something to talk about

[mark kennedy]

This is a duplicate thread of one I started in Creationism. Someone expressed an interest in discussing it openly so I thought I would invite his comments here. Anyone is free to engage as they see fit, I am assuming that the free exchange rules are still in force in the common forum.

Only 29% of the genes in the comparison of the Chimpanzee Genome and the Human Genome sequences are the same. More importantly, with brain related genes I have yet to see one that had a beneficial effect. These are the effects most often seen:

Charcot–Marie–Tooth (CMT) sensorimotor neuropathy
Infantile spasms, dystonia, and other X-linked phenotypes
Schizophrenia
Brain tumors
Alzheimer's disease
Parkinson's disease​

Pick a chromosome, any chromosome and you will find a disease or disorder effecting the human brain as the result of a mutation.

Human Genome Project Landmark Poster

FIGURE 2. Comparative neuroanatomy of humans and chimpanzees. (Genetics and the making of Homo sapiens. Nature April 2003)

Charles Darwin in the preface to ‘On the Origin of Species’ credits Jean-Baptiste Lamarck with being the first man to propose that ‘the doctrine that species, including man, are descended from other species.’ This, Darwin argues, ‘being the result of law, and not of miraculous interposition.’ One of Darwin’s contemporaries, Gregor Johann Mendel, was doing a series of experiments with pea plants that yielded the laws of inheritance that would become the cornerstone of modern genetics. Darwin’s book popularized the idea of common decent while Mendel’s only surviving paper would not be rediscovered for nearly half a century later. Mendelian laws of inheritance became inextricably linked to waves of discovery starting with chromosome theory and culminating in the molecular basis of heredity: The DNA double helix. Darwinism contributed nothing to the waves of discovery but was philosophically commingled with genetics in what has become known as the modern synthesis.

In order to examine the scientific basis for common descent I propose to examine the genetic basis for the common descent of humans from that of apes. The most dramatic and crucial adaptation being the evolution of the human brain. Charles Darwin proposed a null hypothesis for his theory of common descent :

“If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down.” (Darwin, On the Origin of Species)​

With a cranial capacity nearly three times that of the chimpanzee the molecular basis for this giant leap in evolutionary history is still almost, completely unknown. Changes in brain related genes are characterized by debilitating disease and disorder and yet our decent from a common ancestor with the chimpanzee would have had to be marked by a massive overhaul of brain related genes. I propose that a critical examination of common descent in the light of modern insights into molecular mechanisms of inheritance is the single strongest argument against human/ape common ancestry.

Darwin discussed what he called the 'bane of horticulture', this was infertility. Haldane in 'The Cost of Natural Selection indicated "genetic deaths," which is either deaths or it's equivalents in reduced fertility. He said that it would take 300 generations for a beneficial mutation to become fixed with 1667 accrued in 10 million years.

Like Darwin, he used artificial selection to illustrate what would have had to happen in natural settings:

"especially in slowly breeding animals such as cattle, one cannot cull even half the females, even though only one in a hundred of them combines the various qualities desired." (Haldane, The Cost of Natural Selection)​

For us to have evolved from apes it would have required an accelerated evolution of brain related genes. The evolution of the human brain would have had to start it's accelerated evolution on a molecular basis some 2 million years ago and within Homo Erectus (considered human by most creationists) would have had a brain size twice that of the Austropihicene and early Hominids:

Early Ancestors:

A. Afarensis with a cranial capacity of ~430cc lived about 3.5 mya.
A. Africanus with a cranial capacity of ~480cc lived 3.3-2.5 mya.
P. aethiopicus with a cranial capacity of 410cc lived about 2.5 mya.
P. boisei with a cranial capacity of 490-530cc lived between 2.3-1.2 mya.
OH 5 'Zinj" with a cranial capacity of 530cc lived 1.8 mya.
KNM ER 406 with a cranial capacity of 510cc lived 1.7 million years ago.

