I was recently in a long discussion/debate with Tom Melendy, Ph.D. Molecular Biology, on the FaceBook page of a reporter. It is quite long and in-depth… I will include it all here as both a record for myself to reference in the future (for instance I lost the specified debate info I had with a professor of history at the University of Michigan about the Iraq war — many of my responses are encapsulated in my page entitled WMD); and to show others there are good responses to ideas many think are settled science ~ really settled “scientism.” I also post this here because Tom has taken positions and defended some things I think are questionable… but I am no scientist or specialist in the sciences. So this is posted here in order for others to access and dissect (hello Creation.com?!). A definition for scientism that exudes from the below conversation was made by an atheist, and it is apt here:
If science really is permanently committed to methodological naturalism – the philosophical position that restricts all explanations in science to naturalistic explanations – it follows that the aim of science is not generating true theories. Instead, the aim of science would be something like: generating the best theories that can be formulated subject to the restriction that the theories are naturalistic. More and more evidence could come in suggesting that a supernatural being exists, but scientific theories wouldn’t be allowed to acknowledge that possibility.
Bradley Monton, author of Seeking God in Science: An Atheist Defends Intelligent Design ~ Apologetics315 h/t
This conversation started when a reporter, Virginia Heffernan, who has written for the New York Times, Slate, and currently writes for Yahoo News, came out as a creationist — of sorts. I say “of sorts” because even though she takes a creationist position, it is one taken on minimal understanding. I do not point this out as being a bad thing, people often get busy with schooling, careers, and family and lose the time to investigate the grounds and positions of ones own faith. That being said, when someone is then challenged on a subject what often happens is they will abandon their previously held position in lieu of what they think is a more informed position. I touch on the “new medias” influence in this regards in the opening chapter of my book:
The importance of knowing, defining, and dissecting worldviews in our electronic age is more important today than ever. The internet brings a myriad of religious and political opinions right into our living rooms daily. What we were able to confront, and if one so desired, to stop at their doorstep, is now with a touch of a button in our living rooms, children’s bedrooms, our cell phones, and the like, routing the old filter of that doorstep. Facebook, MySpace, Twitter, all these words have entered our vocabulary in less than a decade and they offer a plethora of chances to encounter the world as never before.
TOM, click your picture
Thomas Melendy, Ph.D., associate professor of microbiology and immunology… at the University at Buffalo (SUNY), have been elected fellows of the American Association for the Advancement of Science (AAAS), the world’s largest general scientific society and publisher of the journal Science. he among 450 scientists selected by their peers this year for their “meritorious efforts to advance science or its applications.”
This is what happens often times when children leave a low information cocoon of faith via their parents and their local church and sit in a classroom like that of Dr. Melendy’s. The onus is then, as I see it, on each person of faith to step up to the plate and learn their faith as well as a guy would learn about their favorite sports team or a woman would learn about a character in a novel. In other words, conversation about one’s faith should flow as easily as talking about — say, the Angels baseball team or a Jane Austen novel.
who was Chairman and Cofounder with Max Weismann of the Center for the Study of The Great Ideas and Editor in Chief of its journal Philosophy is Everybody’s Business, Founder and Director of the Institute for Philosophical Research, Chairman of the Board of Editors of Encyclopedia Britannica, Editor in Chief of the Great Books of the Western World and The Syntopicon: An Index to the Great Ideas, Editor of The Great Ideas Today (all published by Encyclopedia Britannica), Co-Founder and Honorary Trustee of The Aspen Institute, past Instructor at Columbia University, Professor Emeritus at the University of Chicago (1930-52)
… was no “dummy,” and said the following about our faith:
“I suspect that most of the individuals who have religious faith are content with blind faith. They feel no obligation to understand what they believe. They may even wish not to have their beliefs disturbed by thought. But if God in whom they believe created them with intellectual and rational powers that impose upon them the duty to try to understand the creed of their religion. Not to do so is to verge on superstition.”
Morimer J. Adler, “A Philosopher’s Religious Faith,” in, Kelly James Clark, ed., Philosophers Who Believe: The Spiritual Journeys of 11 Leading Thinkers (Downers Grove, IL: InterVarsity Press, 1993), 207
So I give kudos to Virginia Heffernan for having the tenacity to “keep the faith,” but this should be a lesson to all who read this that YOU should take the time to know how to defend, explain, and encapsulate your faith well to both inoculate yourself against being tossed by the waves and blown around by every wind of teaching; as well as showing others that faith is not blind, but in what we know.
…and other resources at:
So with this short admonition and the short list of books below to get the person who searches after truth thinking, and thinking well, I will document the professors and my debate/discussion. I start the discussion before I enter for clarity/reference:
Jim K. Starts out by saying
Tom Melendy Gravity is called a law and can be and has been observed. Macro-Evolution has never been observed. I believe in intelligent design This can include creation all the way to evolution by a God. If you want scientific proof on this watch “I do not have enough faith to be an atheist” by Frank Turek. Here are a few youtube websites for you http://www.youtube.com/watch?v=XFzJ8beUDvg
I will emphasize the point that concerned me:
Tom Melendy responds
Jim, Macro evolution has been observed in the laboratory under controlled conditions – within just a few generations you can “breed” fish to be miniature fish, which reproduce and “grow” up while never getting bigger than the size they were bred for. And Jim, I NEVER said that belief in evolution in inconsistent with a belief in God. I am merely saying that the case for evolution is overwhelming and cannot be denied by any rational person who bothers to examine the evidence. Belief in God is based on faith, not evidence; and it would be entirely appropriate to believe that evolution, like the other laws of the universe, are merely the hands of God shaping the world we live in. As for referring to evolution as “intelligent design”, I would have to agree – there can be no more intelligent a design program than the evolution that created the amazing diversity of life on this planet including mankind himself.
James P. hops in
Er Tom, as a biologist I would call what you’ve described as ‘artificial selection’ – not ‘evolution’. In the wild such a change might be called ‘speciation’ if the two varieties didn’t interbreed to produce fertile offspring, however that’s not ‘evolution’ either. There is no evidence for evolution whatsoever – and that’s coming from someone who has studied the subject in detail for 15 years.
