Dr. Andrew J. Petto Speaking Event – June 22nd
Hi Guys!
I am very pleased to announce that Dr. Andrew J. Petto will be here June 22nd at 7:00 pm Eastern ! He is a Professor at the University of Wisconsin in the Department of Biological Sciences. His topic will be: The Best Evidence for Evolution. You will certainly want to be here. He will speak for approximately 30 minutes and then take questions from the room by microphone for an undetermined period of time. Below are links for more information about Dr. Petto. I look forward to seeing you all here for this very special event !!
Senior Lecturer
Science Education, Evolution Education, and Gross Anatomy
http://www4.uwm.edu/letsci/biologicalsciences/facultystaff/petto/index.cfm
https://pantherfile.uwm.edu/ajpetto/www/index.htm
One on One Debates 
17 responses to “Dr. Andrew J. Petto Speaking Event – June 22nd”
Faith in Humanity
June 23rd, 2013 at 02:49
Thank so much for coming Doctor Petto
Andrew Petto
June 23rd, 2013 at 19:50
I am so happy to have met you all and have chatted with some of you
I want to follow up on Neph’s question on the article on the accumulation of deleterious mutations. There are several layers of issues, and I will do that in the next post.
Andrew Petto
June 24th, 2013 at 03:06
Here is the promised comment to Neph’s question about why we have not died 100 or more times over (of course, this is a rhetorical questions; we only die once … each). This will be fairly lengthy, but I will try to communicate clearly so that you all can form questions and see the perspective in which we should be viewing individual research articles.
The article is this one: Kondrashov AS. Contamination of the genome by very slightly deleterious mutations: why have we not died 100 times over? J Theor Biol. 1995 Aug 21;175(4):583-94.
The abstract is here: http://www.ncbi.nlm.nih.gov/pubmed/7475094, but I was able to get a full text copy from my wife’s university library (mine only has issues back to 2005).
Note that this study provided a method for *estimating* the rate of new mutations in the genome based on estimates of disease-causing mutations in human populations (back to that in a minute). It focused on *very slightly deleterious* mutations (VSDMs): those not instantly fatal or disabling, but which do affect the outcome of the DNA sequence in question; and, as I mentioned in the case of Hemoglobin S (sickle-cell trait), the mutation is sometimes helpful and sometimes deleterious; the outcome is contingent on the situation. The issue here is whether there is a limit to the number of VSDMs that a population can tolerate and still be viable.
Now, earlier genetic studies used a rough estimate of the amount of genetic variability in a population called the effective population size (N sub e). This value is an estimate based on an idealized model … one that is seldom observed in real life, but which is often useful in calculating the effects of changes in breeding patterns from one generation or population to the next. So, it is both a familiar and a useful concept, but one that is very much an ideal.
This study is pre-genomic … that is, the study was done before the sequencing of the human genome was compete and before a lot of the contemporary analysis could even be imagined. It presumed that the rate of mutation per individual in an N-sub-e sized population could be extrapolated to the entire genome. And it changed the unit of measurement from the “gene” (which usually involves hundreds of DNA sequences, often in different locations in the genome) to the “individual nucleotide sites” that make up these genes. Think about that for a minute; we go from about 30,000-50,000 genes as the basis for calculating mutation rates to 1.5 Billion nucleotides (the GATC “letters” in a DNA “word”). That is an increase of over 30,000 times in the number of targets we are looking at (now, he may not be wrong that this is the best way to look at it, but this change of scale is significant; even if there were no differences in the rate of accumulation of VSDMs, the raw numbers would be at least 30,000 times higher!).
This model also uses a simplified concept similar to one that Neph was getting at with the random mutation idea … the concept that all parts of the genome accumulate mutations at the same rate with the same probability. But again, this was a simplifying assumption made for the purposes of computational efficiency. It may or may not be true in real time (it certainly does not seem to be true for genes as a whole), but, again, Kondrashov was proposing a heuristic: a way for formulating a question and getting an answer that would be helpful in our attempts to generate understanding of some important process or principle.
Kondrashov’s study in 1995 has been used as a reference in 121 research articles in the past 18 years (and 18 years is not only a very long time in research, but in this case it spans an intellectual chasm of the time before and after the human and man other genomes were sequenced). One of the more recent studies based on Kondrashov’s is this one:
Author(s): Keightley, PD
Rates and Fitness Consequences of New Mutations in Humans
Source: GENETICS Volume: 190 Issue: 2 Pages: 295-304 DOI: 10.1534/genetics.111.134668 Published: FEB 2012
Keightley applied Kondrashov’s model to the human genome and agreed that this estimate gives a very high rate of mutation … BUT … Keightley finds two important qualifying principles from modern genetics: (1) Only about 1/6 of these mutations occurs in “protein-coding” sequences (those that produce essential building blocks of the body’s structure and function); and (2) not all mutations are equal in their impact on reproduction and survival … or at least not in the sense of being fatal to the expected function of the gene. Keightley (among others) uses the terms “hard” and “soft” natural selection to distinguish between the effects on survival and reproduction of individuals bearing those changes.
