Monday, August 28, 2006

Evolutionary Intermediates

A post at iDesign entitled'On Evolutionary Explanations' provides a sharp analytical critique of what passes for evidence for evolution. The post is italicized. My comments are in block print with quotes identified.

Evolutionists and design theorists often have an extremely different notion of what constitutes "proof" of evolution, and this causes a good deal of confusion. Evolutionists complain that the standard of proof required by design theorists is unreasonably high, and design theorists complain that the proofs of evolution in the literature are not proofs at all. You can guess where I fall on that spectrum.

If you pay close attention, whenever evolutionists are engaged in listing the "proofs" for evolution, they almost exclusively list evidence for common descent. Ask them for the mountain of evidence that necessity and stochastic processes are responsible for making the transitions between the similar forms which they just showed you, and they may draw a few pictures and connect them with arrows, but that is all you are likely to get.

Take this model of the evolutionary origin of the bacterial flagellum. It is long, detailed, and testable.

Two separate posts at this site were made in response to this article.

But just what aspects of the model are testable? Precisely the aspects related to homology. The testable claims are about which components may be more ancient that others, which structures may have been intermediate between the Type-III secretory system and the bacterial flagellum, etc. The question of whether natural selection acting on random variation is powerful enough to make the hypothetical transitions is never addressed. Instead it is assumed that proposing intermediates and telling a story about how each might provide an incremental fitness benefit is enough.

During an exchange at Telic Thoughts a commentator known as Smokey made the following remark.
In real science, the job is to produce new data that directly test one's interpretation. That's why ID isn't real science.
Before dealing with the claim that ID is not real science let's take a look at the prior sentence in the context of the referenced paper on the bacterial flagellum. Does the data cited in the paper test the interpretation? The interpretation is that the homologous proteins cited formed precursor systems from which descended the bacterial flagellum through a natural selection process. From the paper:

A new model is proposed based on two major arguments. First, analysis of dispersal at low Reynolds numbers indicates that even very crude motility can be beneficial for large bacteria. Second, homologies between flagellar and nonflagellar proteins suggest ancestral systems with functions other than motility. The model consists of six major stages: export apparatus, secretion system, adhesion system, pilus, undirected motility, and taxis-enabled motility. The selectability of each stage is documented using analogies with present-day systems. Conclusions include: (1) There is a strong possibility, previously unrecognized, of further homologies between the type III export apparatus and F1F0-ATP synthetase. (2) Much of the flagellum’s complexity evolved after crude motility was in place, via internal gene duplications and subfunctionalization. (3) Only one major system-level change of function, and four minor shifts of function, need be invoked to explain the origin of the flagellum; this involves five subsystem-level cooption events. (4) The transition between each stage is bridgeable by the evolution of a single new binding site, coupling two pre-existing subsystems, followed by coevolutionary optimization of components. Therefore, like the eye contemplated by Darwin, careful analysis shows that there are no major obstacles to gradual evolution of the flagellum.

Back to the iDesign comments:

I'm not convinced. You see, I'm a computer scientist. I'm used to looking at incredibly complex, interdependent systems at a high level of abstraction and implementing modifications at the very lowest level. There is very rarely a correlation, even in the most well-designed systems, between what changes appear straightforward at a high level of abstraction and what changes are actually straightforward to implement (by "straightforward" I mean changes which do not require a large number of compensatory changes to other parts of the system). There is not enough detail in the above model (or in most evolutionary models) to evaluate whether or not natural selection is sufficiently powerful to get the job done.

The author is pointing to a parallel experience. In this case the interdependent systems referred to have obvious parallels to biological systems that are component parts of an organism. Shared features include complexity and interdependence. Key to the analogy are low level modifications needed to generate higher level effects. A critical observation on the part of the author is the link between low level changes and the necessity to make even further modifications to other parts of the system to integrate those changes. This suggests a means of testing that would distinguish between an outcome generated through natural selection and one arrived at through intelligent design. Identifying the modifications needed to accomodate intermediate evolutionary changes simultaneously identifies the data needed to test prevailing interpretations. Placing the precursor to a biological system under selective pressure tests the adaquacy of the process. While the outcome and the precursor may be identifiable in detail, intermediates are somewhat speculative. Any outcome entailing the need for more intermediates than can be generated by a selection process would be evidence for intelligent design.

This raises an interesting question: How specific does a model have to be to be convincing? That is, how small do the proposed changes have to be to render it likely that natural selection could have filled in the gaps? I don't know of any formal answer to this, but whatever the answer might be it must be able to test natural selection, not merely assert its ability to move between hypothetical intermediate forms described at a high level of abstraction. Ironically, the only people who seem to be interested in doing this sort of thing are design theorists.

Contrary to Smokey's assertion data can be used to test an interpretation favorable to design. Testing natural selection is also a more authentic means of documenting an evolutionary interpretation than is the citing of homologous proteins and theorized precursor systems.

Wednesday, August 23, 2006

Teaching Evolution in Kansas as Viewed by Daniel Andres

Part of a post from a Spanish language blog known 'El Blog de Daniel Andres' (The Blog of Daniel Andres) is included below. The blog is supportive of intelligent design. The particular post quoted from refers to the recent controversy in Kansas over the teaching of evolution in public schools. I'll summarize the main points in English and then comment on them.

Kansas está inmerso en una discusión sobre los estándares de la educación en las escuelas públicas al respecto del darwinismo. Los críticos de Darwin están lanzando una propuesta llamada Stand Up for Science en la cual buscan reunir firmas para que, empezando por Kansas, la forma en la que se enseña a Darwin sea corregida. En plata blanca esto significa enseñar las fortalezas y debilidades de la teoría pues en USA solo se enseña que Darwin tiene fortalezas, olvidando que toda teoría científica, inclusive el DI, tiene debilidades. De lo que no trata es de enseñar posturas diferentes sobre los orígenes; teorías como el creacionismo, la simbiosis, el DI o la auto-organización compleja. Ninguna de esas busca enseñarse, la reforma solo pide enseñar fortalezas y debilidades de Darwin.

Al enseñar que el darwinismo es tan absoluto como la demostración de un teorema (que solo tiene certezas), se les está diciendo a los estudiantes que no hay forma de negar el evolucionismo. Curiosamente eso la haría dogma, no ciencia, pero eso es algo que les preocupa poco a los fieles de la religión darwinista.

Daniel Andres alludes to the fact that there was an attempt to require that both the strengths and weaknesses of Darwin's theory be taught in public schools. As of now he notes that only supportive data is presented to students and that evolution is presented as undeniable. This is dogmatic not scientific but that, notes the author, is a small concern to followers of the Darwinian religion.

On purely educational or scientific grounds it is difficult to justify withholding data that is problematic for current theories of origin and current beliefs about genetic changes over time. There is much such data. I've referred to some of it in blog entries at this site.

When Darwinists attempt to suppress information, under the guise of protecting science, they ironically arouse the curiosity of youth and whet their appetite for further information about intelligent design. They may gain short term victories like the one in Kansas, but at the expense of unwitting encouragement of a longer range struggle against Darwinian orthodoxy.

Intelligence Generates Information & its Encoding Convention

The following snippet of a post entitled 'Information, Materialism and Free Will' appeared in Dembski's Uncommon Descent blog.

The generation of information where none existed, as well as the accompanying coding convention and information transmitting mechanism, is perhaps the best evidence for an intelligent cause of life. The italicized blog reference follows.

The existence of information is a fundamental refutation of materialism.

Information has no mass. It has no physical dimensions. And it can exist in multiple places at the same time. It has no physical or materialistic properties whatsoever. Put a gigabyte of information on your computer’s blank hard disk, and check out how much more the disk weighs. Back up your hard disk and that information will exist in two places at the same time. You can transmit that information at the speed of light (at which speed nothing with rest mass can travel).

Life is not fundamentally based on atoms, molecules and chemistry. These represent the media and low-level mechanism in which life’s information is stored and expressed.

Monday, August 21, 2006

Protein Folding Malfunction and Disease

A HUM-MOLGEN article entitled 'Protein Folding Lost In Translation' reveals a link between diseases and an accumulation if misfolded proteins. The specific cause of the accumulation is attributed to a malfunction of the translation process which is essential for protein synthesis. The article cited a study of mice and what is referred to as a "sticky mutation." Susan Ackerman and colleagues were involved in the study. The italicized article follows along with my comments in bold print.

A new mechanism that could underlie certain neurodegenerative diseases is published online this week by Nature. The researchers reveal that upsetting the accuracy of translation, the process by which messenger RNAs are coded into proteins, can lead to the accumulation of misfolded proteins.

The reason that accumulated, misfolded proteins become problematic as a result of translation function impairment, lies in the fact that all coded for proteins, containing the amino acid alanine, would be affected by this malfunction. Although amino acid substitution can occur without negating function, the number of substitutions, likely to occur as a result of this type of mutation, indicates that protein malfunction would overwhelm the capacity of coping cellular mechanisms.