(See Smithsonian Human Family Tree)

Homo Erectus Skulls:

Hexian 412,000 years old had a cranial capacity of 1,025cc.
ZKD III (Skull E I) 423,000 years old had a cranial capacity of 915cc.
ZKD II (Skull D I) 585,000 years old had a cranial capacity of 1,020cc
ZKD X (Skull L I) 423,000 years ago had a cranial capacity of 1,225cc
ZKD XI (Skull L II) 423,000 years ago had a cranial capacity of 1,015cc
ZKD XII (Skull L III) 423,000 years ago had a cranial capacity of 1,030cc

Sm 3 >100,000 years ago had a cranial 917cc

KNM-WT 15000 (Turkana Boy) 1.5 million years ago had a cranial capacity of 880cc

(Source: Endocranial Cast of Hexian Homo erectus from South China, AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY 2006)

Homo habilis that would have lived. 2.5–1.5 mya with a cranial capacity of ~600 cc. The next link would have been Homo erectus with a cranial capacity of ~1000cc. KNM-WT 15000 (Turkana Boy) would have lived 1.5 mya and the skeleton structure shows no real difference between anatomically modern humans. The skull while smaller then the average cranial capacity of humans but close to twice that of his ancestors of 2 mya.

That means for our ancestors to have evolved it would have required a dramatic adaptive evolution of the size just under 2 mya sandwiched between two long periods of relative stasis. One such gene would have been the HARf regulatory gene involved in the early development of the human neocortex from 7 to 19 gestational weeks. With only two substitutions allowed since the common ancestor of the of 310 mya the divergence between humans and chimpanzees indicates 18 substitutions as early as 2 mya. (Nature, vol. 443, no. 7108, pp. 167-172 September 14, 2006)The ASPM gene while 99.3% the same for the human–chimpanzee comparison is marked by ten insertions/deletions equal to or longer than 50 bp, all of them located within introns. Primary microcephaly (MCPH) is a neurodevelopmental disorder characterized by global reduction in cerebral cortical volume.(Genetics, Vol. 165, 2063-2070, December 2003) In addition, a total of 2014 genes or ~10% of brain related genes analyzed differed in expression between humans and chimpanzees brains.(Genome Res. 14:1462-1473, 2004 ).

Evolutionists used to be able to use a 10 million year timeline, then it was 5 million years but when it comes to the most important adaptation you are looking at less then 1 million years and realistically it's only half that.

Darwin's null hypothesis for common descent is not unanswerable:

“If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down.” (Darwin, On the Origin of Species)​

If you take the road less traveled and choose to question common descent popularized by Darwin I submit that human brain evolution is prime topic. Darwin's theory is supposed to absolutely break down if a complex organ by decent with modification. My proposal is simply this, the human brain had neither the time nor the means to have evolved from that of apes.


Grace and peace,

Mark

 

[Hentenza]

Mod Hat On
​

Thread moved to Origins Theology.

 

[gluadys]

Only 29% of the genes in the comparison of the Chimpanzee Genome and the Human Genome sequences are the same.

By how much, on average, do these genes differ between chimpanzee and human genomes? Or rather by how much on average do the remaining 71% of genes differ?

Pick a chromosome, any chromosome and you will find a disease or disorder effecting the human brain as the result of a mutation.

What is the evolutionary impact on a species of a malfunctioning gene expressed as disease or disorder in the host of the mutation? This is a question I have posed to you on many occasions and which you have never once responded to. Are you going to ignore it again?

Changes in brain related genes are characterized by debilitating disease and disorder and yet our decent from a common ancestor with the chimpanzee would have had to be marked by a massive overhaul of brain related genes.

Of course, changes in brain-related genes in modern humans are characterized by disease and disorder. But if the evolutionary hypothesis is correct, these are not the genes which existed in the common ancestor. They are the consequences of changes to those ancestral genes. Have you investigated the effect of mutations--especially those related to brain size--on those ancestral genes?