Think, for example, of mutations that caused blood (antigen) types; or various eye colors; of the difference between attached and unattached earlobes, freckles, tongue-rolling, and a whole lot of other features. These differences are certain due to mutations (that is, changes in some part of the DNA sequence that provides instructions for the building blocks and developmental processes that will produce these variants), but none of these would present a serious selective advantage or disadvantage to those who possess them. Even if they have an effect on selective breeding (you love brown eyes or a widow’s peak and so you will always go for a mate who has these over someone who does not), they are seldom fatal to the survival and reproduction of their possessors (because you may choose from among potential mates who are actually available to you, rather than waiting for just the perfect mate … Mr Right … or Mr Right Now?).
Finally, the point to remember is one that I made in the talk and in the Q&A: scientific research papers are not scripture; they are the best understanding that we can generate with the methods, technology, and data available to us *at the time*. Kondrashov’s paper was a thoughtful examination of unanswered questions *at the time*. However, it is wrong to presume that this article published in 1995 is the last word on the issue 18 years later … as the 121 research papers that have spun off from this original paper show us.
What these 121 papers tell us is how the questions raised by Kondrashov can be used to query new data that we have and to resolve the dilemma of the high estimates of mutation load in human populations. Some of these apply the model to specific genetic diseases; others, like Keightley are more interested in how the model works in the context of more complete genomic sequences.
And that is why evolution is a great theory: new knowledge opens up new questions, and the attempts to answer those questions produce new knowledge, which leads to need questions, and so on.
NephilimFree
June 27th, 2013 at 00:33
Dr. Petto, I am not at all surprised that you would say the paper I provided a link to does not provide information that can be relied upon. It is common of evolutionists to explain away all of the evidence from genetics that demonstrates that evolution theory is a pseudoscientific fantasy which requires ignoring the obvious conclusions the evidence points us to. Evolutionists are even quick to throw their own under the bus when they inadvertently provide evidence that the theory is untenable. Methods of estimating fixed mutation rates and the effects of mutation upon a genome or population will always be changing, and hopefully improving. However, the inference we get from the effect of accruing mutation will never change, and will only magnify the anti-science nature of evolution theory. This inference is that mutation is negative and evidence that man has not been around for hundreds of thousands of years, nor will he be around for another hundred thousand.
Are the majority of mutations “silent” as evolutionists have been claiming for so long? Certainly not. We know today that genetic sequences are overlapping and embedded. What effects one is likely to effect another, perhaps several. We know today that the genome is not simply a nucleotide-by-nucleotide, linear book of information. It is sentences which share their characters with other sentences and possesses 3-dimentional hierarchies of information, even when super-coiled as chromatin. Because we cannot measure a cost to the higher percentage of mutations is not reason to believe that they are not negative. We know today that the “junk DNA” paradigm of evolutionists is false, since we have discovered that a) the codes for proteins are located throughout the genome and not neatly packed into a region, b) there is critical function (such as regulatory and developmental) throughout the genome, demonstrating areas of the genome once declared junk are not junk at all, but vital information instead, and c) the very rare beneficial mutation cannot overcome the negative effect of the vast majority of mutations, which are either seemingly silent or clearly negative. This is especially true of mutations which effect anatomy. The list of diseases and deformities which are produced by mutation is extensive.
It is simply a fact that mutation is degrading the genome, and this knowledge is supported by the overwhelming number of genetic studies which discuss observed negative effects produced by mutation. Evolutionists must fake the idea that mutation is not degenerating the human genome, but has and is instead of building it and continuously creating the information necessary for evolution. Natural Selection cannot resurrect the problem for evolutionists, since it is estimated that 70-100 mutations are believed to become fixed in the genome per generation. Natural Selection selects mutants, not individual mutations.
Consider: Chimps have an approximately 10% larger genome than humans. Evolutionists claim that we have a common ancestor. If this were true, then within the length of time from the common ancestor to the present (250,000 to 400-000 yrs. depending upon the evolutionist), evolution has produced both modern humans and modern chimps. Mutation must have therefore built this 10% more genome in chimps during this time span, since the “common ancestor” is the genome from which both diverged. There are 2 possibilities here. The first is that typical mutations did this work. However it is clearly untenable to believe that mutation could do this and produce a viable species. Such a mutation load would be outrageously high. Because beneficial mutations are quite rare, it is irrational to believe that the mutations which could do this work would produce so much functional DNA. The second possibility is that mutation has duplicated large tracts of the genome to produce this material in the chimpanzee genome. But this is untenable too since we observe also that mutations which cause such large, rapid changes to DNA typically produce chromosome disorders and individuals with server disabilities or still birth. Let me remind you that much of the chimp genome was not actually sequenced because doing so was very expensive (millions of dollars) at the time, and because evolutionists believe that they are simply the same (or nearly so) as human because of the evolution paradigm. So it does not help the evolutionist to claim that large tracts of the chimp genome were duplicated, since the chimp genome was never fully sequenced.