Susan Ackerman and colleagues studied mice with the so-called 'sticky' mutation, which develop tremors, movement problems and cellular death of cerebellar neurons. The results of the study implicate the faulty manufacture of transfer RNAs (tRNAs) - the molecules that insert amino acids into their appropriate position during translation - as the reason behind the neurodegeneration seen in sticky mice. The team showed that the sticky mutation disrupts an enzyme called alanyl-tRNA synthetase, which attaches a specific amino acid to tRNA molecules. The mutation causes the production of proteins containing aberrant amino acids, and these proteins cannot fold correctly and so accumulate within neurons, killing them. The researchers propose that some heritable diseases could be caused by mild mutations that disrupt tRNA synthetase enzymes.

Proteins that do not fold correctly lose their functional capabilities. They can then impair other cellular functions. However, cells have mechanisms that identify and degrade such proteins. There is a biochemical concept known as protein turnover. The following alludes to this process.

In healthy adults, the total amount of protein in the body remains constant, because the rate of protein synthesis is just sufficient to replace the protein that is degraded. This process, called protein turnover, leads to the hydrolysis and resynthesis of 300 to 400 g of body protein each day. The rate of protein turnover varies widely for individual proteins. Short-lived proteins (for example many regulatory proteins and misfolded proteins) are rapidly degraded, having half-lives measured in minutes or hours. Long lived proteins, with half-lives of days to weeks, constitute the majority of proteins in the cell. Structural proteins, such as collagen, are metabolically stable, and have half-lives measured in months or years.1

Protein malfunction is natural as are cellular mechanisms to cope with the problem. The article refers to a condition wherein the amount of impaired proteins can accumulate to the point of overwhelming the coping mechanisms. The article and larger issues which encompass it are interesting from the perspective of life's origins and history. Loss of protein function is inevitable. Sometimes it occurs at the outset of the protein synthesis process as indicated in this post. Other times it occurs subsequently as indicated in the quoted reference. In any case misfolded and other malfunctional proteins can become obstacles to the functions needed to sustain life.

Mechanisms that identify and degrade proteins are clearly essential. Essential functions are red flags in objective assessments of the adaquacy of natural history paradigms. Setting aside the matter of how protein synthesis mechanisms come about and how their functionality is acquired, data indicates that some means of coping with malfunctional proteins is required at an early point in theoretical musings about how life came about and subsequently evolved. The implications of this specific issue will be further analysed in future posts about proteins.


1. 'Biochemistry'; Page 244; Pamela C. Champe, Richard A. Harvey and Denise R. Ferrier; Lippencott, Williams & Wilkens; 2005.

Sunday, August 20, 2006

Chicken Little: Part Two

This is the second of a two part post related to an article by Karen Armstrong entitled 'Bush's fondness for fundamentalism is courting disaster at home and abroad.' Parts of the article follow in italics. The title of the post refers to this amusing cartoon courtesy of Mike Gene of Telic Thoughts. My comments are in bold print.

Is there a connection between a religiously motivated mistrust of science, glaring social injustice and a war in the Middle East? Bush and his administration espouse many of the ideals of the Christian right and rely on its support. American fundamentalists are convinced that the second coming of Christ is at hand; they have developed an end-time scenario of genocidal battles based on a literal reading of Revelation that is absolutely central to their theology. Christ cannot return, however, unless, in fulfilment of biblical prophecy, the Jews are in possession of the Holy Land. Before the End, the faithful will be "raptured" or snatched up into the air in order to avoid the Tribulation. Antichrist will massacre Jews who are not baptised; but Christ will defeat the mysterious "enemy from the north", and establish a millennium of peace.

This grim eschatology, developed in the late 19th century, was in part a reaction to the "social gospel" of the more liberal Christians, who believed that human beings were naturally evolving towards perfection and could build the New Jerusalem here on earth by fighting social injustice. The fundamentalists, however, believed that God was so angry with the faithless world that he could save it only by initiating a devastating catastrophe; they would see the terrible battles of the first world war, which showed that science could be used to lethal effect in the new military technology, as the beginning of the End.

The "reaction to the social gospel" hypothesis is very dubious. Armstrong greatly distorts beliefs of conservative Christians who believe that God is both sovereign and in control of events. These Christians believe the saving event was the atoning death of Christ on the cross. There is no need to save it a second time through catastrophies.

The fundamentalists' rejection of science is deeply linked to their apocalyptic vision. Even the relatively sober ID theorists segue easily into Rapture-speak. "Great shakings and darkness are descending on Planet Earth," says the ID philosopher Paul Nelson, "but they will be overshadowed by even more amazing displays of God's power and light. Ever the long-term strategist, YHVH is raising up a mighty army of cutting-edge Jewish End-time warriors."

It has become increasingly evident that this quote of Paul Nelson is a fabrication. The story was well covered here and in subsequent posts. Despite being caught committing a grave journalistic offense neither author Karen Armstrong nor the publication 'The Guardian' has yet to either acknowledge the problem or apologize for it.

Friday, August 18, 2006

Irreducibly Complex Protein Folding Mechanism

A post at iDesign@UCI entitled 'Chaperonin Design' is based on an article in 'Nature' about proteins known as chaperonins. The italicized article follows along with my comments in bold print.

A recent article in Nature explored the means by which certain proteins called chaperonins work. Chaperonins are proteins which help other proteins fold correctly. Specifically, they provide a "cage" in which the target protein can fold without interference. Artificially growing or shrinking the size of the cage can make certain proteins fold more quickly or slowly, but the overall size of the cage seems to be optimal given the number of proteins which this chaperonin interacts with.

There are a number of indicators of intelligent causality alluded to in this post. The indicators, which fall within the purview of circumstantial evidence, will be individually identified. There is an optimal relationship between the two proteins; specifically the size fit. Alone this signifies very little. However when considered in conjunction with other factors, which include the alternative stochastic process said to generate the cited proteins, the optimal fit becomes a relevant factor.

Because the cell is so crowded with large molecules, it is energetically favorable for newly transcribed proteins to fold compactly, reducing the volume they occupy. If it weren't for chaperonins, this tendency would cause partially complete amino acid chains to bind with each other (there are many of these chains in close proximity because mRNA is transcribed by many ribosomes at once).

Chaperonins counteract a natural tendency for proteins to fold following transcription. Folding without chaperonins would result in dysfunctional tertiary structures.

The upshot is that chaperonins use the energetic effects of crowding to stimulate folding while at the same time eliminating the negative effects of crowding - promiscuous binding to anything in the area. This is a neat trick. In the final paragraph of the article, the author (who, of course, credits natural selection with chaperonin design) even exhorts human designers to follow the example of chaperonins:

"It is a testament to the ingenuity of natural selection that the chaperonin cage not only combats aggregation caused by crowding outside the cage but also uses crowding to accelerate protein folding inside the cage. Nanoengineers trying to improve the yield of therapeutic proteins could profit from studying the tricks of the chaperonin nanocage."

Good suggestion. However should natural selection be credited with generating this phenomenon? What experimental evidence validates the belief that such protein pairings co-evolve? Note that the function of the chaperonin enables the functionality of its partner protein. Precision and necessity are descriptive of the protein relationship. There is no indication that either qualities allow for compromise in function i.e. an envisioned scenario wherein a fit becomes progressively more precise while lesser function becomes gradually maximized. Yet that would be what a natural selection paradigm would generally call for.

If chaperonin function is dependent on an exact fit to the folding protein and the folding protein lacks function without a chaperonin then we have a purposeful relationship. This one enables a more complex cellular function through a problem solving device in the form of the chaperonin protein. Does this type of phenomenon yield to a natural selection explanation? Why? Based on what experimental evidence?

What experimental evidence would implicate an intelligent cause? One could argue that evidence is already at hand in the form of purpose, precision and necessity. The argument against this has been the adaquacy of a non-telic (in the sense that the generating process is actually stochastic in nature and outcomes selected as theorized) natural selection based explanation. Natural selection then would be the testing target and coding genes for the cited proteins the experimental focus in an appropriate organism.

Wednesday, August 16, 2006

Darwinism: Part Two

An article by David Stove entitled 'So You Think You Are a Darwinian?' contains a list of ten Darwinian beliefs. The last five are listed in this post. The article is italicized.

6. '…no one is prepared to sacrifice his life for any single person, but everyone will sacrifice it for more than two brothers [or offspring], or four half-brothers, or eight first-cousins.'

This is a quotation from the epoch-making article by Professor Hamilton to which I referred a moment ago. The italics are not in the text. Nor are the two words which I have put in square brackets; but their insertion is certainly authorized by the theory of inclusive fitness.

7. Every organism has as many descendants as it can.

Compare Darwin, in The Origin of Species, p. 66: ‘every single organic being around us may be said to be striving to the utmost to increase in numbers’; and again, pp. 78-9, ‘each organic being is striving to increase at a geometrical ratio’. These page references are to the first edition of the Origin, (1859), but both of the passages just quoted are repeated in all of the five later editions of the book which were published in Darwin’s lifetime. He also says the same thing in other places.

But it would not have mattered if he had not happened to say in print such things as I have just quoted. For it was always obvious, to everyone who understood his theory, that a universal striving-to-the-utmost-to-increase is an essential part of that theory: in fact it is the very ‘motor’ of evolution, according to the theory. It is the thing which, by creating pressure of population on the supply of food, is supposed to bring about the struggle for life among con-specifics, hence natural selection, and hence evolution. As is well known, and as Darwin himself stated, he had got the idea of population permanently pressing on food, because of the constant tendency to increase, from T. R. Malthus’s Essay on Population (1798).