Tom Melendy responds
“Er” I’m a PhD biologist myself James, and I’ve been studying evolution for 25 years. Evolution is a result of the combination natural selection (and yes, in the lab it would be artificial – same thing except in nature you have to wait until conditions change so selection is usually slower) AND speciation. Speciation is a much more complicated process that occurs on a much slower time scale. By definition (when two sub-species can no longer productively interbreed to create a group that can reproduce) – however, things are more complicated than that! As any biologist will tell you, the devil is in the details – some “speciation” can be a result of behavior – two subspecies may no longer ever mate due to changes in mating behavior and/or geographic separation. Others are due to cytogenetic changes – while a donkey and a horse are genetically 99+% identical at the gene sequence level, the cytogentic changes make their common hybrid (the mule) generally sterile (non-dysjunction during gamete formation), EXCEPT in a very rare cases where the chromosomes happen to align in just the right formation – there are a few documented and proven cases where mules were able to effectively cross-breed with horses or donkeys. Horses and donkeys are far down the speciation path so sexually reproductive hybrids are extraordinarily rare. Zebras show an intermediate cytogenetic phenotype/structure between those of horses and donkeys, and as such their progeny (zebroids) have much greater success at matings with either parental species. The “mules” for lion-tiger matings (ligers and tigons) are fairly functional reproductively and can fairly readily interbreed with their parent species (so much more like the zebroids), so these are less far down the speciation path, even though tigers and lions are still considered different species. There are examples of interspecies hybrids that can reproduce, thereby creating a hybrid species. This shows cases where the two species are even more closely related. One example is the American Red Wolf, which is a hybrid between the Gray Wolf and the Coyote. (There are other know cases too.) And finally there are sub-species which don’t generally mate, but can and when they do they produce offspring that can mate with either parental species or their own hybrid-type; examples of this would be Bengal and Siberian tigers mating or Kodiak bear or Grizzly bear matings with Polar Bears. The time-scale require for speciation is much greater than that for natural selection, but is the aspect of evolution that drives speciation (essentially ‘nails down’ the changes that build up over time in sub-species, and starts preventing backcrosses from homgenizing the two species). These cytogenetic changes are much like those that occur in all animals during the early stages of somatic cancers, but of course only the most conservative changes can be heritable (any gametes with the more significant cytogenetic changes would not survive development). So as you can see James, while it is not feasible to reproduce the ‘slow’ aspect of evolution (cytogenetic speciation) in the laboratory (because of the great time scales required), there is a wealth of evidence of how this process occurs in the natural world around us – showing species and sub-species at all levels of speciation. There is an extraordinary wealth of proof of evolution not only at the fossil level (which is dramatically greater than the state 20 years ago, the supposed “holes” creationists point to no longer exist), but also now at the genetic level (as many extinct species have had their genomes sequences with new high-throughput sequencing techniques, many within just the last couple of years), and this information complements and clarifies the fossil data wonderfully. And here I’ve told you about examples of speciation that are currently ongoing in the world today, and they are present in a wide range of levels. Anyone with a biology background who claims to see no evidence of evolution is being willfully blind!
Tom Melendy again responds
And Jon, you can put whichever “label” you want on it, model or theory, I don’t really care – either way it’s happened throughout the natural history of this world, and it continues to happen today.
This is where I wade in, and I concern myself with a single point that takes a while to get to. I keep this point alive throughout.
Tom Melendy, I missed the observation MACRO evolutionary proof. Please explain what this observation has been. Is there a peer reviewed article you can refer me to.
Tom Melendy responds
read it again, there’s an extensive outline of the paleontological, genetic, cytogenetic evidence. If you can’t understand it, let me know the part you can’t understand and I can explain it to you.
Is there a peer reviewed article on the Macro evolutionary evidence observed in the laboratory? I get every reasonably priced science mag (the Nature journal is too expensive for me). I have about 5,000 books in my home library, many are materialist — from Grecian times till today, neo-Darwinian topics (Mayr, Gould, Asimov, Miller, etc.), and other texts. About half of my library are views opposite of mine.
In other words, I have yet to meet, read, or watch proof of one species, say the Canis lupus, changing into a Felis silvestris catus. Centimeter changes in beaks of birds on an island is micro evolution (change within species).
Canis lupus being able to mate with the Canus domesticus, or Polar Bears with Grizzlies, or rabbits separated by a canyon [they are different species... but can mate... just cannot due to separation] … these are the same kind: in other words, a rabbit, is a rabbit, is a rabbit.
A Great Dane and a Chihuahua cannot mate, but they are still dogs.
Take note Tom refers to his education and position a lot. There is an ego, or, an emotion, involved here that drives his position more than the evidence. Although God is not mentioned yet, the topic is on “creationism,” so the below quote is perfect to set the stage for the “bias” behind the bias:
Naturalism and materialism are not scientific conclusions; rather, they are scientific premises. They are not discovered in nature but imposed upon nature. In short, they are articles of faith. Here is Harvard biologist Richard Lewontin: “We take the side of science in spite of the patent absurdity of some of its constructs, in spite of its failure to fulfill many of its extravagant promises of health and life, in spite of the tolerance of the scientific community for unsubstantiated just-so stories, because we have a priori commitment, a commitment [a faith] — a commitment to materialism. It is not that the methods and institutions of science somehow compel us to accept a material explanation of the phenomenal world, but, on the contrary, that we are forced by our a priori adherence to material causes to create an apparatus of investigation and a set of concepts that produce material explanations, no matter how counter-intuitive, no matter how mystifying to the uninitiated. Moreover, that materialism is an absolute, for we cannot allow a Divine Foot in the door.”
Dinesh D’Souza points to this in his recent book, What’s So Great about Christianity (Washington, DC: Regnery Publishing, 2007), 161 (emphasis added).
I just explained to you “speciation”, which is the basis behind macro-evolution. I showed you how different species can sometimes mate (Canis lupus can mate with Canis latrans – two different species – and produce offspring that can reproduce with themselves), I explained as you move farther away evolutionarily the species can hybridize and hybrids show some, but decreasing ability, to successfully mate as the species are more distantly related (are you going to tell me lions are tigers, or zebras are horses or donkeys?) I pointed out how a macroevolutionary experiment cannot be done in the laboratory because of the time frame required for cytogenetic changes to occur (do you know what those are?). So unless you can provide a time machine, those experiments cannot be completed for many lifetimes. But that doesn’t mean that you can’t evaluate and measure the genetic and cytogenetic changes that are in the midst of occurring throughout the world in the many examples I’ve given of species, sub-species, and closely related species showing every step along the way toward speciation. In spite of your readings, you seem to lack some basic understanding of not only biology, but how to objectively evaluate biological data. But I guess that’s the case isn’t it – reading the Bible does not make one a minister, reading biology books does not make one a biologist, anymore than knowing an opera by heart makes one a opera performer. Reading something is different than the skill set to actually DO it. I am a biologist trained (and hired) at some of the best institutions in the world – I don’t write the textbooks, I do the research that ends up being written about by textbook authors.
Yes, Lions are tigers. They are cats, whether they can breed or not. They are a kind.
First Statement by You:
1) Macro evolution has been observed in the laboratory under controlled conditions – within just a few generations you can “breed” fish to be miniature fish, which reproduce and “grow” up while never getting bigger than the size they were bred for.
2) I pointed out how a macroevolutionary experiment cannot be done in the laboratory because of the time frame required for cytogenetic changes to occur.
Miniaturizing a fish is not macro-evolution!? You have a Ph.D. alright — in obfuscating terms.
- American Heritage Science Dictionary: “Evolution that results in the formation of a new taxonomic group above the level of a species.”
- From an old 1962 textbook (Holt, Rinehart, Winston, … probably when you were going through school?) Evolution and Genetics: “The Modern Theory of Evolution:Quantum evolution, also known as mega- and macroevolution, is the term applied to the rapid shift of a population to a new equilibrium distinctly unlike the ancestral condition, thus leading to the origin of higher taxonomic categories such as new orders and classes.”
- What Is Evolution, Ernst Mayr: “Evolution above the species level; the evolution of higher taxa and the production of evolutionary novelties, such as new structures.”