I feel it necessary to remind you, since you are an evolutionist and evolutionists operate today by disavowing evidence that argues against their paradigm and accept any that they can obfuscate into evidence of evolution, that the “junk DNA” paradigm is dead, so arguing that this difference of 10% in the chimp genome is or ever was “junk” is not supportable since if it is not true for humans it is not true for chimps as well:
“The complexity of our biology resides not in the number of our genes but in the regulatory switches,” – Eric Green, director of the National Human Genome Research
Institute and collaborator on the ENCODE project, in a press briefing September 5, 2013
ENCODE Project Writes Eulogy for Junk DNA
http://www.sciencemag.org/content/337/6099/1159.summary
ENCODE – The Junk DNA concept must be consigned to history
http://www.arn.org/blogs/index.php/literature/2012/09/10/encode_the_junk_dna_concept_must_be_cons
“These findings reveal there are secrets within the genomes of humans and other animals that scientists are still uncovering, and the old belief that life has useless junk DNA is more false than ever, scientists added.” http://science.nbcnews.com/junk-dna
Weird molecular hoops dispel ‘junk DNA’ myth http://science.nbcnews.com/_news/2013/03/01/17147699-weird-molecular-hoops-dispel-junk-dna-myth?lite
The obvious inference from this is that mutation did no such thing as create the genomes of humans and chimps, or any other organism. I find it to be an embaressment to science itself that evolutionists are still claiming that mutation is the base mechanism of some imaginary process that has created all of the types of life and built their genomes. I understand that evolutionists can’t let go of this idea since the entire house of cards of evolution theory comes down if they do, but evolutionists simply can no longer hide behind the claim that mutation is the builder of all of the genetic information that constitutes the genomes and functions of life. This is especially true since we know today that the information alone does not define organisms. The information of the cell’s structures, including cortical inheritance, is passed down to an organism, and this is a severe problem for evolution, since the inherited information is not determined by genes.
The eulogy for evolution theory has been written by all fields of science, especially genetics and biology. Evolutionists simply refuse to accept the eulogy exists. It is inevitable that the camp will dwindle into extinction in the coming decades because evolution theory simply cannot survive another century of scientific discovery. From the early 19th century to the mid-20th century was enough time for the world to cough up the idea that molecular interactions design organisms. The 21st century will be it’s demise. Scientists will inevitably tire of making themselves look foolish by proclaiming evolution in light of what has been and will continue to be learned about life at the microscopic level.
“I had one reviewer tell me that he didn’t care what the data said, he knew that what I was finding wasn’t possible. I wrote back and said, “Well, what data would convince you?’ And he said, ‘None.'” — Mary Schweitzer
“It is, in fact, a common fantasy, promulgated mostly by the scientific profession itself, that in the search for objective truth, data dictate conclusions. If this were the case, then each scientist faced with the same data would necessarily reach the same conclusion. But as we’ve seen earlier and will see again and again, frequently this does not happen. Data are just as often molded to fit preferred conclusions.” — Roger Lewin
“Today, our duty is to destroy the myth of evolution, considered as a simple, understood, and explained phenomenon which keeps rapidly unfolding before us. Biologists must be encouraged to think about the weaknesses of the interpretations and extrapolations that theoreticians put forward or lay down as established truths. The deceit is sometimes unconscious, but not always, since some people, owing to their sectarianism, purposely overlook reality and refuse to acknowledge the inadequacies and the falsity of their beliefs.” — Pierre Grasse
Andrew Petto
July 2nd, 2013 at 20:38
This is a long, complex post, and I will respond in bits. First of all, I am hard pressed to find the sentiment in my post that you attribute to me; in particular “does not provide information that can be relied upon” and “throw their own under the bus.” These are nothing like what I wrote or what I meant here.
I said that the paper from almost 20 years ago was a rethinking of what it would mean to study the problem from the point of view of the genome rather than the individual and so it generated a heuristic — a way of estimating the impact of a particular type of genetic change. I also said that it had been cited by at least 121 other studies in the mean time, including the one that I suggested was a reasonable culmination of this line of thinking … now that there actually are genomic data to test the heuristic. And that paper suggests that the heuristic is valuable, but the details should be modified.
If that is what you mean by “throwing someone under the bus” or “the original paper cannot be relied upon”, then you are really missing the point … both of my note and the process of science.
For example, Darwin expected evolutionary change to be constant and gradual in all cases. In less than a century, scientists had accumulated many examples in which that did not seem to be the case. Were we saying that evolutionary theory could not be relied on because not all change appeared to be constant and gradual? I would say no, but your response seems to say yes.
And, as far as heuristics go … they do not need to be correct or to correspond to real events to be useful. Almost everyone who takes biology learns the “Hardy-Weinberg” equilibrium model (heuristic) for measuring the allelic composition in stable populations. However, the model make several presumptions (in addition to that of a stable population) that are almost never met in the real world. Does that mean that we consider HWE to be something that cannot be relied upon? Absolutely not! But it means that we have to understand the assumptions, limitations, and details of its application to use it properly.
And those two examples illustrate the heart of my assessment of this paper … mostly driven by what researchers in the field are saying about that paper when they use it as a foundation for their own research.
So, please do not attribute to me behaviors and attitudes that are patently false.
In the next reply, I will consider the evidence that you offer. However, there is no point in amassing quotations … especially without context. I am well aware of the writings of the people whose quotes you have extracted, but these are proximate complaints about the human institution that is the practice of science. No one said it was perfect; but it does not rely on the actions of a few individuals (despite how we are taught the history of science) and it does go down some wrong (unproductive) roads. And science has its share of pedants, bullies, and just plain jerks.But it moves on.