Still, that every organism has as many descendants as it can, while it is or may be true of most species of organisms, is obviously not true of ours. Do you know of even one human being who ever had as many descendants as he or she could have had? And yet Darwinism says that every single one of us does. For there can clearly be no question of Darwinism making an exception of man, without openly contradicting itself. ‘Every single organic being’, or ‘each organic being’: this means you.

8. In every species, child-mortality - that is, the proportion of live births which die before reproductive age - is extremely high.

Compare Darwin in the Origin, p. 61: ‘of the many individuals of any species which are periodically born, but a small number can survive’; or p. 5, ‘many more individuals of each species are born than can possibly survive’. Again, these passages, from the first edition, are both repeated unchanged in all the later editions of the Origin.

Proposition 8 is not a peripheral or negotiable part of Darwinism. On the contrary it is, like proposition 7, a central part, and one which Darwinians are logically locked-into. For in order to explain evolution, Darwin had adopted (as I have said) Malthus’s principle of population: that population always presses on the supply of food, and tends to increase beyond it. And this principle does require child-mortality to be extremely high in all species.

Because of the strength and universality of the sexual impulse, animals in general have an exuberant tendency to increase in numbers. This much is obvious, but what Malthus’s principle says is something far more definite. It says that the tendency to increase is so strong that every population, of any species, is at all times already as large as its food-supply permits, or else is rapidly approaching that impassable limit. Which means of course that, (as Malthus once put it), the young are always born into ‘a world already possessed’. In any average year, (assuming that the food-supply does not increase), there is simply not enough food to support any greater number of the newborn than is needed to replace the adults which die. But such is the strength of the tendency to increase that, in any average year, the number of births will greatly exceed the number of adult deaths. Which is to say, the great majority of those born must soon die.

Consider a schematic example. Suppose there is a population, with a constant food-supply, of 1000 human beings. Suppose - a very realistic supposition, in fact a conservative one - that 700 of them are of reproductive age. Suppose that this population is already ‘at equilibrium’, (as Darwinians say): that is, is already as large as its food can support. According to Malthus’s principle, people (or flies or fish or whatever) will reproduce if they can. So, since there are 350 females of reproductive age, there will be 350 births this year. But there is no food to support more of these than are needed to replace the adults who die this year; while the highest adult death-rate which we can suppose with any approximation to realism is about 10%. So 100 adults will die this year, but to fill their places, there are 350 applicants. That is, there will this year be a child-mortality of 250 out of 350, or more than 70%.

It was undoubtedly reasoning of this kind from Malthus’s principle which led Darwin to believe that in every species ‘but a small number’ of those born can survive, or that ‘many more’ are born than can survive. What did Darwin mean by these phrases, in percentage, or at least minimum-percentage, terms? Well, we have just seen that Malthus’s principle, in a typical case, delivers a child-mortality of at least 70%. And no one, either in 1859 or now, would dream of calling 30 or more, surviving out of 100, 'but a small number’ surviving. It would be already stretching language violently, to call even 23 (say), surviving out of 100, ‘but a small number’ surviving. To use this phrase of 30-or-more surviving, would be absolutely out of the question. So Darwin must have meant, by the statements I quoted above, that child-mortality in all species is more than 70%.

Which is obviously false in the case of our species. No doubt human child-mortality has often enough been as high as 70%, and often enough higher still. But I do not think that, at any rate within historical times, this can ever have been usual. For under a child-mortality of 70%, a woman would have to give birth 10 times, on the average, to get 3 of her children to puberty, and 30 times to get 9 of them there. Yet a woman’s getting 9 of her children to puberty has never at any time been anything to write home about; whereas a woman who gives birth 30 times has always been a demographic prodigy. The absolute record is about 32 births. (I neglect multiple births, which make up only 1% of all births.) As for the last 100 years, in any advanced country, to suppose child-mortality 70% or anywhere near it, would be nothing but an outlandish joke.

It is important to remember that no one - not even Darwinians - knows anything at all about human demography, except what has been learnt in the last 350 years, principally concerning certain European countries or their colonies. A Darwinian may be tempted, indeed is sure to be tempted, to set all of this knowledge aside, as being of no ‘biological’ validity, because it concerns only an ‘exceptional’ time and place. But if we agreed to set all this knowledge aside, the only result would be that no one knew anything whatever about human demography. And Darwinians would then be no more entitled than anyone else to tell us what the ‘real’, or the ‘natural’, rate of human child-mortality is.

In any case, as I said earlier, Darwinians cannot without contradicting themselves make an exception of man, or of any particular part of human history. Their theory, like Malthus’s principle, is one which generalizes about all species, and all places and times, indifferently; while man is a species, the last 350 years are times, and European countries are places. And Darwin’s assertion, that child-mortality is extremely high, is quite explicitly universal. For he said (as we saw) that ‘of the many individuals of any species which are periodically born, but a small number can survive’, and that ‘many more individuals of each species are born than can possibly survive’. Again, this means us.

9. The more privileged people are the more prolific: if one class in a society is less exposed than another to the misery due to food-shortage, disease, and war, then the members of the more fortunate class will have (on the average) more children than the members of the other class.

That this proposition is false, or rather, is the exact reverse of the truth, is not just obvious. It is notorious, and even proverbial. Everyone knows that, as a popular song of the I 930s had it,

The rich get rich, and
The poor get children.

Not that the song is exactly right, because privilege does not quite always require superior wealth, and superior wealth does not quite always confer privilege. The rule should be stated, not in terms of wealth, but in terms of privilege, thus: that the more privileged class is the less prolific. To this rule, as far as I know, there is not a single exception.

And yet the exact inverse of it, proposition 9, is an inevitable consequence of Darwinism all right. Malthus had said that the main ‘checks’ to human population are misery - principally due to ‘famine, war, and pestilence’ - and vice: by which he meant contraception, foeticide, homosexuality, etc. But he also said that famine - that is, deficiency of food - usually outweighs all the other checks put together, and that population-size depends, near enough, only on the supply of food. Darwin agreed. He wrote (in The Descent of Man, second edition, 1874), that ‘the primary or fundamental check to the continued increase of man is the difficulty of gaining subsistence’, and that if food were doubled in Britain, for example, population would quickly be doubled. But now, a more-privileged class always suffers less from deficiency of food than a less-privileged class does. Therefore, if food-supply is indeed the fundamental determinant of population-size, a more-privileged class would always be a more prolific one; just as proposition 9 says.

William Godwin, as early as 1820, pointed out that Malthus had managed to get the relationship between privilege and fertility exactly upside-down. In the 1860s and ‘70s W. R. Greg, Alfred Russel Wallace, and others, pointed out that Darwin, by depending on Malthus for his explanation of evolution, had saddled himself with Malthus’s mistake about population and privilege. It is perfectly obvious that all these critics were right. But Darwin never took any notice of the criticism. Well, trying to get Darwin to respond to criticism was always exactly like punching a feather-mattress: ‘suddenly absolutely nothing happened’.

The eugenics movement, which was founded a little later by Darwin’s disciple and cousin Francis Galton, was an indirect admission that those critics were right. For what galvanized the eugenists into action was, of course, their realisation that the middle and upper classes in Britain were being out-reproduced by the lowest classes. Such a thing simply could not happen, obviously, if Darwin and Malthus, and proposition 9, had been right. But the eugenists never drew the obvious conclusion, that Darwin and Malthus were wrong, and consequently they never turned their indirect criticism into a direct one. Well, they were fervent Darwinians to the last man and woman, and could not bring themselves to say, or even think, that Darwinism is false.

A later Darwinian and eugenist, R. A. Fisher, discussed the relation between privilege and fertility at length, in his important book, The Genetical Theory of Natural Selection, (1930). But he can hardly be said to have made the falsity of proposition 9 any less of an embarrassment for Darwinism. Fisher acknowledges the fact that there has always been, in all civilized countries an inversion (as he calls it) of fertility-rates: that is, that the more privileged have always and everywhere been the less fertile. His explanation of this fact is that civilized countries have always practised what he calls ‘the social promotion of infertility’. That is, people are enabled to succeed better in civilized life, the fewer children they have.

But this is evidently just a re-phrasing of the problem, rather than a solution of it. The question, for a Darwinian such as Fisher, is how there can be, consistently with Darwinism, such a thing as the social promotion of infertility? In every other species of organisms, after all, comparative infertility is a sure sign, or even the very criterion, of comparative failure. So how can there be if Darwinism is true, a species of organisms in which comparative infertility is a regular and nearly-necessary aid to success?

Fisher’s constant description of the fertility-rates in civilized countries as ‘inverted’, deserves a word to itself. It is a perfect example of an amazingly-arrogant habit of Darwinians, (of which I have collected many examples in my forthcoming book Darwinian Fairytales). This is the habit, when some biological fact inconsistent with Darwinism comes to light, of blaming the fact, instead of blaming their theory. Any such fact Darwinians call a ‘biological error' an ‘error of heredity’, a ‘misfire’, or some thing of that kind: as though the organism in question had gone wrong, when all that has actually happened, of course, is that Darwinism has gone wrong. When Fisher called the birth-rates in civilized countries ‘inverted’, all he meant was that, exactly contrary to Darwinian theory, the more privileged people are the less fertile. From this fact, of course, the only rational conclusion to be drawn is, that Darwinism has got things upside-down. But instead of that Fisher, with typical Darwinian effrontery, concludes that civilised people have got things upside-down!