Like Darwin, he [Haldane] used artificial selection to illustrate what would have had to happen in natural settings:

"especially in slowly breeding animals such as cattle, one cannot cull even half the females, even though only one in a hundred of them combines the various qualities desired." (Haldane, The Cost of Natural Selection)​

http://www.talkorigins.org/indexcc/CB/CB121.html

With only two substitutions allowed since the common ancestor of the of 310 mya the divergence between humans and chimpanzees indicates 18 substitutions as early as 2 mya.

Is this figure derived from Haldane's incorrect estimate?

(Nature, vol. 443, no. 7108, pp. 167-172 September 14, 2006)The ASPM gene while 99.3% the same for the human–chimpanzee comparison is marked by ten insertions/deletions equal to or longer than 50 bp, all of them located within introns. Primary microcephaly (MCPH) is a neurodevelopmental disorder characterized by global reduction in cerebral cortical volume.(Genetics, Vol. 165, 2063-2070, December 2003)

I don't think I have seen you answer a question related to this gene. A single mutation in this gene reduces brain size drastically. If one takes a small brain size to be the original condition, is it not possible that microencephaly is due to a mutation that reverses the one that initially enlarged the brain? If one mutation decreases brain size dramatically, why can one mutation not increase brain size dramatically?

 

[mark kennedy]

By how much, on average, do these genes differ between chimpanzee and human genomes? Or rather by how much on average do the remaining 71% of genes differ?

The answer is rapidly changing:

In order to focus on human-specific changes that have functional importance, we first identified a set of genomic regions which are at least 100 bp in length and identical between chimp (P. troglodytes), mouse (Mus musculus), and rat (Rattus norvegicus) in at least 96% of alignment columns...Bioinformatic analysis of the 34,498 predicted functional elements shows that they are very similar to previously described highly conserved elements in the human genome. Only 19.6% overlap coding regions of human genes, while the remaining non-coding regions are mostly intergenic (45.4%) and intronic (31.0%)...​

Forces Shaping the Fastest Evolving Regions in the Human Genome

Along the lineage leading to modern humans we infer the gain of 689 genes and the loss of 86 genes since the split from chimpanzees, including changes likely driven by adaptive natural selection. Our results imply that humans and chimpanzees differ by at least 6% (1,418 of 22,000 genes) in their complement of genes, which stands in stark contrast to the oft-cited 1.5% difference between orthologous nucleotide sequences. This genomic “revolving door” of gene gain and loss represents a large number of genetic differences separating humans from our closest relatives.​

The Evolution of Mammalian Gene Families

What is the evolutionary impact on a species of a malfunctioning gene expressed as disease or disorder in the host of the mutation? This is a question I have posed to you on many occasions and which you have never once responded to. Are you going to ignore it again?

The answer won't change no matter how many times you pretend it hasn't been answered:

Examples of this are legion, exceptions are virtually non-existent. This is not a minor point, random mutations do bad things to brain related genes

Different classes of homeobox genes tend to be expressed in different regions of the brain and are critical to the development of that specific region. Thus, mutations of the Hox genes disrupt the hindbrain and cause loss of many of the cranial nerves. Mutations in the Engrailed genes disrupt the development of the cerebellum and midbrain. Finally, mutations of the Dlx genes affect differentiation in the basal ganglia, while mutations of the Emx and Otx genes affect the cerebral cortex.

Several generalizations can be made from these studies. The defects in the mutant animals are frequently subtle. This is because there are often several highly related transcription factors in the same tissue, and the closely related gene products are able to take over the function of the mutated gene. Thus, to determine further the effects of these genes on development, investigators are now creating “double knock-outs” in which both genes are removed. When animals have mutations in two of these related genes, they often have much more severe abnormalities. For instance, mutation of Dlx-2 affects one type of interneuron in the olfactory bulb, whereas mutation of both Dlx-1 and Dlx-2 appears to affect all of the interneurons in this region.