Species is the key… you seem to be conflating it a bit.
So are you positing that this “smaller fish,” which in one breath you say is evidence of “Quantum evolution” a new taxonomy? Or is it [Quantum evolution] not able to be done in the laboratory because of the time frame required for cytogenetic changes to occur is not long enough in human terms?
So, Macroevolution is not observable, correct?
re-read!!! – I never said “macro” evolution could be observed. I was referring to the microevolutionary changes. When you brought up macro I started telling you about the cytogenetic changes required for speciation or macroevolution. Both steps, micro and macro, are required for evolution. Pay attention!
Man, you are not a very astute student are you?
Yes, according to your own citation above, lions and tigers are separate species. As I stated above. Very good Sean.
Let us get into the nitty-gritty later, I want to define terms first.
SPECIES and MACROEVOLUTION:
Species is not well defined. Example: Canis Domesticus (say, a, German Shepherd) and Canis Lupus (wolf) are classified as two separate species. But they can interbreed (i.e. a Wolf and a German Shepherd). But a Chihuahua and a Great Dane cannot breed, but they are both Canis Domesticus (the same species). The arctic hair cannot breed with the Florida hair, but both breed with the Dakota hair. Evolutionists recognize certain bowerbirds as distinct species even though they often interbreed.
Or consider the case of two different kinds of squirrels separated by the Grand Canyon. The Kaibab squirrel inhabits the north side of the canyon, while the Abert squirrel inhabits the south side. It seems evident the two descended from one original population. Rarely, however, can squirrels from both populations come together, and thus there is no interbreeding between them. And, for some time biologists have disagreed as to whether the squirrels had reached the level of two separate species.
Look, you could go to Galapagos Islands and get a pair of finches and bring them back to a laboratory and just let them have sex. After a few generations you will have small beaked, medium beaked, large beaked finches. The information is already in there genome, nothing new was created, specificity was lost if anything. Now if you simulate a drought, like on Galapagos, so that the seeds become hard and more beak strength is needed to open them, then of course the larger beaked finch will survive. A creationist came up with the survival of the fittest twenty-four years prior to Darwin. After all the other “parent” finches die off, you are left with only large beaked finches in the laboratory. This is not evolution; no new information was gained in the process. There are limits to its change, strep-throat may change into a flesh eating virus, but it loss specificity to get to that point or already had the information in its genome. It’s still strep-throat.
That finch didn’t turn into a dinosaur; that dog didn’t turn into a cat; that ape didn’t turn into a man, etc.. The genetic barriers wont and don’t allow it. You can post all the sites in the world, but you will never be able to find one proof of macroevolution in the fossil record or in the living world. All we have ever seen is what evolutionists’ call “subspeciation” (variation within a type), never “transpeciation” (change from one type to others). The primrose is a prime example of my point. The alleged new species of primrose that de Vries thought he had “discovered” were not new species at all but rather mere variations of the same species.
This “sport” (a certain primrose that de Vries created), with it’s doubled chromosome [no new information was added, it merely doubled the information that was already there], is still a primrose. Stickleback fish may diversify into fresh-water dwellers and salt–water dwellers, but both remain sticklebacks. One fruit fly may breed on apple trees and another on hawthorn trees, but both remain fruit flies. Speciation is a means of creating diversity within types of living things, but macroevolution is much more than diversity.
Macroevolution requires an increase of the gene pool, the addition of new genetic information, whereas the means to speciation discussed above represent the loss of genetic information (how so?). Both physical and ecological isolation produce varieties by cutting a small population off from its parent population and building a new group from the more limited genetic information contained in the small population. A large population carries genetic reserve, a wealth of concealed recessive genes. In a small group cut off from the parent population, some of these recessive traits may be expressed more often. This makes for interesting diversity, but it should not blind us to the fact that the total genetic variability in the small group is reduced!.
The appearance of reproductively isolated populations represents microevolution, not macro-evolution. Vertical change – to a new level of complexity – requires the input of additional genetic information. Can that information – the ensembles of new genes to make wrens, rabbits, and Hawthorne trees be gleaned from random mutations?
Thus far, there appears to be good evidence that the roles mutations are able to play are severely restricted by and within the existing higher-level blueprint of the organism’s whole genome.
To go from one-celled organisms to a human being means that information must be added to the genetic messages at each step of the way. Mechanisms for the loss of genetic information cannot be used as support for a theory requiring vast increases of genetic information.
Speciation is actually akin to what breeders do. They isolate a small group of plants or animals and force them to interbreed, cutting them off from the larger gene pool to which they belong. A century of breeding testifies to the fact that this produces limited change only. It does produce the open-ended change required by Darwinian evolution. Some think, as do I, that the extinction of the dinosaurs occurred because they didn’t have the genetic diversity to adapt to environmental changes.
Percival Davis & Dean H. Kenyon, with Charles B. Thaxton as Academic Editor, Of Pandas and People: The Central Question of Biological Origins, 2nd Edition (Dallas, TX: Haughton Publishing Co., 1993), 19-20.
I disagree with the very opening aspect of this text. As I cited before while Great Danes and Chihuahuas cannot breed it is only due to physical limitations – artificial insemination would result in a perfectly viable mutt. This is no different than two sub-species which do not interbreed only because they’re on different canyon ridges and do not cross the canyon. This text is ‘popular’ science, it is not a text used by scientists. Some things are misleading.
Macroevolution does NOT require an “increase in the gene pool” – the gene pool of the horse and donkey are virtually identical, yet they are separate species (yet closely related enough to produce sterile offspring). The reason they are different species is due to the cytogenetic changes (note that does NOT involve additional genetic material or a greater gene pool).
Tom, Evolutions says I came from a rock. In fact, it says — ultimately — that a South-East Asian Man who just got home from a hard days work came from an odorless (body-odor), colorless (dark completion) gas. This man can sit down and read Aristotle and learn about the laws of logic that precede any scientific adventure and that are not known to the senses (law of excluded middle, law of identity, law of non-contradiction, etc), and use these “mind” (I would say “Mind”) reasoning tools to critique a fallacious statement… that, this south-east Asian man would expect someone half-way around the world to be able to understand.
So information added to the gene pool is not the topic I wish to zero in on, yet.
You are telling me that a donkey and a horse are a donkey ARE proof of macroevolution? You are telling me as well that Cats (Felidae) are a diverse group of carnivores that includes domestic cats, lions, tigers, ocelots, jaguars, caracals, leopards, mountain lions, lynx and many other groups of cats are not the same kind?
Let me restate that, wolves and a few other dog kind (Canidae) have all the genetic information in them that breeders are then able to change through intelligent input. So a Chihuahuas is still a Canidae, but with much less specified complexity — the bottom of the gene pool so-to-speak. [Left to its own devices with no help from man, the wolf, coyote, etc would survive, but the Chihuahuas would probably die out.]
You seem to be conflating “species” with other classification titles (http://tinyurl.com/3npkel8) [*SEE YOUR OWN STATEMENT BELOW* ~ not capitalized to yell, merely to emphasize]. I want you to be clear and concise so a high school student from L.A. Unified can understand you: “are you saying small changes in specie level adaptation (centimeter beak change in birds, or Brussels sprouts to hit a bit closer to home to your point [http://creation.com/eat-your-brussels-sprouts]) are more than that, they are evidence of macroevolution?