So, just to take Mary Schweizer’s example, she had a reviewer who would not be convinced by the evidence she provided (and we have all had that experience), BUT her paper appeared in the journal SCIENCE, one of the most prestigious in the world. So, though her complaint is valid, it is not a condemnation of science so much as of a wrong-headed reviewer. Her work on the recovery of soft tissues from dinosaurs really did challenge the prevailing view that tissues could not be preserved in their natural form for millions of years. Exciting stuff; but neither was she rejected by the scientific community … only by one blockhead.
Andrew Petto
July 3rd, 2013 at 02:30
The ENCODE data:
I will leave this discussion for those of you who are interested in a detailed critique to read what a biochemist has to say about it (I am a functional morphologist and not a biochemist or a geneticist): http://sandwalk.blogspot.ca/2012/09/the-encode-data-dump-and-responsibility.html and related posts that are linked to that one.
For those of you not reading it, here is the nub: (1) New biochemical techniques have allowed us to record bits of DNA that does not primarily code for specific structural proteins that do, under some conditions, undergo transcription to RNA; and others whose binding sites (the places where signaling proteins attach to activate DNA) are occupied. (2) The idea that the structural proteins are all that is active in the genome (so-called one-gene–one-protein model) has been dead for decades (though, unfortunately, this is often what is still taught in K-12); so the general public (incuding, unfortunately general-assignment reporters and even some science reporters) are genuinely surprised and amazed when they learn about (1). (3) Aside from the fact that we know that this former “junk DNA” is bound with signal proteins and at least sometimes is transcribed into RNA products, we still do NOT know the functions of the touted 80% of this DNA or of its products … at least not yet.
Whether Larry Moran (or Ewan Bailey) is right or wrong on this has yet to be established. But it puzzles me that anyone would argue that this is the death knell of evolutionary theory … which only says (REMEMBER THIS! It is the CRITICAL part) that biologic variation among living things should form a pattern related to the degree of common ancestry among the organisms that we study. I see neither any claims nor any evidence in the ENCODE project to refute that proposition.
Whether we are correct about a particular model or the contribution of a particular process to the evolution of life on earth is not a test of the theory … it is a test of these models. What would test the theory is a pattern of variation that (a) was not phylogenetic; and (b) could not be explained by known biologic processes (which could also be tested).
Next up: Why do chimps have more genetic variation than humans?
Andrew Petto
July 3rd, 2013 at 02:52
On CHIMPS.
On the question of the genetic variation in populations of 2 lineages of descendants from a common ancestor: Here is where we have lots of evidence from living species to help us out.
The question was how mutation could cause chimps to have more genetic variation than humans. Interesting question, but the wrong one. Mutation probably is not the reason for this … though if we use the term mutation correctly, it simply means change in the DNA and it does not have to be harmful (that is another misconception that our K-12 science teaching seems to perpetuate).
The best explanation for the REDUCED genetic variation in humans compared to chimps lies in something called “founder effect” … which is a term used to describe why genetic variation is reduced in migrating populations compared to their ancestral populations. Put very simply … if a band of chimpanzees breaks off from its ancestral population and becomes isolated in a different habitat, we would expect (a) that this band would retain only a portion of the total genetic variation that was available in the whole population (that is, they would, within a generation, exhibit a much lower degree of genetic variation); and (b) if they were isolated from their ancestors, then they would not be able to “refresh” the gene pool, so that their genetic make-up would become more and more unique just from the regular process of reproduction and social group formation; and if there were selective pressures on traits that might have been rare among their ancestors, gradually these populations would “settle” into their different degrees of the genetic variation.
If these also happen to exploit savanna habitats and begin to walk upright, then we have a population of early hominins with reduced genetic variations vis-a-vis their chimpy ancestors.
We can’t go back and check this, of course, but we have modern examples. The best example is in the study of genetic variation in Africa, where all human species emerged, and the rest of the world. African populations have the MOST genetic variation within them; populations in Europe, Asia, and the Americas have measurably less (though the amount varies and is correlated with the degree to which “gene flow” or intercontinental mating occurred historically). We also have smaller-scale examples, such as the founder effect associated with the Bounty mutineers and their descendants on Pitcairn Island. All of these point to the same thing; migration and the separation of populations (geographic, behavioral, political, etc) can result in significantly reduced genetic variation in one of the descendant populations without any need to propose a mutational mechanism.
Of course, a model of random mutational change SHOULD predict that modern humans would have more variation than modern chimps WITH RESPECT TO THEIR FOUNDING populations … and this is because humans have bigger populations over a much wider geographic range. But, it appears that the genetic bottleneck was so stringent in early human evolution that all the extra people did was intensify the difference.
The other thing that is going on with the chimps…and this is VERY important…is that their mating and social systems much more closely resemble the “pan-mictic” (no pun intended) state that genetic models presume. That is … they are much more likely to have multiple mates in multiple social groups, so everyone’s genes has a chance to stay in the pool. This can (somewhat) counter the effects of a smaller population … IF there are enough individuals of opposite sexes with the combinations of genes (and we are back to the N-sub-e concept here).
So, it is not mutation that is responsible for the higher degree of genetic variation in chimps vs humans … or at least that is not the ONLY explanation we can test for this situation.
Andrew Petto
July 3rd, 2013 at 03:15
On switching the unit of analysis from the individual to the genome.
