The “law” will take into account both the qualities of the transcendent information and the qualities of the “entropic” material upon which the information is inlaid.

There is no information without the capacity for entropy of some sort. Shannon’s famous paper defining information defined it in relation to some notion of entropy. The two notions can’t be separted.

But there are piles of subtleties that haven’t been quite worked out.

As he developed these ideas, Shannon needed a name for the incompressible stuff of messages. Nyquist had used intelligence, and Hartley had used information. In his earliest writings, Shannon favored Nyquist’s term [intelligence]…..
John von Neumann…advised Shannon to use the word entropy….Use “entropy” and you can never lose a debate, von Neumann told Shannon–because no one really knows what “entropy” means….Shannon accepted von Neumann’s suggestion. He used both the word “entropy” and its usual alebraic symbol,H. Shannon later christened his Massachusetts home “Entropy House” — a name whose apporopirateness was apparent to all who set eys on its interior.

“I didn’t like the therm ‘information theory’” Robert Fano said, “Claude didn’t like it either.” But the familiar word “information” proved too appealing….

William Poundstone
Fortune’s Forumula

Further:

The introduction of information theory and its application to thermodynamics has led to the conclusion that entropy, a basic concept of that science, is a measure of the observer’s ignorance of the atomic details of the system. When we measure the pressure, volume, and temperature of an object, we have a residual lack of knowledge of the exact position and velocity of the component atoms and molecules. The numerical value of the amount of information we are missing is proportional to the entropy. In earlier thermodynamics, entorpy had represented, in an engineering sense, the energy of the system unavailable to perform external work. In the modern view, the human mind enters once again, and entropy relates not just to the state of the system but to our knowledge of that state.

Harold Morowitz
Emergence of Everything

At issue with the debate over mutation. When is a mutation informative and when is it entropy? I’m very hesitant to class ALL mutations soley as “entropy”. The issues are much more subtle than most people suppose.

Measuring things in terms of selection (as in beneificial or detrimental) is a too crude a way to characterize biology. To see why read: Airplane magnetos, contingency designs, and reasons ID will prevail. Lewontin and Andreas Wagner came to the same conclusions independently.

I agree that some mutations in speciation are “designed” and frontloaded in to the parent species, Yet the overall functional information of the original parent species is decreased since the variability of the sub-species is now more limited than the variability of the parent species. Wouldn’t you agree that overall genetic entropy is being strictly adhered to even in speciation?

I wanted to ask you what do you think the final foundational law of biology will look like? Will it look more like Dembski’s conservation of information principle or do you think the final law of biology will take on a more entropic nature? as this subject compares and relates to the first and second laws of thermodynamics?

The notion of specified complexity (CSI) is more primitive than entropy (as in decay of CSI) since the notion of such an entropy has no defintion appart from the definition of CSI.

It might be a worthy project to express Genetic Entropy as the decay of CSI and thereby unify the two notions under one concept.

That was one of the minor criticism of Sanford’s book in that Sanford relied more on Werner Gitt’s notions of biological information rather than Bill Dembski’s. But that is a minor point.

Also, using the notion of CSI, it might be possible to distinguish designed mutations from those that would be considered random, undesirable noise.

I want to get away from the notion that ALL mutation necessarily implies genetic entropy. The varieties of diversity we see in biology strike me as a designed feature, not a defect.

That a llama an camel can descend from one ancestor, or a wolf, dog, jackal, and fox can descend from a common ancestor, or that cabbage, broccoli, cauliflower descended from wild mustard strikes me as designed mutation, not genetic entropy. These were front-loaded, designed mutations in the highest sense. Spetner’s NREH and Baraminology and probably Behe’s front-loading strongly argue for these notions.

How Vaccines Compromise the Immune System

http://en.epochtimes.com/news/6-2-11/38052.html

Plus I wanted to ask you scordova or one of you other guys this question;

I wanted to ask you what do you think the final foundational law of biology will look like? Will it look more like Dembski’s conservation of information principle or do you think the final law of biology will take on a more entropic nature? as this subject compares and relates to the first and second laws of thermodynamics?

they are completely non random. And none of them is transmitted genetically.

Thank you for your informative and detailed explanation, gpuccio.

In the human immune system the mutations are not transmitted genetically. But by way of slight extension, if the mutations in the immune system were designed, it would stand to reason at least some genetically inherited mutations are designed to evolve populations as well.