…. I still think this statement by you @Tom Melendy is a bit of an overreach:
Jim, Macro evolution has been observed in the laboratory under controlled conditions – within just a few generations you can “breed” fish to be miniature fish, which reproduce and “grow” up while never getting bigger than the size they were bred for.
Please give me the name of the fish you referenced… and through observed “quantum evolution, also known as mega- and macroevolutionary” what other Order this fish became under observation. You see Tom, we are still at one of your opening statements, which you have not clearly, eruditely, and concisely explained. So you lied to Jim? Or you were mistaken in your wording? What.
My apologies for the lack of clarity on my part. When this thread first started we were talking about common evolution in the lab. This is commonly seen with microorganisms. Someone asked what about non-microorganisms. I responded that you could see macro evolution in the lab in fish (macro just to differentiate from micro-organisms). Once you began defining your terms as micro and macro evolution as being the small changes due to variation and selection, versus the larger changes that produce different species that of course made my previous point unclear – I was referring to micro-evolution (variation and selection) being studied in a macroorganism (fish). It wasn’t an over-reach, it was a miscommunication due to us not having established an accepted nomenclature prior to that statement. Often different branches of science will utilize the same term to mean different things in different fields. As to your question of which fish – Atlantic silversides. Here’s the website showing you the surprising result that within just a handful of generations the fish size could be decreased dramatically. http://evolution.berkeley.edu/evolibrary/article/0_0_0/conover_04
Tom posts a few followups
….Once you defined what you were discussing through the terms of micro versus macro evolution, all of my other statements made still stand as written
….As to your longer question about evolution above and how it relates to species and higher orders. There are many elements you have of confusion there. One simple one that makes me concerned is that you state a chihuahua has “much less specified complexity” amongst the Canids. Not at all true! It’s complexity is just a great, but everything has just been bred to be on a smaller scale – larger doesn’t inherently mean more complexity Sean.
As for your comment about my conflating species with genus or family – that is exactly my point Sean! The very definition of evolution is the creation of new species. The formal definition of a species is that it cannot interbreed and create viable young with another species. Yet we know of several cases where that does indeed occur – you give some examples yourself Canis lupus and Canis familiaris. Whereas most species do follow the rule that they cannot interbreed with others at all. There are other genuses or even families of organisms where there is still some interbreeding that can occur, but their ability to produce offspring vary – and I gave you examples of different species of bear that can produce viable offspring, but different species and even genuses of the horse family that can produce offspring with varying degrees of ability to interbreed successfully. I have even given you some information on why these various equines produce progeny of differing ability to interbreed – their speciation is being driven by cytogentic changes – in the cases of this group horses, donkeys and zebras all have very similar genetics (about 99% of their genes are the same) yet those genes are divided up amongst a different number of chromosomes (donkeys have more smaller chromosomes, horses the fewest larger chromosomes, zebras are intermediate in number and size). These cytogenetic differences are what limits production of offspring with a full ability to reproduce (due to nondysjunction during meiosis, production of gametes). And these are the type of cytogenetic changes that, as I was describing earlier, over time begin to prevent back-crossing, which allows the microevolutionary changes (like those we see with the fish) to over time become more permanent, driving the diversity of the evolutionary tree. My point has been that all these examples show speciation at different stages: while wolves and dog, or wolves and coyotes, are different species (by most criteria), they can still produce viable offspring – they have not truly become fully independent species as per the formal criteria; bears are somewhat similar as polar bears can produce viable offspring with Kodiak bears and grizzly bears and North American brown bears, any offspring produced with European brown bears do not survive to adulthood – speciation was achieved between polar bears and European brown bears, but is incomplete between polar bears and North American brown bears; equines are a third example, where all three discussed, horses, donkeys and zebras – which belong to not just different species, but even different sub-genuses, can produce offspring, but those offspring cannot interbreed successful, and have varying ability to produce offspring with the parent species (donkey-horse, extraordinarily rarely, horse-zebra or donkey-zebra, much more often) – so the equines are much further down the speciation path than Canis or Ursid, yet not nearly as far as some species which cannot produce offspring at all. So THIS Sean, is macroevolution – no one would say a polar bear is the same species as a grizzly or a brown bear – yet they are only partway along the path to speciation. Similarly donkeys and zebras are clearly not the same species as horses, yet these are further along the way to speciation. These are the examples where I’m showing you that evolution is occurring in the here and now, and that we can see different groups of animals at different stages of speciation. This is the best we can do in describing the individual steps in macroevolution as we cannot carry out speciation/macroevolution in the laboratory because of the time frame required to generate stable cytogenetic changes in organisms – selection can occur over just a few generations, cytogenetic changes occur over generations upon generations.
Tom has FINALLY mentioned the specific experiment he mentioned, as well as backing away from his previous statement of macroevolution being observed. But if you notice he beats around the bush quite a bit to still try and “save face” at the same time of still trying to obfuscate the issue of species.
Okay, that helps. The changes you mentioned were merely within a species and no new information was added to the genome, merely “rearranged” (layman terms) to get a specified output. In fact, this arrangement could be considered “less specified” from the parent population (like the Chihuahua). Examples of bacteria resisting anti-biotics exemplify this loss of information to the parent population/strain. Darwinism requires the opposite.
Thank you for the link to the fish, this helps. All creationists, intelligent design adherents, and the neo-Darwinian and cladists believe in change within species. If an evolutionists says evolution equals “change,” and then shows an experiment where no new information was added to the genome. nothing in that fish experiment disproves or challenges the creationist perspective:
…. For some years now, many fisheries management authorities around the world have instituted legal minimum size requirements for various fish species. Thus anglers must return ‘undersized’ fish to the water unharmed. Similarly, commercial fishermen use large-meshed nets to spare the smaller fish—with the aim of ensuring the long-term viability of the fishery.
However, the fish that are genetically predisposed to mature at larger sizes are the ones most likely to be caught before they can reproduce. Thus there has been a strong selection pressure favouring scrawny fish that never reach the minimum legal size. Hence the genes for late-maturing larger-sized fish have been progressively lost from many fish populations, leaving early-maturing smaller-sized ones to dominate the gene pool. (So, ironically, by catching only the biggest fish and letting the others go, humans have unintentionally selected against that which they desire most!)
Note that this is not evolution because the selection pressure—which is essentially an artificially-imposed version of ‘natural selection’—simply favours certain genes over others; it cannot generate any new genetic information. Neither such ‘artificial’ nor ‘natural’ selection can turn plaice into people; it can only operate on (i.e. cull out) genetic information that already exists.
Fisheries scientists David Conover and Stephan Munch, of the State University of New York, observed that size-specific culling of Atlantic silversides rapidly changes the genetic makeup of the population.7 After just four generations, fish populations from which the largest 90% of silversides were removed before breeding averaged just half the size of fish in populations from which the smallest 90% had been culled. In other words, removing big fish soon results in a population of little fish (and vice versa).