This was the original thread, as I recall … the “Why haven’t we died 100 times” question.
And there is one important aspect of this change in perspective that needs to be remembered. The human genome is NOT one sequence of DNA that we all share. In fact, the Human Genome Variation Project aims to characterize all the variation in the human genome.
This recent article (http://www.ncbi.nlm.nih.gov/pubmed/20981092) looks at how existing variation in DNA sequences for groups of individuals (1000) leads to an estimate of a mutation rate in the whole genome (note that this is still the same approach generated by Kondrashov, but conducted on real human data, rather than estimates). Based on these data, the authors calculated a rate of mutation (in the genome) of 10^-8 per base pair (compared to 10^-6 in Kondrashov); that is 2 orders of magnitude, or 100 times lower. And since Kondrashov argued that his estimated rate is the equivalent of 100 lethal mutations, then the new estimate drops that to 1.
So, again, not throwing K under the bus, but taking his heuristic and extending and refining it with newer data that he did not have.
There is another point here, as well. When we speak of a mutation at some point in the 1.5 billion pairs of DNA bases in the genome, we must recognize that this change that happens in an individual is not simultaneously occurring in the other 6+ billion people on the planet. The genome is not a singular thing like an oversoul in which we all share.
A mutation (for good or ill) in the “genome” is a change in the DNA in an individual, who may or may not pass it along to another individual if s/he can mate successfully, and IN COMBINATION WITH the DNA bases inherited from the other parent, these sequence may or may not result in some observable, measurable change in the offspring. These interactions among genes and among the products in the tantalizing findings of ENCODE are still largely a matter for speculation. It is difficult to imagine that they have NO effect, but, as I understand it, we are still not clear on what they DO mean.
What we ARE sure of is that the ENCODE data are a confirmation of the major shift in genetics since the 1970s AWAY FROM the one-gene–one-protein model. However, there were people in the 1940s (Waddington, inter alii) and the 1970s (Lovtrup inter alii) who had already begun proposing how the actions and products of genes may be affected or influenced by other parts of the genome. They have been vindicated in large part, and it has gotten a lot more complex and a lot more interesting.
NephilimFree
July 4th, 2013 at 10:29
“For example, Darwin expected evolutionary change to be constant and gradual in all cases. In less than a century, scientists had accumulated many examples in which that did not seem to be the case. Were we saying that evolutionary theory could not be relied on because not all change appeared to be constant and gradual? I would say no, but your response seems to say yes.”
The concensus in the scientific community is that the profound absence of transtitional fossil forms is a nagging and persistent problem for evolution. Many prominant scientists have admitted this ever since Darwin and still do to this day, and because of this absence the concept of Punctuated Equalibrium was invented to explain it away. An absence of evidence is not evidence that evolution has proceded with leaps. I am sure that you would be willing to throw these scientists under the bus for their admissions:
“What is missing are the many intermediate forms hypothesized by Darwin, and the continual divergence of major lineages into the morphospace between distinct adaptive types.” – Carroll, Robert L. Curator of Vertebrate Paleontology, Redpath Museum, McGill University, Canada, “Towards a new evolutionary synthesis,” Trends in Ecology & Evolution, 2000, Vol. 15, pp.27-32, p.27.
“Major transitions in biological evolution show the same pattern of sudden emergence of diverse forms at a new level of complexity. The relationships between major groups within an emergent new class of biological entities are hard to decipher and do not seem to fit the tree pattern that, following Darwin’s original proposal, remains the dominant description of biological evolution.” – Koonin, Eugene, “The Biological Big Bang model for the major transitions in evolution,” Biology Direct, 2007, 2:21.
Many, many more such admissions have been made. Nothing has changed for evolution since Darwin’s time. The expected transitions are still absent. Punctuated Equalibrium does not fix the problem. Pointing to creatures which similar morphology which do not show any gradualistic change and proclaiming them transitional does not evidence transition any more than pointing to creatures which have different morphologies and doing the same. Had dogs become extinct in the past, it’s quite certain that evolutionists would point to the fossil of a Collie and that of a Chiuahua and proclaim transtion because of the difference in body size and the shape of the skull, despite the fact that there is not difference in morphology between them. And yet we know that dog breeds are not evidence of evolution since they are products of gene expression. There is no new genetic information, but instead a loss of it by the turning off of genes. There is no morphological difference. There is no evidence that one anatomy is becoming a different one. There is no evolution here, nor in any supposedly transitional forms which have a difference in shape and size. For example, evolutionists point to whales which have ischium and proclaim this transitional, while it is known that these bones are part of the reproductive system (anchors for the penis) and there are no forms between whales and creatures such as ambulocetus and pacicetus. These creatures are not transitions, but animals of a different morphology from that of whales. The transitional forms would show the dissapearing of bones towards the whale. Evenso, it’s Punctuated Equalibrium to the rescue for evolutionists, and the transition exists in their imagination. “See the bones dissapearing?” No, we do not. Only the evolutionist does. This is how evolutionists point to creatures of different morphology and proclaim transition. Punctuated Equalibrium rescues nothing. The absence of evidence is not evidence that the evolutionist’s imagined transition happened quickly enough that it left no forms behind.
