2015-11-13

Hi guys,

I'm having a weekly chat/debate with a very nice creationist, I'm an atheist myself.

The topic has come onto DNA, and he seems to be suggesting that some scientists are showing that life cannot have evolved and DNA could not have started due to the time it takes for mutations to get 'fixation'

Right, I'll admit it. This is way above my head - I'm not a scientist (neither is he), and analytically less intelligent that the average participant in this forum! But i am sure that if this proof existed, almost every scientist/biologist would be a creationist. But actually the trend is the opposite.

So I wonder if you could help me, and perhaps you could show me where his argument contains holes? (possible in layman terms?)

Any thoughts would be greatly appreciated

Here is what he has said:

------ --------------- --------------- --------------- --------------- --------------- --------------- --------------- --------------- --------------- -------

Time and mutations

One of the areas raised on both our documents is whether there was enough time for evolution by mutation and natural selection. Sternberg, for example, calculated that it would take 43 million years to achieve ‘fixation’ of two required co-ordinated mutations in a land animal that was the precursor of a whale. Sternberg’s example was a simplified one: for the sake of an argument he supposed that the changes needed to the male testes in the land animal, that is becoming internal and with a cooling system to keep them functional, could be achieved by just two mutations. In reality, of course, it would take many more than that. You stated that this did not seem logical, etc.

Fixation is the process by which genetic traits become widespread. The time taken to achieve fixation can be calculated using population genetics models. Sternberg based his calculation on a paper by Rick Durrett and Deena Schmidt (both of whom are advocates of neo-Darwinism). This paper, which is admittedly complicated, can be read at http://www.genetics.org/content/180/3/1501.full . )

As interesting as this is, I was more interested in the original purpose of the paper: it was intended to be a refutation of Behe’s calculation regarding the time needed to produce such changes. Behe pointed out some flaws with the application of their model (http://www.genetics.org/content/181/2/819.full), some of which they accepted (http://www.genetics.org/content/181/2/821.full ) and some of which they didn’t. Behe’s analysis of their paper is at http://behe.uncommondescent.com/2009/03 ... ns-part-1/ and it is worth reading all 5 parts as it does make Durrett & Schmidt’s paper easier to understand.

Durrett and Schmidt, in addition to using their model to test Behe’s observations, also used it to calculate mutation fixation rates in humans. Their model shows that time needed for two co-ordinated mutations to achieve fixation in humans is, after being adjusted for the number of generations calculated, 162 million years. Their assumption is that the fist mutation is either benign or just slightly detrimental. Behe considers this to be too optimistic – if the first mutation is significantly detrimental (see the fruit fly example below) then their calculations will be significantly optimistic.

They acknowledge that this figure, 162 million years, is problematic. In an attempt to overcome it they suggest multiplying the DNA neighbourhood by 1,000. Behe points out that this is ‘the gratuitous multiplication of probabilistic resources’ and that it would not solve the problem because ‘in almost any particular situation, almost all possible double mutations (and single mutations and triple mutations and so on) will be useless... it is a common conceptual mistake to naively multiply postulated “helpful mutations” when the numbers initially show too few’.

Is it necessary for multiple mutations to occur to achieve macroevolution? Logic would answer yes – just looking at the list of things needed to change a land animal into whale it is obvious that many, probably thousands, are needed. Would co-ordinated ones be needed? Again, the answer is obviously yes. To illustrate this, mutation experiments on fruit flies have caused some to develop an extra set of wings. However, this was not beneficial because that mutation did not generate the necessary muscles to make them operative – the fruit fly with the extra wings was unable to fly at all. Another mutation (at least) would be needed to make those extra wings viable. A simple example, but one that illustrates the problem. (See http://www.biomedsearch.com/nih/Muscle- ... 74495.html )

Durrett and Schmidt’s figures concerning humans also have consequences. The image of the human evolutionary tree at the Smithsonian National Museum of Natural History (http://humanorigins.si.edu/evidence/human-family-tree ) claims that Sahelanthropus tchadensis is the oldest known species in the human family tree and it lived 6 to 7 million years ago.

If Durrett and Schmidt’s model is correct then this is simply not credible. Interestingly, Behe points out that when their model is correctly applied to malaria it produces approximately the same figures as his calculations, which were based on a different model, for the time taken to fix two coordinated mutations in malaria. As the calculations they use are based on the accepted science of populations genetics and Genetics magazine published their algorithms, it is highly unlikely that their maths is wrong. That their model and Behe’s empirical research can yield similar results tends to validate them both.