Homeobox genes regulate processes ranging from the specification of the identity of brain regions to the growth of these regions to participating in the differentiation of specific cell types or axon tracts. Mutation of Emx-2 eliminates the dentate gyrus of the hippocampus, and mutation of Emx-1 primarily reduces the corpus callosum. In addition, in humans, mutations of Emx-2 result in a type of cerebral cortical malformation called schizencephaly. Thus, these genes are essential for major aspects of brain development, and their absence or mutation causes abnormalities in specific cell types or in the “wiring” within the brain. Mutations or subtle variations in the activity level of some of these master control protein deficits are hypothesized to be associated with the more commonly seen neuropsychiatric disorders. ( Development of the Cerebral Cortex: V. Transcription Factors and Brain Development. John L.R. Rubenstein, M.D., Ph.D. emphasis mine)​

Germ cell mutations are the only why that the up regulation of the human brain is possible. What we could expect from the introduction of germ cell mutations is:

Neuroepithelial tumors , Non-neuroepithelial tumors , rhabdoid tumors , carcinomas of the breast and adrenal cortex , brain tumors, and acute leukemias , Neural Degeneration, sickle-cell disease , cystic fibrosis , Huntington's disease , fragile X syndrome , Burkitt's lymphoma , Duchenne Muscular Dystrophy , HUMAN BRAIN, BREAST AND PROSTATE CANCERS, rhabdomyosarcoma . In discussing the 68,000 indels discovered in a comparison of Chimpanzee chromosome 22 and Human chromosome 21 there is only one explanation for they're introduction to into the respective genomes, mutations. Never mind that there is no demonstrated mechanism for evolution on this level Darwinian's never question the universal descent model. Here is a list of diseases and disorders associated with Human Chromosome 21:

Coxsakie and adenovirs recptor, Amyloidosis, cerebroarterial, Dutch trype, Alzheimer disease, APP-related, Schizophrenia, chronic, Usher syndrome, autosomal recessive, Amytrophic lateral scerosis, Oligomycin sensitivity, Jervell and Lange-Nielsen syndrome, Long QT syndrome, Down syndrome cell adhesion molecule, Homocystinuria, Cataract, congential autosomal dominant, Deafness autosomal recessive, Myxovirus (influenza resistance, Luekemia, acute myeloid, Myeloproliferative syndrome, trasient, Leukema transient of Daown syndrome, Enterokinase defiency, Multiple carboxylase deficiency, T-cell lymphoma invasion and metastasis, Mycobacterial infection, atypical, Down syndrome (critical region), Autoimumne ployglandular disease, tye 1, Bethlem myopathy, Epilepsy, progressive myoclonic, Holoprosencephaly, alobar, Knocloch syndrome, Hemotiytic anemia, Breast cancer, Platelet disorder, with myeloid malignancy.​

Human Chromosome 21

Of course, changes in brain-related genes in modern humans are characterized by disease and disorder. But if the evolutionary hypothesis is correct, these are not the genes which existed in the common ancestor. They are the consequences of changes to those ancestral genes. Have you investigated the effect of mutations--especially those related to brain size--on those ancestral genes?

Do you have a single reason why I should think it changed?

http://www.talkorigins.org/indexcc/CB/CB121.html

Your kidding right?

Is this figure derived from Haldane's incorrect estimate?

I have never derived anything from Haldane except that even beneficial effects from mutations are fixed with steep physiological costs.

I don't think I have seen you answer a question related to this gene. A single mutation in this gene reduces brain size drastically. If one takes a small brain size to be the original condition, is it not possible that microencephaly is due to a mutation that reverses the one that initially enlarged the brain? If one mutation decreases brain size dramatically, why can one mutation not increase brain size dramatically?

Because these are random mutations that cause a stop codon to be inserted resulting in a truncated protein.