Nothing changes regarding the fossils. It never will. A new, large-scale study confirms Gould’s statement regarding stasis made over 40 years ago:
“No matter how many presentations I give where I show these data, no one (including myself) has a good explanation yet for such widespread stasis despite the obvious selective pressures of changing climate.”
Donald R. Prothero, et. al., “Size and shape stasis in late Pleistocene mammals and birds from Rancho La Brea during the Last Glacial–Interglacial cycle,” Quaternary Science Reviews, 56(21):1-10, 2012.
It’s not just the fossils that exhibit stasis. Biology does the same damage to evolutionism:
Epistasis as the primary factor in molecular evolution
“The main forces directing long-term molecular evolution remain obscure. A sizable fraction of amino-acid substitutions seem to be fixed by positive selection1, 2, 3, 4, but it is unclear to what degree long-term protein evolution is constrained by epistasis, that is, instances when substitutions that are accepted in one genotype are deleterious in another.”
http://www.nature.com/nature/journal/v490/n7421/full/nature11510.html#/methods
Even the rates at which evolution must have produced different morphologies is another example of Punctuated Equalibrium to the rescue:
“However, differential rates of change and the evolutionary mechanisms driving those rates result in pervasive phylogenetic conflict. These drivers need to be uncovered because mismatches between evolutionary processes and phylogenetic models can lead to high confidence in incorrect hypotheses. Incongruence between phylogenies derived from morphological versus molecular analyses, and between trees based on different subsets of molecular sequences has become pervasive as datasets have expanded rapidly in both characters and species.” – Understanding phylogenetic incongruence: lessons from phyllostomid bats, Dávalos LM, Cirranello AL, Geisler JH, Simmons NB. Department of Ecology and Evolution, State University of New York at Stony Brook, 2012
The morphological immutability and fixity of species was argued in Darwin’s day, and the creationists have been right all along. So much so, that evolutionists are confirming the creationist’s argument from over 150 years ago, and the evolutionist camp is breaking down. Many have tired of beating their heads against a wall. This will continue until there are no more pushers of evolutionism:
“Evolutionary biologists have been loosely divided into two camps. One group believes that all characteristics of an organism are equally malleable by evolutionary pressures, with the result that an organism can in theory take any shape. The other camp has the view that there are fundamental properties of each organism that are quite immutable. In his commentary, Wagner discusses new work on the complexity of organisms and a paper by Waxman and Peck in this week’s issue and argues that these results tip the balance in favor of the group that believes in a fundamentally immutable set of characteristics for each organism.” – Science 20 February 1998:
Vol. 279 no. 5354 pp. 1158-1159, referring to “Complexity Matters”, Günter Wagner, Department of Ecology and Evolutionary Biology, Yale University, 1998
“And, as far as heuristics go … they do not need to be correct or to correspond to real events to be useful. Almost everyone who takes biology learns the “Hardy-Weinberg” equilibrium model (heuristic) for measuring the allelic composition in stable populations. However, the model make several presumptions (in addition to that of a stable population) that are almost never met in the real world. Does that mean that we consider HWE to be something that cannot be relied upon? Absolutely not! But it means that we have to understand the assumptions, limitations, and details of its application to use it properly.”
We do not need assumptions for anything in science except for the formation of hypothesis. Evolutionists rely heavily on assumptions that are refuted by the evidence and use of the Scientific Method, which they sumarily ignore to proclaim, “We haven’t got all of the facts yet, but they will be revealed in time.” And yet, nothing changes. The facts don’t change, so the evolutionist concocts additional assumptions, calls them sub-theory, and tell the world they have the answer, it’s only that the actual evidence is not yet discovered. So long as assumptions can be put forth as something evidenciary, evolutionists go about their business as usual.
And those two examples illustrate the heart of my assessment of this paper … mostly driven by what researchers in the field are saying about that paper when they use it as a foundation for their own research.
“However, there is no point in amassing quotations … especially without context. I am well aware of the writings of the people whose quotes you have extracted, but these are proximate complaints about the human institution that is the practice of science.”
Ah yes. The ole’ “quote mining” argument. Scientists do not make statements lightly. Removing the assumptions and speculations form and evolutionist’s statement and providing their admission does not make the assumptions and speculation “fixers” become evidence, as I stated above.
“So, just to take Mary Schweizer’s example, she had a reviewer who would not be convinced by the evidence she provided (and we have all had that experience), BUT her paper appeared in the journal SCIENCE, one of the most prestigious in the world. So, though her complaint is valid, it is not a condemnation of science so much as of a wrong-headed reviewer.”
Science? Not science, but evolution theory. Science says nothing. Creationists enjoy science. It is not science that we have a beef with. It’s the misuse of it.
“Her work on the recovery of soft tissues from dinosaurs really did challenge the prevailing view that tissues could not be preserved in their natural form for millions of years. Exciting stuff; but neither was she rejected by the scientific community … only by one blockhead.”
More blockheads than one have tried tossing her under the bus. She was even fired for not backing down from her data. Many in the scientific community disavowed her evidence because of it’s implications.
NephilimFree
July 4th, 2013 at 10:54
“But it puzzles me that anyone would argue that this is the death knell of evolutionary theory … which only says (REMEMBER THIS! It is the CRITICAL part) that biologic variation among living things should form a pattern related to the degree of common ancestry among the organisms that we study.”