This is not evolution, as the genes for big or little fish were already present in the population beforehand. Note that the limits to how big or little the fish can be in the final population are determined by the amount of pre-existing genetic variety. Conover and Munch wrote: ‘Management tools that preserve natural genetic variation [i.e. pre-existing variety] are necessary for long-term sustainable yield.’ In other words, we need to leave at least some of the big fish in the water, so that their desirable genes (from a human perspective) remain in the fish population.
Despite this anti-evolutionary insight, their research paper refers to fish demonstrating ‘evolutionary effects’ and having ‘evolved rapidly’. That last claim took many of their fellow evolutionists by surprise. David Conover reported: ‘Even some fisheries’ scientists have been unwilling to accept that evolution is happening within a few fish generations.’ ….
I make this point in my earliest debate with a neo-Darwinist, in which I end with:
Theodosius Dobzhansky, one of the twentieth centuries leading Darwinists, acknowledged this:
“And yet, a majority of mutations, both those arising in laboratories and those stored in natural populations, produce deteriorations of viability, hereditary diseases, and monstrosities. Such changes, it would seem, can hardly serve as evolutionary building blocks.”
Mr. Hitchings: “On the face of it, then, the prime function of the genetic system would seem to be to resist change: to perpetuate the species in a minimally adapted form of response to altered conditions, and if at all possible to get things back to normal. The role of natural selection is usually a negative one; to destroy the few mutant individuals that threaten the stability of the species.”
Goldschmidt said: “It is true that nobody thus far has produced a new species or genus, etc., by macromutation. It is equally true that nobody has ever produced even a species by selection of micromutaions.”
Goldschmidt would have known – he bread gypsy moths for twenty years and a million generations in various environments. All he ever got was more gypsy moths. Anyone who thinks that an accumulation of mutations (information-losing processes) can lead to Macroevolution (a massive net gain of information) “is like the merchant who lost a little money on every sale but thought he could make it up on volume.” (Spetner)
(I have a .com now, this is my old blog)
So the example of the fish is something that if defined properly doesn’t support the grand changes that Darwinism implies. Nor, if properly defined, no creationist finds anything wrong with it… other than someone takes this loss of information and applies it to the past spuriously [stepping out of science and using a meta-narrative to state something that is unobservable] to say, “see, I am related to a banana in the tree of life.” THAT is bananas.
About the author of the linked Creation.com article:
B.Ag.Sc. (Hons) [University of Adelaide, South Australia]—Honours thesis title: The effects of applied nitrate on nitrogen fixation by subterranean clover (1982)
Ph.D. [University of New England, New South Wales, Australia]—Thesis title: The contribution of tree legumes to the nitrogen economy and forage production in the humid tropics (1988)
Dr. David Catchpoole was once an ardent atheistic evolutionist, before being challenged to look critically at the problems of evolution, and the scientific evidence for creation and the Bible.
Dr. Catchpoole is an expert neither on evolution nor on genome integrity (one of my fields of expertise). He is not qualified.
I am merely pointing out that others exist with advanced degrees (that you mentioned about yourself) who write on “change,” does it matter if a young earth creationist got us to the moon, invented the MRI, and is a leading pediatrician who had a movie made about him (“Gifted Hands”). Belief about origins (historical science) and science in the lab are thus — provably — two areas that are separate.
I merely argue that “Darwinism” is a historical science that IS THE MATRIX that must be placed on the Atlantic silversides [and the loss of specificity compared to the parent population] in order to church out of the hopper “evidence” for Darwinian evolution. Circular.
And you’re wrong again, resistance to antibiotics is due to a GAIN of genetic material, not a loss. You talk a good game Sean, but the fact is that you don’t know enough facts about basic biology to support your thoughts. This is what we need to explain to college students who figure that once they read a text and can pass an exam, they must be experts; and why can’t they just do whatever they want in life (being an expert on something) because they can always ‘find’ the answers they need online or in a book. The problem is that you need a solid basis upon which to build – if you don’t have the basic material you really can’t support your ideas and arguments. (kind of like needing to have a vocabulary of words before you can write a paper). You Sean have collected a great number of books and ideas, but you don’t REALLY know the science behind what you’re talking about – which leaves your theories and positions full of holes/flaws. It’s been an interesting discussion but I can’t continue this indefinitely – I have work to do. If you don’t understand the concept that evolution is a continuum of small changes and selections, punctuated by larger cytogenetic changes that prevent back-breeding, ultimately leading to speciation (different species). And if you can’t understand how all I’ve shown you supports both aspects of that – then I suggest you head back to school for a degree in Biological Sciences – you clearly have the interest.
When I say “loss of specificity to the parent population,” what I mean is that if it were possible to kill all Canidae’s except the Chihuahua… wolves would be extinct. the information left in the Chihuahua is a loss that can never be regained. It is less specified.
No Sean, your last comment is very wrong. It wasn’t their advanced degrees in other areas that make them capable in other things. In each case those individuals had to study and learn a whole new area to become capable. Furthermore, development does not always come from an expert – some people do not full understand what they develop or contribute to. Invention does not always come from the greatest knowledge.
I have to start work. This is a great example, bacteria, for the conversation. Will check in this evening. thank you for your patience and willingness to talk.
That’s actually not true either Sean – are you saying that the genetic information in a wolf contains that of the chihuahau, but not the reverse? That’s not true at ALL. You don’t understand basic genetics. Selective breeding over enough time can create either from the other.
Okay, Home. I would love to get your thoughts on this.
No, there is specificity lost from the parent population:
Artificial breeding/selection is a good analogy. The original mongrel dog/wolf population had more genetic variety than any of the many individual breeds of dog today, but because of continual mixing up of the genes/alleles due to free inter-breeding (out-breeding), the outward appearance of the dogs/wolves would not generally have shown extreme variety. But selecting rare dogs with Chihuahua-like features and breeding them together (inbreeding) for many generations results in the concentration of alleles that give Chihuahua-likeness and the elimination of a lot of the other alleles—ones for ‘large dog’ for example. So you could never breed a Great Dane from a Chihuahua; the genetic information required has been depleted by the very process that has generated the extreme features.
Bacterium & Evolution II
This is part II of a debate I had
It has been proven that resistance to many modern antibiotics was present decades before their [the antibiotics] discovery. In 1845, sailors on an ill-fated Arctic expedition were buried in the permafrost and remained deeply frozen until their bodies were exhumed in 1986. Preservation was so complete that six strains of nineteenth-century bacteria found dormant in the contents of the sailors’ intestines were able to be revived! When tested, these bacteria were found to possess resistance to several modern-day antibiotics, including penicillin. Such traits were obviously present prior to penicillin’s discovery, and thus could not be an evolutionary development. (Medical Tribune, December 29, 1988, p. 1, 23.)
In 1998, the National Academy of Sciences published and distributed a book to public schools and other institutions entitled Teaching About Evolution and the Nature of Science. Jonathan Sarfati, Ph.D., F.M., wrote a book, Refuting Evolution, which is a topic by topic rebuttal to this Academy of Sciences publication. Under the evidence for evolution in the evolutionist text is the following quote:
The continual evolution of human pathogens has come to pose one of the most serious health problems facing human societies. Many strains of bacteria have become increasingly resistant to antibiotics as natural selection has amplified resistant strains that arose through naturally occurring genetic variation.