​

Indels involving one or two base pairs (or multiples thereof) can have devastating consequences to the gene because translation of the gene is "frameshifted". This figure shows how by shifting the reading frame one nucleotide to the right, the same sequence of nucleotides encodes a different sequence of amino acids. The mRNA is translated in new groups of three nucleotides and the protein specified by these new codons will be worthless. Scroll up to see two other examples (Patients C and D).

Frameshifts often create new STOP codons and thus generate nonsense mutations. Perhaps that is just as well as the protein would probably be too garbled anyway to be useful to the cell.

Indels of three nucleotides or multiples of three may be less serious because they preserve the reading frame (see Patient E above). Mutations ​

Because it just doesn't work that way and you know it because I have showed you this more then once:

We identified a homozygous mutation introducing a premature stop codon into the predicted ASPM (abnormal spindle−like microcephaly associated) open reading frame in each of the four affected families. The four mutations are 719−720delCT (exon 3), causing a frameshift leading to a premature termination 15 codons downstream. ASPM is a major determinant of cerebral cortical size ​

 

[gluadys]

The answer is rapidly changing:

Yes, I notice how you like to mix and match different figures as if they were all referring to the same thing e.g numbers of genes, composition of genes, numbers of base nucleotides, number of changes in DNA sequences.

It is not so much that the answer is rapidly changing as that you do not discriminate between one figure and another.

The answer won't change no matter how many times you pretend it hasn't been answered:

And you still have not answered the question. Apparently you still haven't even understood the question. Are you ever going to learn the difference between the deleterious effect of a mutation on its host and the potential impact of the mutation on the evolution of the species?

Repeating your catalogue of what can go wrong when a mutation occurs, does not answer the question about the evolutionary impact on the species. It only indicates one of three things:
a) you know the answer but refuse to state it
b) you don't know the answer, but refuse to admit your ignorance
c) you don't even understand the question.

I'm placing my money on c).

Do you have a single reason why I should think it changed?

I introduced the question with a hypothetical: "But if the evolutionary hypothesis is correct,..." The point is that you demonstrate nothing if you assume the genes were the same 2-5 million years ago and note the consequences of mutations to the genes as they are now. That is not the evolutionary hypothesis you wish to falsify. The evolutionary hypothesis is that the modern genes did not exist in their present form back then. So the effect of mutations in today's genes is not a problem from that perspective. It is the effect of mutations on their ancestors you need to think about.

Or demonstrate that today's genes are identical to the ancestral genes. But that can't be the case, because there were no large human brains 2 million years ago.

Your kidding right?

I don't think they are.

I have never derived anything from Haldane except that even beneficial effects from mutations are fixed with steep physiological costs.

Something he was wrong about. But if you did not get the limit of only two substitutions allowed from him, where did you get it from?

Because these are random mutations that cause a stop codon to be inserted resulting in a truncated protein.

So if the original protein was shorter and a mutation lengthened it, you get the human ASPM gene and a large brain. Now when a mutation introduces a premature stop codon, it decreases the size of the brain. Why is this out of the question?

Alternatively it could have been a different mutation, not just the reverse of a truncation, that allowed for brain size to increase. The question remains: if a single mutation can reduce brain size more than half, why can a single mutation, (either the reverse of this or a different independent mutation) why can such a mutation not increase brain size by the same amount?

Because it just doesn't work that way and you know it because I have showed you this more then once:

All you have shown me is a frameshift I already knew about. I have read Kimball's site too. It doesn't answer the question. We know that a single mutation produces microencephaly--a significant reduction in brain size. Why can a single mutation not have dramatically increased brain size 2 mya?

 

[birdan]

Pick a chromosome, any chromosome and you will find a disease or disorder effecting the human brain as the result of a mutation.

...

Changes in brain related genes are characterized by debilitating disease and disorder and yet our decent from a common ancestor with the chimpanzee would have had to be marked by a massive overhaul of brain related genes.