Fisher, who died in 1962, is nowadays the idol of ultra-Darwinians, and he deserves to be so: he was in fact a sociobiologist ‘born out of due time’. And the old problem for Darwinism, to which he had at least given some publicity, even if he did nothing to solve it, remains to this day the central problem for sociobiologists. The problem (to put it vulgarly) of why ‘the rich and famous’ are such pitiful reproducers as they are.

Of course this ‘problem’ is no problem at all, for anyone except ultra-Darwinians. It is an entirely self-inflicted injury, and as such deserves no sympathy. Who, except an ultra-Darwinian, would expect the highly-privileged to be great breeders? No one; just as no one but an ultra-Darwinian would expect women to adopt-out their babies with maximum expedition. For ultra-Darwinians, on the other hand, the infertility of the privileged is a good deal more than a problem. It is a refutation.

But they react to it in accordance with a well-tried rule of present-day scientific research. The rule is: ‘When your theory meets with a refutation, call it instead "a problem", and demand additional money in order to enable you to solve it.’ Experience has shown that this rule is just the thing for keeping a ‘research program’ afloat, even if it leaks like a sieve. Indeed, the more of these challenging ‘problems’ you can mention, the more money you are plainly entitled to demand.

10. If variations which are useful to their possessors in the struggle for life ‘do occur, can we doubt (remembering that many more individuals are born than can possibly survive), that individuals having any advantage, however slight, over others, would have the best chance of surviving and of procreating their kind? On the other hand, we may feel sure that any variation in the least degree injurious would be rigidly destroyed.’

This is from The Origin of Species, pp. 80-81. Exactly the same words occur in all the editions.

Since this passage expresses the essential idea of natural selection, no further evidence is needed to show that proposition 10 is a Darwinian one. But is it true? In particular, may we really feel sure that every attribute in the least degree injurious to its possessors would be rigidly destroyed by natural selection?

Which slight advantage would enhance survival chances? There are hundreds if not thousands in individual organisms. There are also about an equal number of slightly disadvatagous traits. The central idea of natural selection is fatally flawed. There is little empirical evidence supporting the "slight advantage" concept. It was a logical, as opposed to empirical, concept when first introduced and remains so to this day.

On the contrary, the proposition is (saving Darwin’s reverence) ridiculous. Any educated person can easily think of a hundred characteristics, commonly occurring in our species, which are not only ‘in the least degree’ injurious to their possessors, but seriously or even extremely injurious to them, which have not been ‘rigidly destroyed’, and concerning which there is not the smallest evidence that they are in the process of being destroyed. Here are ten such characteristics, without even going past the first letter of the alphabet. Abortion; adoption; fondness for alcohol; altruism; anal intercourse; respect for ancestors; susceptibility to aneurism; the love of animals; the importance attached to art; asceticism, whether sexual, dietary, or whatever.

Each of these characteristics tends, more or less strongly, to shorten our lives, or to lessen the number of children we have, or both. All of them are of extreme antiquity. Some of them are probably older than our species itself. Adoption, for example is practised by some species of chimpanzees: another adult female taking over the care of a baby whose mother has died. Why has not this ancient and gross ‘biological error’ been rigidly destroyed?

‘There has not been enough time’, replies the Darwinian. Well, that could be so: perhaps there has not been enough time. And then again, perhaps there has been enough time: perhaps even twenty times over. How long does it take for natural selection to destroy an injurious attribute, such as adoption or fondness for alcohol? I have not the faintest idea, of course. I therefore have no positive ground whatever for believing either that there has been enough time for adoption to be destroyed, or that there has not. But then, on this matter, everyone else is in the same state of total ignorance as I am. So how come the Darwinian is so confident that there has not been enough time? What evidence can he point to, for thinking that there has not? Why, nothing but this, that adoption has not been destroyed, despite its being an injurious attribute! But this is palpably arguing in a circle, and taking for granted the very point which is in dispute. The Darwinian has no positive evidence whatever, that there has not been enough time.

Mercifully, Darwinians nowadays are much more reluctant than they formerly were, to rely heavily on the ‘not-enough-time’ defence of their theory against critics. They have benefited from the strictures of philosophers, who have pointed out that it is not good scientific method, to defend Darwinism by a tactic which would always be equally available whatever the state of the evidence, and which will still be equally available to Darwinians a million years hence, if adoption (for example) is still practised then.

The cream of the jest, concerning proposition 10, is that Darwinians themselves do not really believe it. Ask a Darwinian whether he actually believes that the fondness for alcoholic drinks is being destroyed now, or that abortion is, or adoption - and watch his face. Well, of course he does not believe it! Why would he? There is not a particle of evidence in its favour, and there is a great mountain of evidence against it. Absolutely the only thing it has in its favour is that Darwinism says it must be so. But (as Descartes said in another connection) ‘this reasoning cannot be presented to infidels, who might consider that it proceeded in a circle’.

What becomes, then, of the terrifying giant named Natural Selection, which can never sleep, can never fail to detect an attribute which is, even in the least degree, injurious to its possessors in the struggle for life, and can never fail to punish such an attribute with rigid destruction? Why, just that, like so much else in Darwinism, it is an obvious fairytale, at least as far as our species is concerned.

It would not be difficult to compile another list of ten obvious Darwinian falsities; or another one after that, either. But on that scale, the thing would be tiresome both to read and to write. Anyway it ought not to be necessary: ten obvious Darwinian falsities should be enough to make the point. The point, namely, that if most educated people now think they are Darwinians, it is only because they have no idea of the multiplied absurdities which belief in Darwinism requires.

Saturday, August 12, 2006

Testing ID Hypotheses

An instructive exchange between me and another commentator took place at the blogsite Telic Thoughts. The topic centered around the origin of life. The entire thread can be viewed at the website. The exchange, which spanned multiple posts, is reproduced. My comments are preceeded by B and the other commentator by the letters OC. My blog comments are in bold print.

OC: The problem with an ID hypothesis for the origin of life is that it doesn't seem to make predictions other than by exclusion–"there are no conditions in which random chemical reactions can self organize to produce something that reproduces with heritable variation".

This is an objection to ID based on personal preference. "Heritable variation" is a phrase loaded with dubious assumptions. The belief that catalytic qualities of RNA are sufficient evidence that "reproduction with heritable variation" would proceed has not been demonstrated. Various RNAs do exhibit catalytic properties. Cleavage of phosphodiester bonds has been demonstrated but the scope of RNA catalysis is not nearly as broad as that found in proteins. More importantly heritable variation needs a coding context. That context is the genetic code. Its existence provides functional meaning to the nucleotide content and order of DNA. Without an in place code different nucleotide sequences are meaningless. For that matter the alphanumeric symbols of the English language are meaningless without a convention by which their identity and sequences acquire meaning. Random sequences of RNA nucleotides then are heritably useless without the simultaneous existence of a governing encoding convention.

It's easy enough to demonstrate the weaknesses of origin of life hypotheses as well as the subjective nature of preferred predictions but what about OC's point? Are there design predictions and ways of testing them? Continuing:

B: I'll give you a reason that is testable. Found universally are error detection and repair mechanisms that maintain genomic integrity. Causes of genomic mal-function include factors that were present on earth at life's origins. The prediction is that such mechanisms are absolutely essential to the viability of a genome and a test involves observing replication without such mechanisms. If the rate of information loss exceeds gains a generation mechanism is fatally compromised.

OC: So once again, the best that you can come up with is a negative prediction: reproduction without separate error correction mechanisms will never be observed.

Note the way OC frames the issue- in negation form. Consider this instead:

An indicator of intelligent causality is an outcome that would not otherwise occur through natural forces alone. Nucleic acid sequences naturally become disordered with time. In the absence of error detection and repair mechanisms the rate of decay will exceed possible increases in genomic information resulting from selected changes. Experimental verification of this hypothesis would establish the alluded to indicator of intelligence.

The presentation is positive but for OC the message is negative. It's about the message and some dislike the concept that intelligence is detectable.

B: Predictions entailing negations are useful. Physical realities can reflect one option or its opposite. Why assume one is valid without testing? It is an irrational approach.

In this case negations have an affirmative flip side. There are two possibilities. An outcome (life) was either the result of an intelligently directed process or one that was undirected by intelligence. Evidence against one is necessarily evidence favoring the opposite.

OC: Obviously, such a prediction cannot be confirmed in a finite amount of time.

B: We can get a very good indication of what occurs under varying conditions and if the data is overwhelmingly lopsided after much testing a conclusion can be drawn. Confirming events of natural history may be intrinsically difficult but the best fit will win out in the end.

B: Predictions entailing negations are useful. Physical realities can reflect one option or its opposite. Why assume one is valid without testing?

OC: As a rule they are not useful. Scientifically, they are almost always dead ends, because people who make negative predictions never actually seem to try to test them. It is just human nature–people find it hard to motivate themselves to attempt something that they believe to be impossible. Essentially all scientific progress is made on the basis of positive predictions. For example, even though you have tried to frame this as a prediction of ID, there are no ID advocates attempting to test it. All of the work on testing origin of life scenarios is being done by people who hypothesize that such a mechanism exists.

A prediction about competing rates: one a theorized addition of information and the second a measurement of its loss can be viewed positively. Which process is predominant? The implications are enormous for more than just life's origins.