It should? Because you have a paradigm or because of the evidence? The evidence is clear: Stasis in biology, stasis in the fossils, fixity of species, the degretaory nature of mutation… Nothing changes, yet the paradigm gones on, and on, and on…
“The question was how mutation could cause chimps to have more genetic variation than humans.”
No, the qwuestion was how could random mutation create 10% more genetic material in chimps than in humans. You have moved the goalpost. Naughty naughty!
“Put very simply … if a band of chimpanzees breaks off from its ancestral population and becomes isolated in a different habitat, we would expect (a) that this band would retain only a portion of the total genetic variation that was available in the whole population (that is, they would, within a generation, exhibit a much lower degree of genetic variation); and (b) if they were isolated from their ancestors, then they would not be able to “refresh” the gene pool, so that their genetic make-up would become more and more unique just from the regular process of reproduction and social group formation; and if there were selective pressures on traits that might have been rare among their ancestors, gradually these populations would “settle” into their different degrees of the genetic variation.”
Regarding “a)” The problem here is that continual changes to allelic frequency reduces the available genetic information in a population – the opposite of what evolution requires: a continuous input of new genetic information. Producing varieties of dog (breeds) demonstrates this beautifully.
Regarding “b)” There is no morphological difference between any two varieties of chimpanze. Differences of size and even shape do not support evolution.
“If these also happen to exploit savanna habitats and begin to walk upright, then we have a population of early hominins with reduced genetic variations vis-a-vis their chimpy ancestors.”
Whoa! I can’t imagine why the absence of a locking knee joint, different number of skul bones, different number of ribs, lack of forward curve to the illiac blade of the pelvis (needed for bipedalism) rear-oriented formane magnum are going to help evolutionists argue that the fossil of an extict chimp or one of the estimated 8,000 extict primates is some kind of tansitional form. You seem to be doing a Punctuated Equalibrium leap here as well.
“The best example is in the study of genetic variation in Africa, where all human species emerged, and the rest of the world. African populations have the MOST genetic variation within them; populations in Europe, Asia, and the Americas have measurably less (though the amount varies and is correlated with the degree to which “gene flow” or intercontinental mating occurred historically).”
The out of Africa idea is refuted by human language and history. It seems out of the near-east is the truth:
“Our work indicates that the protolanguage originated more than 6,000 years ago in eastern Anatolia [eastern Turkey] …” Thomas V. Gamkrelidze and V. V. Ivanov, “The Early History of Indo-European Languages,” Scientific American, Vol. 262, March 1990, p. 110.
“Human language appears to be a unique phenomenon, without significant analogue in the animal world. . . . There is no reason to suppose that the “gaps” are bridgeable. There is no more of a basis for assuming an evolutionary development of “higher” from “lower” stages in this case, than there is for assuming an evolutionary development from breathing to walking.” – Noam Chomsky, Language and Mind (New York: Harvourt, Brace, Jovan-ovich, 1972), pp. 67,68.
“Language is perhaps the most important single characteristic that distinguishes human beings from other animal species. . . . Because of the different structure of the vocal apparatus in humans and chimpanzees, it is not possible for chimpanzees to imitate the sounds of human language, so they have been taught to use gestures or tokens in place of sounds . . . but chimpanzees never attain a level of linguistic complexity beyond the approximate level of a two-year-old child.” – Stephen Matthews, Bernard Comrie, and Marcia Polinsky, editors: Atlas of Languages: The Origin and Development of Languages Throughout the World (New York: Facts on File, Inc., 1996), p. 10.
Sanskrit was the ancient and classical language of India. Sir William Jones (1746-1794), was an accomplished scholar in this language, and in 1786 he wrote: “The Sanskrit language, whatever may be its antiquity, is of wonderful structure; more perfect than Greek, more copious than Latin, and more exquisitely refined than either; yet bearing to both of them a stronger affinity, both in the roots of verbs and the forms of grammar, than could have been produced by accident; so strong that no philologer could examine all three without believing them to have sprung from some common source which no longer exists.”
In his respected two-volume work on Genesis, Dutch scholar G. Ch. Aalders has this comment: “A famous Assyriologist made the amazing discovery that there is a clear relationship between the languages of some of the native people in Central and South America and some of the Islands, on the one hand, and the ancient Sumerian [the oldest known language] and Egyptian languages, on the other. This scholar, who formerly had considered the account in Genesis 11:1-9 to be no more than a myth, came to the conclusion that the biblical narrative is more credible than had been supposed (1981, 254).”
Dr. Harold Stigers has an interesting summary of this matter: “Though there are countless languages and dialects [approximately three thousand currently known], yet ultimate derivation from a parent language is revealed through the continuing studies being made across the boundaries of the major language families. Common features of syntax and vocabulary, which are similar enough, yet different enough not to be labeled borrowings, indicate that one must posit a common ancestor (1976, 130).”
“We also have smaller-scale examples, such as the founder effect associated with the Bounty mutineers and their descendants on Pitcairn Island. All of these point to the same thing; migration and the separation of populations (geographic, behavioral, political, etc) can result in significantly reduced genetic variation in one of the descendant populations without any need to propose a mutational mechanism.”
Varieties exhibit cosmetic differences, not morphological ones. There is no evidence of evolution to be found in cosmetic variation.
