Home » Darwinism, Intelligent Design » Coffee!!: A message from “so-called Denyse O’Leary” …

Coffee!!: A message from “so-called Denyse O’Leary” …

Yesterday, I was at the Canadian Science Writers’ Association convention, held in Ottawa this year, and noted an evolution display by the British Council..

In its obsequies to Darwin, the Council advises the public that

Darwin gathered a mass of information to support his ideas. The types of evidence he used – from fossils to distribution of species – are all much more developed 150 years later. The proliferation of living forms in the so-called Cambrian explosion around 530 million years ago, for example, has been studied in enormous detail.

What I want to draw your attention to is the use of the term “so-called” Cambrian explosion.

I have usually heard the fossil find in Canada’s Burgess Shale called the “Cambrian explosion” – where most phyla of life forms appeared in a short period, some went extinct, and others continued. Darwin, famously, knew it was a problem for his gradualist theory of evolution, and blamed the imperfect fossil record. A more perfect fossil record has not helped much.

The big question is why it is so important for the British Council to defend Darwin’s theory of evolution on this and other questions, when other theories of evolution might more reasonably account for this sequence of events.

I think I shall take to calling that organization the “so-called British Council”.

Oh, and another piece of misinformation on the page is, “The spread of bacteria that can resist antibiotics is a good example of evolution in action.” Yes, if evolution means tossing out working equipment, to avoid detection and destruction. But most people want to know how the equipment was created, and – to the handwringing of Darwinists – find their particular theory unconvincing.

Here is an example: You are a pro-democracy dissident in a totalitarian regime, and you type a newsletter. You get a tip that the secret police are coming, and you row out into the middle of a nearby lake and throw your whole system into it.

Of course, the secret police could arrest you without cause, but they would prefer to have a cause, so that the government-supported and -funded media can trumpet you as a villain.

Now you don’t have that system any more. You are reduced to getting unwanted books at lawn sales and writing messages at agreed pages, known only to the person whose page it is. Then you arrange discreet delivery at the homes of democracy supporters, by various covert means. Still, you manage. They really want the messages.

But someone rats, under torture. Now, you are reduced to hiding baggie-wrapped messages in grapefruits, delivered by a sympathetic travelling fruit vendor. Soggy, but not without information value. Until …

Maybe, messages could be hidden in leafy thickets or in their root systems … I mean, if you inserted them carefully, in plastic – because they grow variously, so they will not likely be watched. But the recipient must be warned. This works, until …

Still, the system goes on because there is an intelligence that wants to hear the news about dissent from the Totality.

Okay, this is the evolution!! of a communications system – if you, as a total Darwinist, like the British Council – believe that bacterial resistance shows evolution in action.

Sure it does, Amoeba. Now let me no longer detain you, but dump you quickly into your latest new pond.

Otherwise, read Mike Behe’s Edge of Evolution: The Search for the Limits of Darwinism.

Note: Behe’s title is curious, because – if you go by current science guff – Darwinism explains everything, so there are no limits, and taxpayers must be forced to fund Darwinism.

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10 Responses to Coffee!!: A message from “so-called Denyse O’Leary” …

  1. I have usually heard the fossil find in Canada’s Burgess Shale called the “Cambrian explosion” – where most phyla of life forms appeared in a short period, some went extinct, and others continued. Darwin, famously, knew it was a problem for his gradualist theory of evolution,…

    According to the link, the Burgess Shale fossils were discovered in 1909 – 27 years after Darwin died. I hope the problem is obvious.

    Oh, and another piece of misinformation on the page is, “The spread of bacteria that can resist antibiotics is a good example of evolution in action.” Yes, if evolution means tossing out working equipment, to avoid detection and destruction. But most people want to know how the equipment was created, and – to the handwringing of Darwinists – find their particular theory unconvincing.

    We’ll skip over goal-post moving (yes, how new machinery evolved is an important problem, but it is not the whole of evolution: adaptation to the environment is just as much evolution, and if that involves loss of function, so what?). But if we look at the following mechanisms of antibiotic resistance listed by Wikipedia, we see:

    1. Drug inactivation or modification: e.g. enzymatic deactivation of Penicillin G in some penicillin-resistant bacteria through the production of ?-lactamases.
    2. Alteration of target site: e.g. alteration of PBP—the binding target site of penicillins—in MRSA and other penicillin-resistant bacteria.
    3. Alteration of metabolic pathway: e.g. some sulfonamide-resistant bacteria do not require para-aminobenzoic acid (PABA), an important precursor for the synthesis of folic acid and nucleic acids in bacteria inhibited by sulfonamides. Instead, like mammalian cells, they turn to utilizing preformed folic acid.
    4. Reduced drug accumulation: by decreasing drug permeability and/or increasing active efflux (pumping out) of the drugs across the cell surface.