OC: As a rule they are not useful. Scientifically, they are almost always dead ends, because people who make negative predictions never actually seem to try to test them. It is just human nature–people find it hard to motivate themselves to attempt something that they believe to be impossible.

B: In this case testing genomic corruption as well as biological mechanisms designed to prevent it yields very useful data related to disease and cancer. It is no doubt true that funding could be problematic for an ID oriented study and anti-IDers would want to fry any publisher of adverse test results. But that's the political dimension of it.

I get the impression that motivation is less of a problem for IDers than is funding.

Friday, August 11, 2006

Embryonic DNA Repair

An article entitled 'DNA repair in mammal embryos is a matter of timing' offers some food for thought. A part of the article appears in italics.

Investigators at St. Jude Children's Research Hospital have discovered that the cells of the developing nervous system of the mammalian embryo have an exquisite sense of timing when it comes to fixing broken chromosomes: the cells use one type of repair mechanism during the first half of development and another during the second half.

The team also showed that blocking a repair pathway causes the cell to commit suicide, a process called apoptosis; and that preventing this attempt at apoptosis keeps the damaged cell alive and able to become cancerous. Moreover, the type of cancer that develops depends on which repair pathway was originally disrupted.

DNA error detection and repair mechanisms are clearly crucial to keeping an organism free of disease and cancer. They are also interesting from an evolutionary point of view. The mechanisms cited here are coupled to a second mechanism- apoptosis. Both need to function together effectively to keep a mammal healthy.

These findings reflect the meticulous timing of an important aspect of embryo development and help to explain the origin of a variety of cancers from muscle tumors to brain tumors, researchers said. A report on these results appears in the online prepublication issue of Proceedings of the National Academy of Science.

Specifically, the St. Jude researchers showed that the DNA repair pathway called homologous recombination (HR) works primarily during the first half of embryo development, when many cells are dividing inside the growing body. In contrast, the pathway called non-homologous end joining (NHEJ) becomes an important repair mechanism midway through development, when cells begin to assume their final form and take on specific roles.

Two different repair pathways correspond to stages of development.

HR and NHEJ repair a type of DNA damage called a double-strand break (DSB), which cuts completely through the DNA. DNA exists as two individual strands that associate to form its double-stranded, twisted-ladder—shaped structure.

The researchers also discovered that a protein called ATM is required for apoptosis that is triggered by blocking NHEJ. However, apoptosis triggered by blocking HR does not require this protein. ATM is a critical DNA damage-signaling factor that is required to prevent a severe human neurodegenerative syndrome called ataxia telangiectasia. This new work points to the specific DNA repair pathway that ATM is required to monitor in order to prevent neurodegeneration.

The protein ATM is an essential part of apoptosis (cellular suicide) and has a monitoring function.

The HR pathway fixes a broken chromosome by using that chromosome’s exact “twin” as a blueprint to guide the repair job, according to Peter McKinnon, Ph.D., an associate member of Genetics and Tumor Cell Biology at St. Jude and senior author of the PNAS paper. However, such twins only exist in cells that are preparing to divide into two new cells, a process called mitosis, he noted. Then, as the cell starts to divide, each member of the sister chromatid pair moves into a different new cell.
Because HR is active only during the first half of embryo development, it is the critical repair pathway for the rapidly multiplying precursor and stem cells—cells that populate the body during early development with “daughter” cells—that later take on specific roles, according to researchers.

“Therefore, if HR-related apoptosis is blocked during the early part of embryo development, precursor and stem cells are affected. And since those cells give rise to many different types of cells and tissues, many different types of cancers can arise, such as skin cancer and sarcomas (cancers of bone, cartilage, fat, muscle or blood vessels),” McKinnon said.

An apoptosis malfunction can easily be fatal.

But as cells acquire specialized structures and functions, they stop dividing and no longer produce sister chromatids. “When cells begin assuming specific roles in the brain, they stow away most of their chromosomes into tightly wrapped strings of DNA and use only those genes required to survive and allow them to perform these roles,” McKinnon explained. “In the absence of sister chromatids to use as blueprints, the NHEJ repair pathway uses various chemical means to join the broken ends of DNA strands.”

Since the cell uses NHEJ only when many cells are becoming specialized, cancers that arise in the absence of this pathway are more specific, such as cancer of a type of cell that produces only immune cells called B lymphocytes. The wide variety of cancers that can form represents the fact that HR and NHEJ are important throughout the developing body, and not just in the developing nervous system.

There are many chicken-egg scenarios in biology. Since apoptosis is involved with pathways unrelated to this study one might surmise that it would have evolved first. Then again that same line of reasoning would apply to any other repair pathway so when did the apoptosis function evolve? What would have initially triggered it?


Darwinism: Part One

An article by David Stove entitled 'So You Think You Are a Darwinian?' contains a list of ten Darwinian beliefs. Five are listed in this post. The article is italicized.

Most educated people nowadays, I believe, think of themselves as Darwinians. If they do, however, it can only be from ignorance: from not knowing enough about what Darwinism says. For Darwinism says many things, especially about our species, which are too obviously false to be believed by any educated person; or at least by an educated person who retains any capacity at all for critical thought on the subject of Darwinism.

Of course most educated people now are Darwinians, in the sense that they believe our species to have originated, not in a creative act of the Divine Will, but by evolution from other animals. But believing that proposition is not enough to make someone a Darwinian. It had been believed, as may be learnt from any history of biology, by very many people long before Darwinism, or Darwin, was born.

What is needed to make someone an adherent of a certain school of thought is belief in all or most of the propositions which are peculiar to that school, and are believed either by all of its adherents, or at least by the more thoroughgoing ones. In any large school of thought, there is always a minority who adhere more exclusively than most to the characteristic beliefs of the school: they are the ‘purists’ or ‘ultras’ of that school. What is needed and sufficient, then, to make a person a Darwinian, is belief in all or most of the propositions which are peculiar to Darwinians, and believed either by all of them, or at least by ultra-Darwinians.

I give below ten propositions which are all Darwinian beliefs in the sense just specified. Each of them is obviously false: either a direct falsity about our species or, where the proposition is a general one, obviously false in the case of our species, at least. Some of the ten propositions are quotations; all the others are paraphrases. The quotations are all from authors who are so well-known, at least in Darwinian circles, as spokesmen for Darwinism or ultra-Darwinism, that their names alone will be sufficient evidence that the proposition is a Darwinian one. Where the proposition is a paraphrase, I give quotations or other information which will, I think, suffice to establish its Darwinian credentials.

My ten propositions are nearly in reverse historical order. Thus, I start from the present day, and from the inferno-scene - like something by Hieronymus Bosch - which the 'selfish gene’ theory makes of all life. Then I go back a bit to some of the falsities which, beginning in the 1960s, were contributed to Darwinism by the theory of ‘inclusive fitness’. And finally I get back to some of the falsities, more pedestrian though no less obvious, of the Darwinism of the 19th or early-20th century.

1. The truth is, ‘the total prostitution of all animal life, including Man and all his airs and graces, to the blind purposiveness of these minute virus-like substances’, genes.

This is a thumbnail-sketch, and an accurate one, of the contents of The Selfish Gene (1976) by Richard Dawkins. It was not written by Dawkins, but he quoted it with manifest enthusiasm in a defence of The Selfish Gene which he wrote in this journal in 1981. Dawkins’ status, as a widely admired spokesman for ultra-Darwinism, is too well-known to need evidence of it adduced here. His admirers even include some philosophers who have carried their airs and graces to the length of writing good books on such rarefied subjects as universals, or induction, or the mind. Dawkins can scarcely have gratified these admirers by telling them that, even when engaged in writing those books, they were ‘totally prostituted to the blind purposiveness of their genes Still, you ‘have to hand it’ to genes which can write, even if only through their slaves, a good book on subjects like universals or induction. Those genes must have brains all right, as well as purposes. At least, they must, if genes can have brains and purposes. But in fact, of course, DNA molecules no more have such things than H20 molecules do.

2 '…it is, after all, to [a mother’s] advantage that her child should be adopted’ by another woman.

This quotation is from Dawkins’ The Selfish Gene, p. 110.

Obviously false though this proposition is, from the point of view of Darwinism it is well-founded, for the reason which Dawkins gives on the same page: that another woman’s adopting her baby ‘releases a rival female from the burden of child-rearing, and frees her to have another child more quickly.’ This, you will say, is a grotesque way of looking at human life; and so, of course, it is. But it is impossible to deny that it is the Darwinian way.

("Rival female?" This type of Darwinian fundamentalism undermines healthy thinking.)

3. All communication is ‘manipulation of signal-receiver by signal-sender.’

This profound communication, though it might easily have come from any used-car salesman reflecting on life, was actually sent by Dawkins, (in The Extended Phenotype, (1982), p. 57), to the readers whom he was at that point engaged in manipulating. Much as the devil, in many medieval plays, advises the audience not to take his advice.

4. Homosexuality in social animals is a form of sibling-altruism: that is, your homosexuality is a way of helping your brothers and sisters to raise more children.