Again, it is clear some mutations in the human body are clearly at variance with the teleological goals of the system, wherease some mutation (like in the immune system) are not.

It is entirely possible there is an anologous situation with the mutations found in bacteria or HIV. Some of the mutation could be classified as designed optimized toward a goal, and some can be classified in terms of a degrading entropy. But in either case, the mutations seem to be limited in the transformations which they can effect, and thus the Edge of Evolution still holds.

The purpose of the mutation, however, is very different at the two different levels where it happens.

The first level is the “ontogenic” maturation of the immune cells, and the purpose of the mutation is to create a wide repertoire of basic antibodies, which can cover with some laxity the space of possible antigens (more correctly, epitopes), so that the organism is endowed with a basic repertoire to react, usually at low affinity, with (almost) any possible epitope in nature. We should notice that, at this first level, nothing is known to the organism of any specific antigen, so the process is just the very intelligent utilization of a randomly created diversity to cover a potential space of information. No selection takes place at this level, except for the very important, and very designed, removal of the clones reacting with the “self”.

The second level, instead, takes places when there is a specific primary immune response to an antigen. The first antibodies produced versus a new antigen are the compatible “basic” ones from the general repertoire. Typically, the specifity of these immediate antibody response is low (in other words, the antibodies have a low avidity for the antigen). But, in a few months, the response becomes refined, and the avidity of the antibodies becomes high. How does that happen?

Although the process has been discovered quite recently, and not everything is understood, it seems that the organism again uses a process of designed random mutation, aimed at the existing immune cells producing the first, low affinity, antibody. But this time the process is very different. A very specific and intelligent selection determines the output. Though the mutations themselves are probably random, they:
a) are directed at an existing conformation (the first antibody) which alredy corresponds roughly to the target (the antigen, or rather the epitope).
b) are specifically selected according to a known information (the epitope itself).

In other words, the organism already possesses all the necessary information aout the “mirror” target (the epitope of the antigen). We have to remember that, at the start of the immune response, epitopes are processed by the immune system, in particular by the antigen presenting cells. That information is obviously stored someway, and is used again by the immune system to “select” the clones with mutations which have yielded an antibody with higher affinity to the antigen, and to block all the others.
So, in this case, we have a very efficient, designed selection according to a pre-existing information (the antigen itself) which has been acquired by the immune system from the outside world. No significant new information is randomly created. The system uses an existing information (the antigen) to mold a specular information (the high affinity antibody), starting with an existing approximate information (the low affinity antibody) selected from a generic repertoire by means of the antigen itself. Random mutation is used only as a “molding” technique, followed by specific intelligent selection, because the system, though knowing the information about the antigen, has no idea about how to model the corresponding antibody. So, a trial and check algorithm is used through the means of designed random mutation in a strictly controlled context.

Doesn’t all that sound so very very much as intelligent design?

And, just to avoid misinterpretations, all these mutations happen exclusively in a very definit subset of somatic cells (the pertinent immune cells). In that sense, they are completely non random. And none of them is transmitted genetically. The basic repertoire is built again each time by each new organism, but through the same method. And the high affinity antibodies against a specific antigen are present only in those individuals who have had an immune response to that antigen, at least a few months before. Nothing of that is transmissable. Only the processes are genetically transmitted.

By the way, the T cell system undergoes the same process (first level) to build the necessary repertoire of T cell receptors (cell immunity). The process is the same, but the interested genes and cells are completely different. I am not aware, anyway, of any knowledge about a “maturation” of the affinity after the first immune response (second level), but I have not really checked.

Whether this is posted as a comment or not, I hope the mod will check out the videos:

http://www.youtube.com/watch?v=zZuPMp-60jg

and

http://www.youtube.com/watch?v=FxdSB8Ky8FI

if we drift to far from this optimal median position the bacteria or organism will quickly lose “survivability”.

CORRECT! And designed mutation can help restore some of the necessary variation back into the population if it gets too specialized — unless of course the specialization results in a serious loss of information (like cave fish or moles losing their ability to see).

The human immune system is constantly dumping variable B-cells into the system. If the B-cells were too specialized we would die!

Again, we have to be careful to distinguish :

1. mutation that is the result of real genetic entropy

2. mutation that is the result of design

We tend to think mutation is always accident, but that is not necessarily so as Royal Truman pointed out.