    Some of these (e.g. 3) are clearly a loss of function. But all of them? How is the production of an enzyme throwing out old equipment?

  2. Heinrich, in Chapter 9 of Origin, Darwin addressed what he knew – that the fossil record was a problem for his theory. You are right in saying that the Burgess Shale discovery itself came later. But there was already enough evidence to set him worrying, and Burgess sure didn’t help his fan club.

    I guess they were lucky that the Smithsonian’s Walcott put them in a drawer where they stayed for, what, forty years?

    I will leave the technical stuff about antibiotic resistance to a bacteriologist, but none of this sounds to me like the beginning of any new species, and most of it probably does involve a loss of function for the current one.

    For one thing, the need to respond to an ongoing lethal stress would usually involve loss of function.

    That happens with humans, too.

    Some survive, but they do not produce new species.

    We need a real theory of evolution, not this stuff.

    My guess is, it will be a hybrid theory, involving a number of vectors, and will owe little to the Darwin lobby, which is basically, just in the way now. I will write more on this later.

  3. Darwin spent a lot of years of meticulous effort in the development of his theory and it seems to me he devoted much thought to whatever details might be relevant for the theory. He made a ground-breaking effort and did his best to discuss and qualify his conclusions. As far as I can tell, he was not in the habit of making bold assertions about subjects he did not have enough knowledge. It seems to me some of the critics of evolutionary theory might take a lesson from Darwin. And maybe also aim their effort at evolutionary theory as it stands today rather than at Darwin, 150 years after Origins. Natural selection still is the overriding paradigm but some progress has been made since Darwin and criticism of the theory as it stands today may be more relevant than criticism of Darwin. It has overtones of strawmanism.

    Darwin:

    the periods during which species have been undergoing modification; though very long as measured by years, have probably been short in comparison with the periods during which these same species remained without undergoing any change.
  4. I will leave the technical stuff about antibiotic resistance to a bacteriologist, but none of this sounds to me like the beginning of any new species, and most of it probably does involve a loss of function for the current one.

    (a) Evolution is not just about speciation, so you’re attempting to move goalposts. Again.
    (b) If you’re not going to deal with the technical stuff, then don’t write things like “most of it probably does involve a loss of function”: at the very least you could do the minimum reseach, like reading what wikipedia has to say on the matter: of the 4 mechanisms listed, only one (the third) seems to be a loss of function. The others might lead to a loss of function in some cases, but I don’t see that this is a necessity, and the examples given aren’t loss of function.

    Please treat your readers with some respect: either do some research before opining, or don’t express opinions that are based on your own ignorance.

  5. Heinrich, I cannot imagine any reasonable person paying attention to Wikipedia, where I was “Diane” O’Leary for months.

    If evolution is not about speciation, what could it possibly be about?

    I don’t need to hear how one amoeba leads to another – or how one guy leads to another. We have a satisfactory explanation for both, even if evolution never occurred.

    The mechanisms you suggest seem vastly unable to do what is required.

    I am regularly told, however, that Darwinism (not “evolution”) explains everything from the origin of the universe to human consciousness.

    And, like most sensible laypeople, I just do not believe that.

    I am one of the people who did not invest in bust banks or drop-the-key-off-in-the-mailbox mortgages.

    Putting me down will not help. I will not invest in Darwinism’s bust bank, and many others will not either.

  6. Heinrich-

    You are a shining example of respect aren’t you?

  7. “1. Drug inactivation or modification: e.g. enzymatic deactivation of Penicillin G in some penicillin-resistant bacteria through the production of ?-lactamases.

    2. Alteration of target site: e.g. alteration of PBP—the binding target site of penicillins—in MRSA and other penicillin-resistant bacteria.

    3. Alteration of metabolic pathway: e.g. some sulfonamide-resistant bacteria do not require para-aminobenzoic acid (PABA), an important precursor for the synthesis of folic acid and nucleic acids in bacteria inhibited by sulfonamides. Instead, like mammalian cells, they turn to utilizing preformed folic acid.

    4. Reduced drug accumulation: by decreasing drug permeability and/or increasing active efflux (pumping out) of the drugs across the cell surface.[32]”

    All of these could be due to some loss of function or some kind of compromise, they could be the result of minor mutations in specific enzymes and proteins, or they could be wholly new functions. It seems the first two options are far more likely, but it would require a knowledge of each specific event in question and a knowledge of the relevant proteins and how they interact with the antibiotic and the cell, etc. etc. For now, it seems that the “compromise” model is about right although it would be interesting if you (Heinrich) had any examples to the contrary.