This very-believable proposition is maintained by Robert Trivers in his book Social Evolution, (1985), pp. 198-9. Professor Trivers is a leading light among ultra-Darwinians, (who are nowadays usually called ‘sociobiologists’). Whether he also believes that suicide, for example, and self-castration, are forms of sibling-altruism, I do not know; but I do not see what there is to stop him. What is there to stop anyone believing such propositions? Only common sense: a thing entirely out of the question among sociobiologists.

5. In all social mammals, the altruism (or apparent altruism) of siblings towards one another is about as strong and common as the altruism (or apparent altruism) of parents towards their offspring.

This proposition is an immediate consequence, and an admitted one, of the theory of inclusive fitness, which says that the degree of altruism depends on the proportion of genes shared. This theory was first put forward by W. D. Hamilton in The Journal of Theoretical Biology in 1964. Since then it has been accepted by Darwinians almost as one man and has revolutionized evolutionary theory. This acceptance has made Professor Hamilton the most influential Darwinian author of the last thirty years.

Thursday, August 10, 2006

Protecting Chromosomes

Information derived from John Hopkins researchers reveals the vital role of specific proteins in protecting chromosomes. Part of an article entitled 'CELL SURVIVAL DEPENDS ON CHROMOSOME INTEGRITY' is shown in italics. My comments are included.

As part of a large National Institutes of Health-funded Technology Centers for Networks and Pathways project, Johns Hopkins researchers have discovered protein machinery important for cells to keep chromosomes intact. Without such proteins, their experiments show that yeast cells experience broken chromosomes and DNA damage that in human cells are well known to lead to cancer.

Such proteins are necessary to preserve the integrity of this eukaryotic genome.

“Maintaining genome integrity is crucial for cell survival,” says Jef Boeke, Ph.D., Sc.D., the report’s senior author, a professor of molecular biology and genetics and co-director of the High Throughput Biology Center of the Institute for Basic Biomedical Sciences at Hopkins. The report will appear online July 6 in Current Biology.

Boeke and colleagues show that removing from yeast cells two proteins called sirtuins - Hst3p and Hst4p - causes cells to become hypersensitive to chemical agents and temperature and to spontaneously break and/or lose chromosomes. In humans, the loss or breakage of chromosomes can cause cells to lose control of when and if they are supposed to divide, becoming cancerous.

Nearly every human cell contains about six feet of DNA packaged into chromosomes. Chromosomes consist of DNA wrapped around a scaffold-like structure made of proteins called histones. Each time a cell divides into two, all of this DNA must be copied exactly and repackaged properly with histones to form chromosomes in the new cell.

During the copying process, new chromosomes often have breaks in them that need to be sealed before the chromosome is considered “finished” and the cell is ready to divide into two. All cells have damage control mechanisms that can sense nicks and breaks in chromosomes - DNA damage - and repair them.

Damaged chromosomes are inevitable. How would a mechanism designed to detect and repair the damage not also be indispensible the moment a eukaryotic genome came into existence?

“We think acetylation somehow marks the newly copied DNA so the cell knows to repair the breaks,” says Boeke. “Once the breaks are repaired, the acetyl groups no longer are needed and are removed in normal cells.”

Sirtuins Hst3p and Hst4p are proteins required to remove these specific chemical “decorations” - called acetyl groups - from specific sites on histones. The acetyl groups are added to lysine-56, an amino acid in the histone protein chain. Chromosomes in yeast cells missing Hst3p and Hst4p become hyperacetylated on lysine-56 - it appears that every lysine-56 in every histone has attached an acetyl group.

“This is the first time we’ve ever seen such a huge effect,” says Boeke. “The chromosomes just light up with acetyl groups - they’re just saturated” when cells are missing these sirtuins.

Earlier work showed that yeast cells initially need the lysine-56 decorations to repair breaks or other damage to DNA that occur when the DNA is copied, an essential process that also has the potential to seriously damage DNA. This new work shows that it is even more critical for yeast cells to remove these decorations once repair has been completed. Thus, there is an endless cycle of putting the acetyl groups on whenever there is damage or the danger thereof and taking them off again. Failure to take off the “decorations” leads to loss of entire chromosomes and other problems with the DNA.

Thus, yeast cells need to carefully coordinate acetylation and deacetylation of lysine-56.

An irreducibly complex function is in evidence.

The team concludes that by putting an acetyl group on lysine-56, the cell is signaling that its DNA is newly made and as a result possibly contains dangerous breaks. Acetylation on lysine-56 may be a universal mechanism for cells to mark damaged DNA. DNA damage can be caused by exposure to chemical mutagens, chemotherapy or even sunlight.

“There are a million mutagens in our environment,” says Boeke. Once cells repair the DNA damage, it is important to shut off repair machinery and return to normal state. The cells require proteins like the sirtuins Hst3p and Hst4p to act as guideposts to help identify dangerous DNA lesions. If the DNA repair machinery does not fix these lesions to maintain chromosome integrity, the cell would lose control of growth or death.

Moving forward, the team hopes to further understand what controls these sirtuins to remove acetyl groups and how hyperacetylation can lead to such dramatic loss of chromosome integrity.

The High Throughput Biology Center, or HiT Center, of the Institute for Basic Biomedical Sciences is an interdisciplinary and interdepartmental effort. The HiT Center combines approaches from a variety of disciplines including biology, physics, chemistry, mathematics, computer science and engineering with the goal of selectively using high-throughput techniques to accelerate hypothesis-driven research and to speed development of new hypotheses.

The Technology Centers for Networks and Pathways of Lysine Modification at Hopkins dissects signaling networks and pathways by developing and applying genetic and computational approaches, proteomics technologies, mass spectrometry technologies, single-cell profiling and other novel methods to detect, quantify and monitor lysine modifications on DNA-coiling histones. Histone modifications are critical for many biological processes, such as epigenetic control of gene expression, which itself dictates the expression of the proteome in all cells. Other lysine modifications include acetylation, methylation, ubiquitylation and sumoylation.

Studies are conducted all the time with inferences favorable to design. Intelligent design encourages critical and innovative thinking about natural history.


Tuesday, August 08, 2006

Limiting Damage to DNA

In an article entitled 'Researchers identify gene as protector of DNA, enemy of tumors' a single gene is the target of focus. The article is italicized. My remarks are not.

Houston -- A single gene plays a pivotal role launching two DNA damage detection and repair pathways in the human genome, suggesting that it functions as a previously unidentified tumor suppressor gene, researchers at The University of Texas M. D. Anderson Cancer Center report in Cancer Cell.

The advance online publication also reports that the gene - called BRIT1 - is under-expressed in human ovarian, breast and prostate cancer cell lines.

This underscores the necessity to explain the evolution of both a gene of interest and all other genes required to enable its regulation and expression.

Defects in BRIT1 seem to be a key pathological alteration in cancer initiation and progression, the authors note, and further understanding of its function may contribute to novel, therapeutic approaches to cancer.

"Disruption of BRIT1 function abolishes DNA damage responses and leads to genomic instability," said senior author Shiaw-Yih Lin, Ph.D., assistant professor in the Department of Molecular Therapeutics at M. D. Anderson. Genomic instability fuels the initiation, growth and spread of cancer.

A signaling network of molecular checkpoint pathways protects the human genome by detecting DNA damage, initiating repair and halting division of the damaged cell so that it does not replicate.

Indeed. Evolutionists cite natural selection as a directional force responsible for sifting beneficial mutations and preserving them. The existence of a complex of genes needed to detect and repair inevitable damage to DNA is essential to preserve existing functions. This raises the question of how any organism could survive genomic corruption prior to a putative point in time when no such damage limiting mechanisms existed.

In a series of laboratory experiments, Lin and colleagues show that BRIT1 activates two of these checkpoint pathways. The ATM pathway springs into action in response to damage caused by ionizing radiation. The ATR pathway responds to DNA damage caused by ultraviolet radiation.

Note that causes of genomic damage would be present at a point in time when the first life forms appeared. It is not a matter of confronting a challenge presented only to more advanced forms of life.

By using small interfering RNA (siRNA) to silence the BRIT1 gene, the scientists shut down both checkpoint pathways in cells exposed to either type of radiation.

Researchers then used siRNA to silence the gene in normal human mammary epithelial cells (HMEC). The result: Inactivation of the gene caused chromosomal aberrations in 21.2 to 25.6 percent of cells. Control group HMEC had no cells with chromosomal aberrations. In cells with the gene silenced that were then exposed to ionizing radiation, 80 percent of cells had chromosomal aberrations.

Genetic disaster ensues when DNA detection and repair mechanisms are disabled.

"We also found that BRIT1 expression is aberrant in several forms of human cancer," Lin said. The team found reduced expression of the gene in 35 of 87 cases of advanced epithelial ovarian cancer. They also found reduced expression in breast and prostate cancer tissue compared with non-cancerous cells.

Genetic analysis of breast cancer specimens revealed a truncated, dysfunctional version of the BRIT1 protein in one sample.

Loss of the DNA damage checkpoint function and the ability to proliferate indefinitely are two cellular changes required for the development of cancer. Lin and colleagues have now tied the gene to both factors. They previously identified BRIT1 as a repressor of hTERT, a protein that when reactivated immortalizes cells, allowing them to multiply indefinitely.

Cells have multiple interacting components as this one gene illustrates. The necessity of functional regulators is aptly portrayed by the article.