“But, it appears that the genetic bottleneck was so stringent in early human evolution that all the extra people did was intensify the difference.”
I would argue that the genetic bottlenecks found in various creatures are evidence of that 450 ft. long wooden ship that Noah built.
Andrew Petto
July 27th, 2013 at 04:23
Neph has been a VERY bad boy! He has excerpted my comments from the talk I gave, posted them online and then had critical things to say about them.
What is bad are these issues: (a) Neph posted these and then attacked my position without even letting me know that he would do so; (b) Neph posted these and attacked my position without inviting me or otherwise giving me the opportunity to respond. This is the lowest of low behavior—deceitful and unethical. It really challenges the presentation that Neph made of himself that he was really interested in a discussion.
Until and unless there is an appropriate apology for this decidedly uncollegial behavior, I have nothing more to say to Neph’s persistent recitals of creationist talking points … all of which have been adequately dismissed by the scientific evidence (viz: transitional forms, tempo and mode of evolutionary change, phylogenetic patterns in fossil and living forms, and so on.
AJ Petto
taotejing
June 24th, 2013 at 03:23
Thanks for coming, Dr. Petto. I hope when you return you’ll make a comment about how some atheistic scientists use science as a weapon against a belief in God, not merely creationism. From your response to my question, I assume you’re against this misuse of science to destroy all faith and spirituality.
Andrew Petto
June 24th, 2013 at 12:45
I think you understand me on this. There is enough science for scientists to do; they should not be doing theology (IMHO). I think what confuses people is that there are often material (not spiritual) claims made on the basis of Scripture or faith constructs of various types that turn out to be false. And yet people who hold to those faith traditions insist (a) on denying the material evidence in the world; and (b) what is worse, insinuating those sectarian claims into science education. I agree that those claims have no place in science education (or research) and that they cannot replace scientific evidence in real-world problems (agriculture, medicine, ecology, conservation, and so on).
Of course the *values* and the ethics of those religious and spiritual constructs *can* (and probably should) guide our choices about what we do about these real-world problems (for example, famine and disease in the world). But, not all faith traditions apply the same values to everyone in the world—some are pretty harsh on those who follow a different tradition and would refuse them any aid.
But, spiritual entities and concepts are outside the realm of science. Just as science can never prove that there IS a God (or gods or other spiritual powers), it cannot prove that there is not. Science can only prove that in this case (or this class of cases) the normal operation of natural laws and principles can fully account for the observations that we make.
Andrew Petto
June 25th, 2013 at 23:01
Those Inaccurately labeled “living” fossils.
For those of you interested in this issue, please check out this news report from the journal Nature: http://www.nature.com/news/living-fossil-genome-unlocked-1.12809
Within the news report there is a link to the full research article, but the report itself does a nice job of explaining how an organism’s overall anatomic form might not change much in millions of years, while other aspects of its biology might.
Enjoy
MopNGlow
June 27th, 2013 at 19:13
Dr. Petto I thought your presentation was fantastic. You told us that the phylogenetic tree is changing because of so much new information. I was wondering if there is a metric (or metrics) for the stability of the phylogenetic tree?
I guess that would be a graph theory thing, something the biologists would get help from mathematicians on. Would love it if you come back to our room and discuss that.
Thanks again for speaking to our room sir.
Andrew Petto
July 2nd, 2013 at 20:18
There are two answers to your questions. First, the tree is changing because more data are available to bolster our understanding. That is true, But the second point is more important …. it is not changing in any fundamental way. That is, it is still a nested hierarchy, but some of the branches that we thought should be closer to X now appear that they should be closer to Y. This is nothing new. If you read Carol Yoon’s book, _Naming Nature_, you will see how scientists have added new data and new techniques in the process of studying these questions, and the result has been a better understanding of the relevance of certain data for our inquiries and inferences about evolutionary relationships. The trees are pretty stable over all, but genomic data now available have given us a lot more information to consider … and to figure out how and how much of it is directly relevant to phylogenetic patterns, and how much is just local variation.
Andrew Petto
July 27th, 2013 at 04:29
A little follow-up on new genomics research.
I asked a colleague in Europe who is a prominent and long-time researcher into genomics, especially applying these models and principles to the complex inter-relationships among the bacteria.
He was writing about a new article looking at “reduced” genomes.
Here is the article: http://www.nature.com/nature/journal/v498/n7452/full/nature12132.html
And here is what my colleague had to say about it.
I think the whole thing with the ENCODE project is kind of reverse reasoning – we have all this ‘junk DNA’ – therefore it MUST serve some sort of purpose, so sure enough, they can find some reason for it being there. Of course, evolution is great at tinkering with what is there. But the real question should be – is the junk DNA really essential? I think the answer is ‘no’ to that question. For example, have a look at the Nature paper that came out a few weeks ago, about a highly reduced plant genome – the plant is fine, all the same genes are there,and they are regulated the same, just no junk DNA. So if junk DNA is ‘essential’, then how can this plant survive without it?
Here is the ‘quote of the day’ from this article:
“The compressed architecture of the U. gibba genome indicates that a small fraction of intergenic DNA, with few or no active retrotransposons, is sufficient to regulate and integrate all the processes required for the development and reproduction of a complex organism.”