  8. Heinrich:

    From Wikipedia:

    “Geologists as long ago as Buckland (1784–1856) realised that a dramatic step-change in the fossil record occurred around the base of what we now call the Cambrian.[6] Charles Darwin considered this sudden appearance of many animal groups with few or no antecedents to be the greatest single objection to his theory of evolution. He had even devoted a substantial chapter of The Origin of Species to solving this problem.[7]”

    Regarding antibiotic resistance, I would like to mention that, out of the 4 mechanisms mentioned in Wikipedia, only 2 and 3 are usually caused by mutations. Mechanism 1 is mediated by HGT, while mechanism 4 is, I believe, less understood, and depends on variations in the regulation of efflux proteins, which could be adaptive.

    So, classical mutations explain only some forms of resistance. In those forms, the important point is not so much if the “favourable” mutation (certainly useful, as long as the pressure of the antibiotic is present) is achieved with a loss of function or not. I think that both situations occur. As the mutation affect an existing structure, it is logical to think that there will be some loss of function, but it could be minimal or the mutation could change the target enough to compromise the binding of the antibiotic, but be practically neutral for ythe original function. As we certainly don’t know all the mechanisms involved in all cases, I would be careful about the loss of function.

    But again, that’s not the point, really. The point is that all these cases are mediated by simple mutations which, far from creating a new complex function, just modify an existing structure, interfering with the action of the antibiotic. So, even if no other function were lost, at least the “function” (however negative) of binding the antibiotic is disrupted. But no new complex function is created.

    These cases of microevolution obey strictly to probabilistic laws, and are considered very realistically by Behe in TEOE. Just to give an idea of how important is the concept of what I call “coordinated mutations” (that is, mutations which must be present at the same time, even if originated at different times, so that some effect becomes recognizable), I quote here a passage form a non ID paper, “Mutation Frequencies and Antibiotic Resistance”, by J. L. Martinez, and F. Baquero, from Antimicrobial Agents and Chemotherapy, July 2000:

    “Since an antibiotic resistance phenotype can be due to mutations in different bacterial loci, the emergence of an antibiotic-resistant mutant will be a function of an overall mutability value that results from the combination of the independent mutability values for these genes. Classical genetic analysis indicates that when mutations in either one or another gene can produce antibiotic resistance, the overall mutability will be the sum of the independent mutability values. On the contrary, when mutations in both genes are required to reach an antibiotic resistance phenotype, the overall mutability will be the product of the independent mutability values for each gene. Let us consider two genes independently involved in an antibiotic resistance phenotype and with independent mutability values of 10^-8. If mutations in any of the genes can render an antibiotic resistance phenotype (see Independent Mutations below), the overall mutability will be 2 × 10^-8; thus, it is only a little higher than that in the case in which only one gene involved in the resistance phenotype has a mutation. On the contrary, if mutations in both genes are required for resistance (see Cooperative Mutations below), the overall mutability will be 10^-16, which is much lower than that in the case in which only one gene is required.”

    The scenario is completely different if we consider resistance mediated by penicillinase. Here we have a complex set of proteins which have a very complex biochemical function: they inactivate the abtibiotic. Un fortunately, these wonderful proteins are not generated by mutations due to the environmental pressure. They are ancient natural genes, present in many bacterial species, and involved since ancient times in bacterial defense against natural antibiotics. Resistance is acquired only by HGT. So, no evolution here, only the horizontal sharing of ancient intelligent resources.

  9. As far as antibiotic resistance this is the test evolutionists must pass, and pass greater than Behe’s 2 protein-protein binding site limit for the “edge of evolution”.

    For a broad outline of the “Fitness test”, required to be passed to show a violation of the principle of Genetic Entropy, please see the following video and articles:

    Is Antibiotic Resistance evidence for evolution? – “The Fitness Test” – video
    http://www.metacafe.com/watch/3995248

    Testing the Biological Fitness of Antibiotic Resistant Bacteria – 2008
    http://www.answersingenesis.or.....-drugstore

    Thank Goodness the NCSE Is Wrong: Fitness Costs Are Important to Evolutionary Microbiology
    Excerpt: it (an antibiotic resistant bacterium) reproduces slower than it did before it was changed. This effect is widely recognized, and is called the fitness cost of antibiotic resistance. It is the existence of these costs and other examples of the limits of evolution that call into question the neo-Darwinian story of macroevolution.
    http://www.evolutionnews.org/2.....s_wro.html

    List Of Degraded Molecular Abilities Of Antibiotic Resistant Bacteria:
    http://www.trueorigin.org/bacteria01.asp

  10. BTW, I did try to respond to the comments here, but my replies have disappeared.

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