An Opiate for Intellectuals

In an article entitled 'Opium of the Intellectuals' the emotional appeal of Darwinism is explored. Utilizing a twist on a Marxist phrase the author argues that Darwinism's persistence can be attributed to its opiate effect on the intellectual masses. The article appears in italics. My comments in standard form.

John Davidson poses the question, "How has Darwinism Persisted?" He believes there to be two reasons in particular which he explains briefly at Uncommon Descent.

I'd like to suggest a third: Darwinism (by which I mean the view that natural processes are sufficient explanations for the origin and diversity of living things) has persisted because it is the opiate of the intellectual elites. It anesthetizes them to the existential pain of a naturalistic world-view which rips all non-arbitrary meaning, morality and significance out of life. Like a drug it gives them a surge of metaphysical pseudo-strength that enables them to cling to an atheistic materialism which might have made sense a century ago but which no longer does. For the man who simply does not want God to exist, Darwinism is a narcotic.

As Richard Dawkins famously wrote, "Darwin made it possible to be an intellectually fulfilled atheist." Unfortunately, the satisfaction that it offers is much like the satisfaction the opium addict gains from his drug. It doesn't really fill the existential emptiness left by the removal of what has been taken away. It merely masks it. Man cannot live without meaning, and atheistic naturalism tells us that ultimately there simply is no purpose to your life or mine. Death is the end. Man is nothing more than an animal with no dignity or worth. Morality is purely subjective. There's no ultimate justice. Love is just a biochemical response. Consciousness is an illusion. Reason is an unreliable tool in the quest for truth.

The intellectual elites are like a bunch of numbed, unhappy addicts sitting around a room seeking to relieve their pain with a fix of materialistic opium, and Darwinism is the best brand on the market. It holds out the allure of an ersatz purpose, incorporating us into the great drama of biological development, it offers us a wafer-thin veneer of meaning by encouraging us to contribute to the well-being of our species. Like those who seek meaning and transcendence in drugs, however, Darwinism ultimately leaves us empty because if we are doomed to perish utterly nothing at all about this life really matters.

Nevertheless, this life is all the atheist has to hold on to. So, like the man dying of emphysema who keeps sucking on his cigarettes, the intellectual elites embrace their Darwinian world-view in hopes that somehow, against all indications, they'll be able to squeeze out of it a few precious drops of meaning for their lives. They're hooked and can't give it up.

For some self-delusion is easier than repentence.

Monday, August 07, 2006

A Mutation Range by Design

A website of the American Committee for the Weizmann Institute of Science published a news article entitled 'Taming Mutations.' The article follows in italics. My comments are in standard print.

REHOVOT, ISRAEL -- May 4, 2006 -- Everyone knows mutations -- genetic mistakes in DNA, the material of heredity -- are bad: The more mutations in the cell’s DNA, the higher the risk of cancer developing. But in the last few years it has become clear that the very processes that generate mutations, if they take place at a relatively low frequency, can actually protect us from cancer. How does the body know how to keep these processes in check, making sure they don’t rocket out of control, causing a sharp rise in our cancer risk? A preliminary answer to this question has come out of research carried out by Prof. Zvi Livneh and research student Sharon Avkin, along with research student Leanne Toube and Dr. Ziv Sevilya of the Biological Chemistry Department, and Prof. Moshe Oren of the Molecular Cell Biology Department, along with two American colleagues. The results of their study appeared recently in the scientific journal Molecular Cell.

The instruments of DNA copying (which takes place prior to cell division) are members of a family of enzymes called DNA polymerase. DNA polymerase travels along one strand of the double stranded molecule, reading each bit of genetic material and copying as it goes along, to create new DNA that will be passed on to the daughter cell at cell division. This enzyme can be a stickler for accuracy -- if it runs into damage from radiation or exposure to harmful substances on the DNA strand, it can stop in its tracks, unable to continue copying. A stoppage of this sort spells death for the cell. But not all damage to DNA is critical and, to avoid the wholesale death of cells, a second type of DNA polymerase, one that is more “careless” and can improvise when it hits a snag, evolved in the cell. “Error-prone DNA repair,” as it’s called, is based on a compromise: The cell lives, but at the price of allowing genetic mutations to be carried over in cell division.

A trade-off occurs. Cells and the energy required to generate their replacement are conserved at the cost of the replicated cell retaining some genetic mutations. The cost of a small number of mutations is evidently worth it.

The body’s solution to minimizing mutations is to have no fewer than ten different “careless” enzymes. Although this may seem paradoxical -- intuitively, more careless enzymes should mean more mutations -- each of these enzymes is tailored to deal with certain specifics types of DNA damage. This specialization is what keeps the level of mutation, and thus the cancer risk, low. But the existence of this variety of specialist enzymes implies precise regulation of the system -- otherwise copying by the careless enzymes might get out of control and lead to an unhealthy proliferation of mutations.

Prof. Livneh and his team recently discovered a security mechanism that prevents such proliferation of mutations. This mechanism allows the right enzyme to go to work at the right time, and only when it’s needed. The main components in this system are the proteins p53 and p21. p53, named “molecule of the year” several years ago by Science, is well known for its central role in reining in cancer processes in the cell. In this case, the proteins seem to act as supervisors, taming the careless enzymes and keeping them in careful check. The scientists’ research showed that if the functioning of p53 or its relative, p21, is harmed, the activities of the careless enzymes can go into overdrive, leading to more mutations.

Sounds like an irreducibly complex system as defined by Professor Behe. Did it evolve through a selection process is a separate question. A proposal suggesting the sequence of events that led to the evolution of this system would be an interesting subject on which to focus.

The actual mechanism works with a sort of molecular clamp that holds the DNA copying enzyme onto the strand of DNA. When the enzyme encounters DNA damage, a small molecule called ubiquitin attaches to the clamp. The ubiquitin, in this case, serves to anchor replacement DNA polymerase molecules -- careless ones -- to the clamp. p53 enters the picture when it is alerted to the damage and causes p21 to be created. The p21 then acts as a sort of facilitator, helping to fasten the proper ubiquitin in place and clearing stalled DNA polymerase out of the way so its replacement can get to work. Thus, these two proteins manage to help the body’s cells maintain a crucial balance, allowing them to divide and multiply while keeping the mutation rate, and therefore the cancer risk, to a minimum.

Biological systems that identify, repair and regulate mutations are an essential part of maintaining genomic integrity. The capacity to generate and maintain genes critical to the survival of an organism, at all stages of an evolutionary process, is a gauge by which to evaluate the viability of the mutation\selection model.


Saturday, August 05, 2006

Chicken Little: Part One

I'm fond of this Chicken Little illustration courtesy of Telic Thoughts. The facial expression correlates well with sky is falling attitude of opponents of intelligent design. Mike Gene, through the link associated with the word 'Bush,' references an article by Karen Armstrong entitled 'Bush's fondness for fundamentalism is courting disaster at home and abroad.' Snippets from the article appear in italics. My comments are in standard form.

From the very beginning, the conflict between religion and modern science was couched in extreme, even apocalyptic rhetoric. Thomas H Huxley, who popularised the Origin of Species, insisted that people had to choose between faith and science; there could be no compromise: "One or the other would have to succumb after a struggle of unknown duration." In response, conservative Christians launched a crusade against Darwinism. After the first world war, the Democratic politician William Jennings Bryan claimed that there was a direct link between evolutionary theory and German militarism: the notion that only the strong could or should survive had "laid the foundation for the bloodiest war in history. The same science that manufactured poisoned gases to suffocate soldiers is preaching that man has a brutal ancestry."

Note the sequence of events. The Origin of Species is published and then popularized by Thomas Huxley. In doing so Huxley, a Darwinist who set the tone for what was to come, throws down a gauntlet by declaring a take no prisoner approach to religion. The quote: "One or the other would have to succumb after a struggle of unknown duration." Armstrong then states that "in response conservative Christians launch a crusade against Darwinism." According to the author the initial challenge comes from Darwin's bulldog and conservative Christians respond by fighting back. Note that at the very outset evolution is founded on an anti-Christian metaphysical foundation.

The struggle continues - nowhere more so than among the Christian right in the US, who still regard the evolutionary hypothesis as surrounded by a murderous nimbus of evil. In 1925, they tried to ban the teaching of evolution in public schools and developed creation science, based on a literal reading of the first chapter of Genesis. More recently, they have tried to introduce into the school curriculum the teaching of intelligent design (ID), which claims that the irreducible complexity of micro-organisms could not have evolved naturally but must be the result of a single creative act. The issue splits the nation down the middle: fundamentalists want to win a battle for God; liberals and secularists are fighting for truth and rationality.

Follow the logic. According to the author the "Christian right" regards evolution "as surrounded by a murderous nimbus of evil." Well surprise, surprise. A theory of natural history is introduced with unnecessary anti-Christian metaphysical baggage and some Christians think this is evil. Shocking.

Just in case you haven't gathered where the author is coming from note how she frames the conflict. It is "fundamentalists" (the same word attached to murderers and suicide bombers) battling against "liberals and secularists" (who) "are fighting for truth and rationality." Is it rational or truthful to proclaim inaccuracies? There are intelligent design advocates, like Behe, who would take issue with the statement that irreducible complexity must be the result of a single creative act. Behe has accepted common descent but believes it occurred with intelligent input. That does not equate to a single creative act.

