles that are formed bind to specific acceptor sites and are more effective at promoting cholesterol efflux than normal HDL particles. We have also seen that the Apo-AIM antioxidant ability is both sequence and substrate specific. Thus Apo-AIM has not lost "information" by AiG's own measures. If anything it has gained Spetner "information.
After this page was made public [20/4/03] AiG added a paragraph that expands on the concept of specificity. Here they introduce the analogy of "fixing cars" and claim that a statement "fix the porsche" has more information than the statement "fix the car and the truck" as the latter, although having two "functions" is less specific than the first. They then refer readers to Werner Gitt's page.

There are two fundamental problems with this argument. First, as we have shown above, Apo-AIM is not less specific than Apo-AI, and can be reasonably considered more specific by AiG's very own criteria. Apo-AIM produces a more specific range of HDL partical sizes, rather than a broader non-specific distribution, it is more specific in activating ACAT, and it specifically reverses oxidation of lipids binding to a specific recognition sequence - all of which increase the amount of information in Apo-AIM according to AiG's logic. Secondly, they have chosen the wrong analogy to illustrate Apo-AIM's "function", and when applying information theory, one must be very careful of the analogy being used. In this case, the functions are (1) increased cholesterol efflux and (2) repair of damaged proteins, very different to the general "fix the car" scenario AiG discuss. These functions are more akin to the sentence "fill the car with fuel and if the car has a flat tyre, fix it". Does this sentence really have less information than "fix the porsche"? We will address this next, but it is obvious that AiG's conclusion is invalid because of these two fundamental problems.

With this more appropriate analogy we can now approach the question of whether Apo-AIM has more or less information than Apo-AI. We will use a formal approach to information theory called algorithmic information theory which is appropriate for comparing systems with multiple functions and will illustrate the case more clearly. We can formally represent an enzymic function as a computer program which performs a given set of functions. In algorithmic information theory, program size is directly proportional to information content, provided that the programs are written in the same language and written equally efficiently. An enzyme with multiple functions must have a longer program to code for its functions, relative to an enzyme which performs a smaller subset of these functions. Hence, an enzyme performing both functions A and B must necessarily have more information than an enzyme which performs only function A or only function B.
We can represent our more reasonable analogy in algorithmic information theory by envisaging wild-type Apo-AI as a robot which has been programmed with the task of filling a car with fuel (in the spirit of AiG's car analogy, as activation of ACAT fills HDLs with cholesterol). To do this task, a program is required to be a certain number of bits long. Now Apo-AIM would be like a robot that has been programmed to fill cars with fuel and recognise and replace flat tyres (an analogy for the anti-oxidant "repair" activity). It is clear this program must be longer than the program that simply fill the cars with fuel. Therefore, according to algorithmic information theory, the longer program has more bits of information.

More technical information can be found on this page on algorithmic information theory, and this page has a critique of Werner Gitt's ideas. Once again we refer readers to this page on Spetner 's formulation of information for specific critiques of Spetner's ideas. It is important to note that Werner Gitt's information theory formulations and Lee Spetner's applications of information theory have not been published in scientific journals and are not peer-reviewed. Currently, they are simply pseudo-scientific concepts, completely unused by professional research scientists. More importantly, however, even using these formulations we can see that Apo-AIM has more AiG-style "information."…

“Conclusions:

AiG claims that the Apo-AIM mutation, which produces a reduction in risk from heart attack and stroke, results in a loss of specificity. However, these claims are incorrect. Instead, Apo-AIM is 1) of a more complex tertiary structure 2) more stable and 3) activates cholesterol efflux more effectively than Apo-AI. Furthermore, Apo-AIM has an antioxidant activity not present in Apo-AI that is sequence and substrate specific. Thus, far from a loss of specificity, Apo-AIM represents a gain of specificity and "information" by AiG's own measures. Contrary to AiG's suggestion, all current evidence indicates that the Apo-AIM mutation is beneficial for its carriers, whether heterozygous or homozygous.”

So here every claim Dan has made is shown to be false. There is no problem with mutation/natural selection theoretically producing gains in information. There are examples of these kinds of changes that are observable. Lee Spetner's ideas are shown to be erroneous,as the debate with Dr. Max demonstrated to all but avowed creationists. We have shown examples in the scientific literature of information gaining mutations. Additionally, mathematical simulations of these natural processes clearly show these information gains and give us more insight into how they develop.