Your second point above does not logically follow from your first point. There are deleterious mutations for any gene (not just affecting the brain), and there are neutral and beneficial mutations. That there are variations of such neural genes as ASPM and microcephalin in the current human population is proof that not all mutations of these genes are detrimental.

For us to have evolved from apes it would have required an accelerated evolution of brain related genes. The evolution of the human brain would have had to start it's accelerated evolution on a molecular basis some 2 million years ago and within Homo Erectus (considered human by most creationists) would have had a brain size twice that of the Austropihicene and early Hominids:

Your basic premise seems to be that there has to be a correlation between increase in brain size and number of mutations involved. IOW, if an increase in brain size from 1 lb. to 2 lbs. takes x mutations, then an increase from 1 lb. to 3 lbs. would take 2x mutations. Do you have any evidence to back up this assertion? With science's emerging understanding of regulatory areas of DNA, it would seem that a simple mutation could extend the active period of embryonic neural development, thus increasing brain size without any correlation to number of mutations. If you have any evidence that brain size increases have to correspond to number of mutations, I'd like to see it.

The ASPM gene while 99.3% the same for the human–chimpanzee comparison is marked by ten insertions/deletions equal to or longer than 50 bp, all of them located within introns. Primary microcephaly (MCPH) is a neurodevelopmental disorder characterized by global reduction in cerebral cortical volume.(Genetics, Vol. 165, 2063-2070, December 2003)

As mentioned before (and as your 2 points above show), microcephaly is caused by mutations to exons, while the 10 indels you keep citing were to introns. All you do is imply that the ASPM protein structure has been highly conserved.

 

[shernren]

Among the many fallacies in mark's post, this one is most glaring (since I've pointed it out years ago) :

Mutations from the current genetic configuration of our brains are deleterious, no doubt. But the question is how did our current genetic configuration get there in the first place? Just because mutations away from a current configuration are unlikely does not mean that mutations into a current configuration are unlikely. Just because a marble will never roll out of a bowl on its own does not mean it can never roll into a bowl on its own.

Suppose I have a string that says "The black cat". Well, let's try randomly mutating it around a little:

Twe black cat
Phe black cat
Tie black cat
The block cat
The black kat
The black caw

None of these strings have "as much meaning" as my string the black cat. If we then postulate that strings "evolve" in the direction of "more meaning", then by mark's logic, we would conclude that the string "the black cat" could not have "evolved".

However, that is absurd. The "evolution" that takes "tie black cat" -> "the black cat" would be a valid one. So would the "evolution" that takes "the block cat" -> "the black cat". See, if every evolution away from "the black cat" is deleterious, the obvious corollary is that every evolution towards "the black cat" is advantageous.

Indeed, the more deleterious any mutation away from the current genetic configuration of the human brain is,
the more advantageous any mutation towards the current genetic configuration of the human brain, from any previous state, would be.

Isn't that obvious?

 

[mark kennedy]

Yes, I notice how you like to mix and match different figures as if they were all referring to the same thing e.g numbers of genes, composition of genes, numbers of base nucleotides, number of changes in DNA sequences.

I noticed that you like to talk in circles endlessly, in generalities and blindly dismiss the substantive, specifics unconditionally.

It is not so much that the answer is rapidly changing as that you do not discriminate between one figure and another.

I don't like to play these little games, I am certainly not going to let you run me in circles while you ask the same rhetorical question again and again and again, no matter what the answer is.

And you still have not answered the question.

Your only tactic, at least the only one that I have ever seen you use. Just keep asking the same question no matter what the answer is. Never address the well researched and carefully prepared discussion, Oh no, just ask the question again, and again, and again ad infinitum, ad nauseum.

Apparently you still haven't even understood the question.

Notice not a single substantive point addressed, not of the carefully prepared points made or even mentioned. Not a single one of the obvious problems is even considered and no to the inevitable ad hominem attack, which is the weapon of choice for TEs on this board.