Behe concludes: ‘Here’s a final important point. Genetics is an excellent journal; its editors and reviewers are top notch; and Durrett and Schmidt themselves are fine researchers. Yet, as I show above, when simple mistakes in the application of their model to malaria are corrected, it agrees closely with empirical results reported from the field that I cited. This is very strong support that the central contention of The Edge of Evolution is correct: that it is an extremely difficult evolutionary task for multiple required mutations to occur through Darwinian means, especially if one of the mutations is deleterious. And, as I argue in the book, reasonable application of this point to the protein machinery of the cell makes it very unlikely that life developed through a Darwinian mechanism.’

dGRNs

But this is not all. Researches into the field of developmental gene regulatory networks (dGRN) have reached some interesting conclusions. I have attached the entire document. It was written by Eric H Davidson, who sadly died in September, who was an evolutionary scientist and not a creationist. The paper is very technical and I will just highlight a few points from its conclusion – for the sake of brevity.

Davidson states:

‘The overall control principle is that the embryonic process is finely divided into precise little “jobs” to be done, and each is assigned to a specific subcircuit or wiring feature in the upper level dGRN. No subcircuit functions are redundant with another, and that is why there is always an observable consequence if a dGRN subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal, and since the subcircuits are all interconnected, the whole network partakes of the quality that there is only one way for things to work. And indeed the embryos of each species develop in only one way.

Thus we can think of a crown group dGRN as an evolutionarily terminal, finely divided, extremely elegant control system that allows continuing alteration, variation, and evolutionary experimentation only after the body plan per se has formed, i.e., in structural terms, at the dGRN periphery, and in developmental terms, late in the process. It is no surprise, from this point of view, that cell type re-specification by insertion of alternative differentiation drivers is change only at the dGRN periphery, quite a different matter from altering body plan… A general result of these arguments is that considerations of evolutionary change in dGRN structure may at last provide a unified conceptual framework for understanding the stages of crown group evolution, and in the same breath the sequential history of change that has produced the different hierarchical levels of animal dGRNs.

But some things never change, and a principle that must have obtained from early in metazoan evolution is that developmental jobs are controlled through the logic outputs of genetic subcircuits. Thus how evolution of the animal body plan has occurred is a question that in the end can only be addressed in the terms of transcriptional regulatory systems biology.’
(Highlights mine).

dGRNs control the embryological development in animals. Davidson notes that the neo-Darwinism ‘erroneously assumes that change in protein coding sequence is the basic cause of change in developmental program; and it erroneously assumes that evolutionary change in body plan morphology occurs by a continuous process. All of these assumptions are basically counterfactual.’

To put things as simply as I can:

Sternberg and Behe have calculated, using different models, that evolutionary change via genetic mutation takes too long. Durrett and Schmidt’s genetic population model shows the same thing. When applied correctly to malaria, it produces results that match Behe’s. When applied to humans it shows that evolution requiring two or more co-ordinated mutations would take far longer than is available.

Davidson’s research goes beyond how DNA produces genes. He looks at how individual genes are put together to form organisms. As a simple analogy – DNA produces Lego bricks, dGRN then assembles these into structures.

Davidsons points out that simply expecting a change at the DNA level – the production of one or more slightly different bricks – is not going to produce a changed body structure, which is needed for macroevolution. For that to occur, a change to the assembly process, the dGRN is needed. After the dGRN has done its work and the body plan has been produced variety can occur. But that would be microevolution – which isn’t disputed.

I note that his conclusion assumes that dGRNs have evolved but that experiments into fiddling with dGRNs are always catastrophically bad. So, basically, he is hypothesizing something that has not been observed and, actually, is the precise opposite of what has been observed. His experiments have shown that far more is needed than new genetic material to create a new kind of organism. You do need new genetic material, but its existence alone will not produce a new body plan. To get that you also need a new or altered dGRN. Behe, Sternberg & Durrett and Schmidt’s calculations have shown that mutations cannot produce the new genetic material quickly enough for evolution to occur and Davidson shows that much, much more is needed even if it could.

My conclusion is that these studies reduce evolution to a hypothesis. Even if, somehow, mutations could produce the parts needed to make up an organism, something still has to build them into an organism. It has to know how to do this. The presence of a new ‘brick’ produced by a mutation in the DNA does not account for the dGRN making use of it – it too would have had to change in order to do so.

All that I have studied over the last few weeks has convinced me that DNA and dGRN are ‘knowledge systems’ and not mere biochemical processes that work in the way that molecular forces cause crystals or snowflakes to form. Knowledge systems, and I have written many such IT systems, require intelligent design and intelligent design requires an intelligent designer.

Show more