Similar episodes of rapid evolution are occurring in many different organisms. Rats have developed resistance to the poison warfain. Many hundreds of insect species and other agricultural pests have evolved resistance to the pesticides used to combat them – even to chemical defenses genetically engineered into plants.
(Sarfati’s reply – any words in the [boxes] are mine):
However, what has this to do with the evolution of new kinds with new genetic information? Precisely nothing. What has happened in many cases is that some bacteria already had the genes for resistance to the antibiotics. In fact, some bacteria obtained by thawing sources which had been frozen before man developed antibiotics have shown to be antibiotic-resistant [6 different antibiotics in fact, penicillin in modern doses – which is way beyond the strength of natural penicillin found in nature]. When antibiotics are applied to a population of bacteria, those lacking resistance are killed, and any genetic information they carry is eliminated. The survivors carry less information [or specificity], but they are all resistant. The same principle applies to rats and insects “evolving” resistance to pesticides. Again, the resistance was already there, and creatures without resistance are eliminated.
[Much like if we killed all dogs (including Canis Domesticus and Canis Lupus) except for Chihuahuas, we would permanently lose the information of the parent population. You could then breed Chihuahuas for a millennium and not get an Irish Wolfhound]
…In other cases, antibiotic resistance is the result of a mutation, but in all known cases, this mutation has destroyed information. It may seem surprising that destruction of information can sometimes help. But one example is resistance to the antibiotic penicillin. Bacteria normally produce an enzyme, penicillinase, which destroys penicillin. The amount of penicillinase is controlled by a gene. There is normally enough produced to handle any penicillin encountered in the wild, but the bacterium is overwhelmed by the amount given to patients. A mutation disabling this controlling gene results in much more penicillinase being produced.
[Thus, the bacteria found frozen in 1845 already had the mutation to overcome modern medical doses of penicillin. So the mutation wasn’t the result of the penicillin in modern doses, thus seemingly becoming resistant… it already had the resistant mutation – informational or specificity losing – in the population. In other words, no new information was added to the parent population!]
…This enables the bacterium to resist the antibiotics but normally, this mutant would be less fit, as it wastes resources by producing unnecessary penicillinase. Another example of acquired antibiotic resistance is the transfer of pieces of genetic material (called Plasmids) between bacteria, even between those of different species. But this is still using pre-existing information, and doesn’t explain its origin.
So the above [first quote] is an example of, as Dr. Lee Spetner would say, “the transfer of resistance genes already extant in bacteria.” I would say as well that the only other example is the building of resistance as a result of losing genetic data because of mutation.
from one of my favorite posts [not mine] on the topic:
The second type of immunity, which comes about as a result of mutation, is not an example of evolution either. Spetner writes:
… [A] microorganism can sometimes acquire resistance to an antibiotic through a random substitution of a single nucleotide… Streptomycin, which was discovered by Selman Waksman and Albert Schatz and first reported in 1944, is an antibiotic against which bacteria can acquire resistance in this way. But although the mutation they undergo in the process is beneficial to the microorganism in the presence of streptomycin, it cannot serve as a prototype for the kind of mutations needed by NDT [Neo-Darwinian Theory]. The type of mutation that grants resistance to streptomycin is manifest in the ribosome and degrades its molecular match with the antibiotic molecule.
In his book Not by Chance, Spetner likens this situation to the disturbance of the key-lock relationship. Streptomycin, just like a key that perfectly fits in a lock, clutches on to the ribosome of a bacterium and inactivates it. Mutation, on the other hand, decomposes the ribosome, thus preventing streptomycin from holding on to the ribosome. Although this is interpreted as “bacteria developing immunity against streptomycin,” this is not a benefit for the bacteria but rather a loss for it. Spetner writes:
This change in the surface of the microorganism’s ribosome prevents the streptomycin molecule from attaching and carrying out its antibiotic function. It turns out that this degradation is a loss of specificity and therefore a loss of information. The main point is that Evolution… cannot be achieved by mutations of this sort, no matter how many of them there are. Evolution cannot be built by accumulating mutations that only degrade specificity.
To sum up, a mutation impinging on a bacterium’s ribosome makes that bacterium resistant to streptomycin. The reason for this is the “decomposition” of the ribosome by mutation. That is, no new genetic information is added to the bacterium. On the contrary, the structure of the ribosome is decomposed, that is to say, the bacterium becomes “disabled.” (Also, it has been discovered that the ribosome of the mutated bacterium is less functional than that of a normal bacterium.) Since this “disability” prevents the antibiotic from attaching onto the ribosome, “antibiotic resistance” develops.
At this point another person chimes in to compliment the tenor of the conversation so-far. Let me say, that the entire discussion was calmly and very little emotional jabs were taken. In most conversations I post the below in order to put in peoples minds that often time — whne sitting behind a keyboard — one tends to apply feelings to the other persons statements that he or she never intended. Which is why this “legal statement,” so-to-speak, typically precedes conversation:
“By-the-by, for those reading this I will explain what is missing in this type of discussion due to the media used. Genuflecting, care, concern, one being upset (does not entail being “mad”), etc… are all not viewable because we are missing each other’s tone, facial expressions, and the like. I afford the other person I am dialoguing with the best of intentions and read his/her comments as if we were out having a talk over a beer at a bar or meeting a friend at Starbucks. (I say this because there seems to be a phenomenon of etiquette thrown out when talking through email or Face Book, lots more public cussing and gratuitous responses.) You will see that often times I USE CAPS — which in www lingo for YELLING. I am not using it this way, I use it to merely emphasize and often times say as much: *not said in yelling tone, but merely to emphasize*. So in all my discussions I afford the best of thought to the other person as I expect he or she would to me… even if dealing with tough subjects as the above. I have had more practice at this than most, and with half-hour pizza, one hour photo and email vs. ‘snail mail,’ know that important discussions take time to meditate on, inculcate, and to process. So be prepared for a good thought provoking discussion if you so choose one with me.”
this is a remarkable discussion – it is civil!! what a mutation is observed having the ability to do, and what a mutation is observed lacking the ability to do are the strongest reasons to continue questioning macro-evolution(molecules to man). to GIORDANO and MELENDY – your info has been enlightening, and it’s refreshing to see that both of you have refrained from name calling or nasty sarcasm. i feel like I’ve just been through a college bio course.
Okay Sean, finally have a few. In response to your posts above about purebred dogs losing genetic diversity and bacteria – those statements you have reposted have elements of truth, but are written in a misleading fashion (whether purposeful or due to lack of understanding I have no way of knowing, so will not judge). It is true that purebred dogs have lost genetic diversity (variation) – but they have NOT lost genetic material. This is due to breeders continuing to backbreed to select for rare or desired traits. Note this also sometimes selects for genetic problems; as I’m sure you are aware many purebreeds have serious problems – just like humans have problems when backbred (why we have traditions and even laws against very close blood relatives marring and having children). But that loss in diversity is not due to a loss of genetic material (not due to a loss of genes). It is mutations, or slight changes in genes, that cause genetic diversity. This might alter their function, or might even turn the gene all the way off in some cases (Mexican hairless?). So yes, purebred dogs have lost genetic diversity, but all the genes required for them to be a wolf are still there! It would take probably hundreds of years of breeding to re-select for those wolf-characteristics, and some of the small mutations in genes that affect their function would have to re-arise, but it could and would happen. The genes ARE still there.