The same passions are likely to be aroused by President Bush's decision last week to veto the Stem Cell Research Enhancement Act, which would have loosened the restrictions on federal funding for stem cell research. "This bill would support the taking of innocent human life in the hope of finding medical benefits for others," Bush said. "It crosses a moral boundary that our decent society needs to respect."

His opponents point out that while the president zealously champions the rights of the unborn, he is less concerned about the plight of existing American children. The US infant mortality rate is only the 42nd best in the world; the average baby has a better chance of surviving in Havana or Beijing; infant mortality rates are unacceptably high among those who cannot afford adequate healthcare, especially in the African-American community. And, finally, at the same time as Bush decided to veto the stem cell bill, Israeli bombs were taking the lives of hundreds of innocent Lebanese civilians, many of them children, with the tacit approval of the US.

Bush bashing is stylish but the fact is the infant mortality rate in the US was unacceptably high before the advent of the Bush presidency. The healthcare problem preceeds Bush too as do the many positive aspects of America that attract more immigrants than any nation on earth. The last sentence though is classic Chicken Little. After one of the most notorious terrorist groups on earth- Hezbollah- launches missiles into civilian populations and kidnaps Isreali soldiers Chicken Little screams about Isreali countermeasures and the inevitable casualties that occur when the other side deliberately locates launch sites in civilian population centers. If you think this diatribe represents truth and rationality then the sky is ominous. The storm clouds represent a vicious one-sided view of the world and a condemnation of all naysayers.

Friday, August 04, 2006

A Darwinian Trojan Horse: Part Two

This is the second of a two part posting about a Los Angeles Times three book review by Robert Lee Hotz. Parts of the article appear in italics along with my comments in standard print.

Fundamentalist proponents of intelligent design, however, make no broad claim for classroom equality on behalf of all religions because, they insist to the general public, theirs is not a faith-based initiative but "a scientific dissent from Darwinism." But as evolutionary biologist Jerry A. Coyne at the University of Chicago notes, one of intelligent design's leading proponents, William A. Dembski, undermines that objective stance: "[A]ny view of the sciences that leaves Christ out of the picture must be seen as fundamentally deficient." He quotes from Dembski's book "Intelligent Design: The Bridge Between Science & Theology."

Substitute anything for science and you get a classic statement of Christian theology. Christ should be in everything a Christian does. This is no more contrary to good science than the many extra-scientific statements made by noted anti-Christians and atheists throughout the Darwin era. Start with Huxley and then Haldane, Sagan, Dawkins and many others. Why does it matter to Darwinists only when the theistic proclamations are of a pro-Christian nature?

Tufts University philosopher Daniel C. Dennett, however, has no patience with conspiracy theory. The intelligent design movement is simply a "hoax," he writes. Although its proponents claim that theirs is a scientific endeavor, they so far have produced "no experiments with results that challenge any mainstream biological understanding; no observations from the fossil record or genomics or biogeography or comparative anatomy that undermine standard evolutionary thinking."

This is sheer hokum. To begin with results of scientific studies are ideologically neutral. Whether the scientists involved are advocates of evolution, theistic evolution, design, creation or anything else is irrelevant to the data produced. At the outset supporters of Darwin cited data gathered by creationists. There were not many Darwinists around. Did it matter? No. The data and its interpretation is what matters.

What they offer instead is a glib debater's ploy: "First you misuse or misdescribe some scientist's work, provoking an angry rebuttal. Then, instead of dealing forthrightly with the charges leveled, you cite the rebuttal as evidence there is a 'controversy' to teach," Dennett writes. "You can often exploit the very technicality of the issues to your own advantage, counting on most of us to miss the point amid all the difficult details."

Those difficult details are what constitute molecular biology, cellular biology, biochemistry and the like. Issues should be framed around details. That's what science is about. The misuse of a scientist's work is a canard and a tired one at that.

"Christians should embrace modern science for what it has done to reveal the magnificence of the divinity in a depth and detail unmatched by ancient texts," Shermer writes. "In contrast, Intelligent Design creationism reduces God to an artificer, a mere watchmaker piecing together life out of available parts in a cosmic warehouse."

A predictable theological argument. Actually God designs through encoded molecular systems whose sophistication rivals and exceeds codes produced by the human species.

Yet he finally embraced his brainchild, impelled by an unflinching intellectual honesty, the weight of the evidence and the imperative of an undeniable idea. "There seems to be no more design in the variability of organic beings and in the action of natural selection," Darwin wrote, "than in the course which the wind blows."

When is the last time you observed the wind blowing a design resembling an encoding unit replete with a promotor region enabling a transcription polymerase protein to bind with an assist from transcription factors? How relevant is the wind analogy to enhancers that effect the transcription process itself? When is the last time wind created a design comparable to the histone proteins constituting nucleosomes and an ingenious code governing gene expression? Can the authors at least produce a sequence of events consistent with the much touted natural selection explanation detailing how a single gene and its regulatory mechanisms evolved? Would such a sequence of events be based on empirical evidence or the imaginations of the story tellers?

Thursday, August 03, 2006

A Darwinian Trojan Horse: Part One

A Los Angeles Times three book review by Robert Lee Hotz is the pretext for some non-scientific criticism of intelligent design. The review is not notable for its relevancy but rather as a good example of what is wrong with Darwinism. Darwinism is not simply noted for its espousal of evolution as a mechanism by which natural history is understood. It is also an attempt to further non-scientific metaphysical values based on inferences drawn from evolution. Snippets from the article appear here in italics along with my comments in standard print.

In exploring the shortcomings of intelligent design, these writers also highlight a broader struggle over the evidence of existence that is as old as science and revealed religion.

Simply put, Darwin documented the transformational power of sex and death. The struggle to survive and reproduce is the natural engine of variation, he determined. In any species, more are often born than can survive. Even a slight hereditary advantage may favor one over the other. Those who survive will pass their competitive edge on to their offspring. In this way, limbs could become wings and, in 3 billion or 4 billion years, microbes could evolve into men.

Darwin did not document "the transformational power of sex and death." He presented an argument that his natural selection concept explained the diversity of biological organisms. It is critical for those indulging in pseudo-scientific criticism to comprehend two things. First, Darwin did not even attempt to document the origin of life. An initial organism is assumed not empirically documented. This has enormous implications for an intelligent design inference if the likes of Hotz and the authors he references are willing to discuss the issue scientifically.

Secondly, the retention of hereditary traits, theorized as having come about through a stochastic process, is arguable but far from documented, particularly as far as eukaryotic organisms are concerned. Despite claims to the contrary, Haldane's Dilemna has never been satisfactorily resolved.

Modern evolutionary biology emphasizes the underlying unity of life, as amply documented in the genetic code shared by all organisms, which genome mapper and evangelical Christian Francis Collins has called "the language in which God created life."

The underlying unity of life, as illustrated by the genetic code, is not in dispute. What is in dispute is the Darwinian contention that a genetic code, a genome by which hereditary traits are retained and passed on and a complex of nucleic acids and proteins came into existence without some measure of intelligent input.

For those seeking faith-based alternatives to Darwin, however, evolutionary theory commits an unforgivable affront, these authors write. It unseats humanity as master of a divine creation. With its emphasis on the mechanism of natural selection, it puts people on equal biological footing with barnacles and baboons.

This is a revealing comment but its meaning is lost on the author. Human mastery of divine creation is an oxymoronic phrase. There is no human mastery of divine providence. On the other hand let us not ignore the intended mockery. This is the type of comment consistent with one who believes divine creation is a human construct rather than a reality. That's the right of the opinion holder. It is insidious though, that one would assert a scientific debunking of intelligent design clothed in theological garb. There are theistic evolutionists who believe evolution was the tool of divine choice. There are others who believe an intelligent inference is evident at the origin of life about which Darwin had little to say. For both groups the unseating reference is a straw man that the author, like Sancho Panza before him, has valiently but vainly strived to demolish.

"[L]et's be clear: This is not evolution versus God," writes David Quammen in "The Reluctant Mr. Darwin: An Intimate Portrait of Charles Darwin and the Making of His Theory of Evolution." "The existence of God — any sort of god, personal or abstract, immanent or distant — is not what Darwin's evolutionary theory challenges. What it challenges is the supposed godliness of Man — the conviction that we above all other life forms are spiritually elevated, divinely favored, possessed of an immaterial and immortal essence, such that we have special prospects for eternity, special status in the expectations of God, special rights and responsibilities on Earth."

This comment shows why Darwinism has so little support among the general public. ID critics contend it is the ignorance of the general public that is to blame. In reality the general public is smarter than their detractors. Note that the nature of the criticism is metaphysical not scientific. Assume for the sake of argument that evolution occured as theorized. This says absolutely nothing about spirituality and eternity. God could have choosen an evolutionary process if he so desired while simultaneously setting aside humanity as distinctly different from other organisms in a moral context. Evolution would not negate an eternal role for humanity except in the eyes of those who already disbelieve in God and eternity. As I pointed out at the outset Darwinism has some distinctly unscientific metaphysical baggage.

Quammen does not flinch from "the horrible challenge" implied by Darwin's idea: "In plain language, a soul or no soul? An afterlife or not? Are humans spiritually immortal in a way that chickens or cows are not, or just another form of temporarily animated meat?"

The fact that Quammen poses Darwinism in this context goes a long way in showing why Americans correctly reject it. It is metaphysics in scientific garb.