Bacterial selection for antibiotics: for bacteria the situation is a bit different. In addition to their bacterial chromosome, bacteria often also have extrachromosomal DNA that they can pick up from the environment or other bacteria, and that they can pass on to their progeny. Antibiotics generally act against basic physiological pathways that bacteria need to duplicate their DNA, make RNA, synthesize their bacterial proteins, or synthesize their cell walls, among others. As you can imagine stopping any of these processes will stop bacterial cell growth. Antibiotic resistance is not due to a loss of any bacterial genes. In some cases it may be due to some small mutation in a bacterial gene that leaves the protein encoded by that gene still functional, but changes the shape just enough that the antibiotic no longer binds effectively, so no longer works. More often bacteria pick up some DNA (whole genes) from the environment or other bacteria around (and these might be other types of bacteria that do not cause disease) that give the bacteria resistance to the antibiotic. Usually these antibiotic resistance genes act one of two ways: one is the gene may encode an enzyme that breaks down the antibiotic (common with penicillin-resistance); the second is that the gene may encode a molecular pump that pumps a variety of small molecules like antibiotics out of the bacteria. If the bacteria is continuously pumping the antibiotic out, the antibiotic is not effective. So in the case of bacterial antibiotic resistance, again there is no loss of genetic material, actually there is a gain of genetic material.
What these posts don’t recognize is that even when there is a mutation, this is NOT a loss of genetic information! It is a loss of diversity, and possibly function (or altered function). But the gene is still there – and it can be mutated back to full function just as easily as it mutated to lose function.
Also it is obvious why bacteria isolated from soil or from many years ago have these genes, penicillin was discovered in naturally occurring mold. This is in the environment, and some bacteria throughout natural history have had to deal with this as well as related molecules – so these enzymes and molecular pumps in some specific environments would be selected for over time. As we use antibiotics in healthcare (and sadly in animal feed), there is more selection for bacteria to pick up and hold onto these genes. That’s why they’re more prevalent in our environment than they were fifty years ago.
Oh, Sean, I forgot. As for how these antibiotics like beta-lactamase or antibiotic pumps arose though evolution. You can look at the amino acid sequence of these proteins and there are some very closely related proteins in some bacteria that are used for different purposes – they break down something other than beta-lactamase and pump other molecules into or out of bacteria. What has clearly happened is that these genes were duplicated and random mutations occurred. At some point in time, one or more of these mutations led to subtle changes in the protein which made it function in a new way – so that it could break down beta-lactamase (the ring in the penicillin structure). This then provided that bacterium with a selective advantage when it was in an environment with that family of mold. This idea of gene duplication is quite common – we humans also have gene duplications throughout our genomes. Most of these are not expressed and not currently “used” if you will – so don’t provide us any advantage now – but appear to be the place where new genes/functions can arise. There are cases where past pseudogenes have evolved to be used. There are several copies of human hemoglobin. In some other animals only a single hemoglobin is used, and the other copies remain as unused pseudogenes. In humans we still have some unexpressed hemoglobin pseudogenes, but we use more than one hemoglobin; at least one is only expressed and used in utero, and is developmentally turned down (to about 3%) as we are born and mature – then the standard hemoglobin is the primary hemoglobin. It is unclear what advantage the fetal hemoglobin provides in utero, but this is the way we have evolved. We guess there is some advantage to using it.
Okay. But even I would say that all by itself acquisition of antibiotic/pesticide resistance is not evidence for evolution. It’s just one very small brick in a very large wall. It’s consistent with evolution, but by itself it’s just one tiny piece of evidence. If it wasn’t for all the other evidence for evolution, then this by itself might be one little weird anomaly
“In his book Not by Chance, Spetner likens this situation to the disturbance of the key-lock relationship. Streptomycin, just like a key that perfectly fits in a lock, clutches on to the ribosome of a bacterium and inactivates it. Mutation, on the other hand, decomposes the ribosome, thus preventing streptomycin from holding on to the ribosome. Although this is interpreted as “bacteria developing immunity against streptomycin,” this is not a benefit for the bacteria but rather a loss for it. Spetner writes:
This change in the surface of the microorganism’s ribosome prevents the streptomycin molecule from attaching and carrying out its antibiotic function. It turns out that this degradation is a loss of specificity and therefore a loss of information. The main point is that Evolution… cannot be achieved by mutations of this sort, no matter how many of them there are. Evolution cannot be built by accumulating mutations that only degrade specificity.”
This is only partly correct Sean. These mutations that occur in the bacterial chromosomal genes that confer resistance to streptomycin (there are more than one that have been discovered) do indeed alter the structure of the ribosome (the enzyme complex that synthesizes proteins). But they do NOT “decompose the ribosome” as Spetner claims. If they did, the bacteria could not survive, as all bacteria (and larger life forms) require protein synthesis to survive! While these mutations alter the bacterial ribosome somewhat, so streptomycin does not bind, the mutant ribosomes still have enough structure to function. In the absence of streptomycin long-term bacteria with this mutation would be out-competed, as they’re not quite as efficient at protein synthesis – but they’d survive just fine in mixed populations without strong selective pressure. Also, as I said above, there is nothing to prevent these single point mutation from mutating back to the normal “wild-type” configuration in the absence of streptomycin. It doesn’t happen any more efficiently than the original mutation to streptomycin-resistance, but it doesn’t happen any less efficiently either. I’m actually shocked at Spetner’s statements you posted – it shows a clear lack of understanding of basic first year microbial biology! I’m kind of appalled.
Having a few beers with the neighbors, Cost Plus World Market had a sale on some really good micro-brew. Spetner breaks the types of resistance into two categories (have you read his book out of curiosity? If you have not I would be curious to talk to you about when you do read it):
1) The transfer of resistance genes already extant in bacteria.
2) The building of resistance as a result of losing genetic data because of mutation.
So the transfer of antibiotic resistance in this manner (number 1) “… is not the kind that can serve as a prototype for the mutations needed to account for Evolution… The genetic changes that could illustrate the theory must not only add information to the bacterium’s genome, they must add new information to the biocosm. The horizontal transfer of genes only spreads around genes that are already in some species.”
Evolution is not happening here — at least the kind neo-Darwinism needs. No new genetic information is produced: genetic information that already exists is simply transferred between bacteria.
In a debate Dr. Spetner had he summed it up thus with Dr Edward Max (via Talk Origins and True Origins):
It turns out, however, that a microorganism can sometimes acquire resistance to an antibiotic through a random substitution of a single nucleotide, and this is the kind of example Max presented. Streptomycin, which was discovered by Selman Waksman and Albert Schatz and first reported in 1944, is an antibiotic against which bacteria can acquire resistance in this way. But although the mutation they undergo in the process is beneficial to the microorganism in the presence of streptomycin, it cannot serve as a prototype for the kind of mutations needed by NDT. The type of mutation that grants resistance to streptomycin is manifest in the ribosome and degrades its molecular match with the antibiotic molecule. This change in the surface of the microorganism’s ribosome prevents the streptomycin molecule from attaching and carrying out its antibiotic function. It turns out that this degradation is a loss of specificity and therefore a loss of information. The main point is that Evolution A cannot be achieved by mutations of this sort, no matter how many of them there are. Evolution cannot be built by accumulating mutations that only degrade specificity.
In the final paragraph of my original critique, I said the following:
The mutations needed for macroevolution have never been observed. No random mutations that could represent the mutations required by NDT that have been examined on the molecular level have added any information. The question I address is: Are the mutations that have been observed the kind the theory needs for support? The answer turns out to be NO! Many have lost information. To support NDT one would have to show many examples of random mutations that add information. Unless the aggregate results of the genetic experiments performed until now is a grossly biased sample, we can safely dismiss Neo-Darwinian theory as an explanation of how life developed from a single simple source. http://www.trueorigin.org/spetner2.asp
You are saying it is an example of a gain of new information? If all anti-biotics were removed from human application, would the parent population be again the dominant bacterium due to its superior health under less pressure?
Oh! Bacterium transferring resistance laterally also fits with the predictive powers of I.D. (You had said: “It’s consistent with evolution”)
Sean, the point I made above, about how some of the things Spetner states are just plain wrong, makes me question his deductive powers. There are similar things in the sections you’ve posted above. He’ll take one correct point, and then follow it up with a second statement about it or a conclusion about it which is patently wrong! Because he starts with a correct statement, you start giving him credence (and it sounds like he knows what he’s talking about. But then he screws it up completely. I can’t even bear to read the little pieces you’ve posted he because he’s made such a mashup of some correct facts, some incorrect statements, and completely fallacious reasoning – I sorry, I just can’t bear to read his work. His reasoning is just garbage – as I’ve pointed out in the example I gave above.
Point mutations, like the one he describes about Streptomycin, do not “degrade specificity”. They ALTER specificity – and might even bind other things BETTER than the original. Because he uses the words “degrade” and “loss of genetic information” (I pointed out above how that conclusion of his is wrong too), it SOUNDS like his conclusion makes sense – that this “loss of specificity” and “loss of genetic information” could not be a positive for evolution. The problem is his characterization of those mutations as being a “loss” of information is simply incorrect. This is what I was talking about above, where he makes a point that is correct – a mutation can caused decreased binding to streptomycin – but his descriptions after that are incorrect and misleading. Virtually everything you’ve posted by him is like this – he starts with one correct statement, then makes misleading or mischaracterizing statements about it, allowing him to build a fallacious argument. One of two things – either he doesn’t know what he’s talking about, or he’s trying to mislead you – I don’t know which.
To be clear, less fitness is better?
….some mutant bacteria, because they have defective membranes, don’t absorb nutrients well. Fortuitously for them, that inefficiency also prevents their absorbing antibiotics. And so, in this instance also, they survive better than their normal cousins. But the mutation did not make them stronger or create new information, or “evolve” to a higher state.
So you teach your students that a harmful mutation in the oxygen-carrying capacity of the blood (sickle-cell anemia) is “good” — or — or an upward mobility in fitness on the whole and a proof of evolution? Its like air leaking slowly from a tire… it may do well temporarily in sand, but it isn’t an improvement.
Rearranging the same information is a prediction of I.D. AND creation… small changes in “species” is expected in all of the evolutionary models and creation models.
It seemed like from an above statement you couldn’t bear to read Spetner. I would feel fulfilled if I got a promise from you to read ONE book, one book: “Unshakeable Foundation,” by Norman Geisler and Peter Bocchino. I will even buy it for you if you do not feel the need to spend money on it. Let me know.
Any scientist with an agenda is not a scientists but a poor philosopher with dangerous intent…. God is beyond being “proven” or “disproven”, which is of course inherent for a being all-powerful. It is beyond any man to prove or disprove God.
This is the same as saying, “God is indescribable,” which of course is a self-refuting [self-deleting] statement… e.g., incoherent. You mean, according to philosophical naturalism God is unprovable:
- Professor: “Miracles are impossible Sean, don’t you know science has disproven them, how could you believe in them [i.e., answered prayer, a man being raised from the dead, etc.].”
- Student: “for clarity purposes I wish to get some definitions straight. Would it be fair to say that science is generally defined as ‘the human activity of seeking natural explanations for what we observe in the world around us’?”
- Professor: “Beautifully put, that is the basic definition of science in every text-book I read through my Doctoral journey.”
- Student: “Wouldn’t you also say that a good definition of a miracle would be ‘and event in nature caused by something outside of nature’?”
- Professor: “Yes, that would be an acceptable definition of ‘miracle.’”
- Student: “But since you do not believe that anything outside of nature exists [materialism, dialectical materialism, empiricism, existentialism, naturalism, and humanism – whatever you wish to call it], you are ‘forced’ to conclude that miracles are impossible”
Unless, @Tom Melendy, God came into the world… a Christian is one who believes Jesus *IS* God incarnate. Do you believe this Tom?
It’s interesting Sean, I actually agree very much with that point made above “Any scientist with an agenda is not a scientists but a poor philosopher with dangerous intent…. God is beyond being “proven” or “disproven”, which is of course inherent for a being all-powerful. It is beyond any man to prove or disprove God.” – this is actually something I teach my students VERY hard – to not become wedded to a theory, to be willing to let that theory go WILLINGLY, if the data argues against it. I have no agenda here – I neither want to prove nor disprove God (such attempts are silly, if we accept God is all powerful, it is beyond the power of Man to prove or disprove). I only want to look at the data and see what they indicate. I would argue VERY STRONGLY that the scientists you have been posting have an AGENDA – and that agenda is to disprove evolution. Ergo, as per your post above – they are very poor scientists. And based on their writings that you’ve posted, I agree wholeheartedly – their writings are rife with errors and mis-conclusions. Conversely I do not believe that believing in Evolution precludes an all-powerful God. Much of the Bible is written as parable or allegory, and I believe that Genesis is written in much this way – written in a way so mankind at that time could comprehend what was written. So unlike most, I go into the Evolution question with an open mind, without any goal or either proving or disproving God. So if you put that question aside, and ask what the data supports, the data overwhelmingly supports Evolution – otherwise why would there be so many fossils of species showing intermediate forms between ancient life forms and current life forms, otherwise why would gene homologies across both current species as well as compared to ancient species show incremental changes consistent with Evolution. Instead of you probing my knowledge and ability to support Evolution with the biological systems in the world – let me ask you a question. If God created all the species currently on the Earth either 6000 years ago, or through intelligent design, why is there so much evidence that supports Evolution? Why Ancient species, why evidence for intermediate species? If you believe in an all-powerful God, yet don’t believe in Evolution, then why are these fossils there, then why does the genetic code show evidence of intermediates and sequence-relatedness consistent with Evolution? Do you believe God put it all there just to try to confuse us? Seems like a lot of trouble just to play a little mind-game with mankind – ??
…Continued in Part II