Are you ever going to learn the difference between the deleterious effect of a mutation on its host and the potential impact of the mutation on the evolution of the species?

See how this works, first the evidence and argument is ignored and then the argument goes, straight 'to the man':

An ad hominem argument, also known as argumentum ad hominem (Latin: "argument to the man", "argument against the man") consists of replying to an argument or factual claim by attacking or appealing to a characteristic or belief of the person making the argument or claim, rather than by addressing the substance of the argument or producing evidence against the claim. The process of proving or disproving the claim is thereby subverted, and the argumentum ad hominem works to change the subject. Wikipedia​

This is how they do it, they assume, a priori, that all living systems are related by lineage aka universal common ancestry. Never mind that the evidence only indicates many share a common ancestry you must assume all or you are assumed to be incredulous, which is a nice word for stupid. If you don't accept common ancestry as a self evident fact a priori then you are assumed ignorant and the focus is on proving that as a fact, not the specifics of the question being argued.

Repeating your catalogue of what can go wrong when a mutation occurs, does not answer the question about the evolutionary impact on the species. It only indicates one of three things:
a) you know the answer but refuse to state it
b) you don't know the answer, but refuse to admit your ignorance
c) you don't even understand the question.

I'm placing my money on c).

See what I mean, there were really only two choices, I am either ignorant, mentally incapable (same thing really) or I'm a liar by omission. This is stereotypical TE and evolutionist rhetoric and it has nothing to do with science, evolution are Christian thought. It is nothing more then an attack on traditional theistic reasoning.

I introduced the question with a hypothetical: "But if the evolutionary hypothesis is correct,..." The point is that you demonstrate nothing if you assume the genes were the same 2-5 million years ago and note the consequences of mutations to the genes as they are now. That is not the evolutionary hypothesis you wish to falsify. The evolutionary hypothesis is that the modern genes did not exist in their present form back then. So the effect of mutations in today's genes is not a problem from that perspective. It is the effect of mutations on their ancestors you need to think about.

The effect of mutations as they are known now is the only way we can project what would be the affect 2 mya. Now, a much better question would be what are the actually differences in brain anatomy when comparing the human and chimpanzee brain. I say that in all seriousness since the MRCA would have had a brain the same size 2 mya.

If you really want to know the differences there are resources out there that will break it down for you:

Abstract
The human brain is one of the most intricate, complicated, and impressive organs ever to have evolved. Understanding its evolution requires integrating knowledge from a variety of disciplines in the natural and social sciences. Four areas of research are particularly important to this endeavor. First, we need to understand basic principles of brain evolution that appear to operate across broad classes of organisms. Second, we need to understand the ways in which human brains differ from the brains of our closest living relatives. Third, clues from the fossil record may allow us to outline the manner in which these differences evolved. Finally, studies of brain structure/function relationships are critical for us to make behavioral sense of the evolutionary changes that occurred. This review highlights important questions and work in each of these areas.​

Evolution of the Size and Functional Areas of the Human Brain

I have just had a lot of pointless exchanges where the same question keeps getting asked again and again and none of the answers are ever satisfactory. It's a debate technique just like the tag team debaters or the ad hominem attack. If you want to know the actual differences there is a lot of information out there but you are going to have to do some reading, it's as simple as that.

The differences examined in this paper include:

Because humans differ from other species on a number of interesting behavioral dimensions(e.g., communication, ability to harness technology, problem solving, complexity of social relationships; see below), and because the neural processing underlying these is often located in different brain regions,there is no general agreement about what components are most important to study a priori. For this reason, this review covers most of the components for which information is available. These include:

1. Overall brain size,
2. Olfactory bulb,
3. Cerebellum, visual cortex,
4. Temporal lobe, and the
5. Overall frontal cortex and its components:

* primary motor,
* premotor, and
* prefrontal cortices

Or demonstrate that today's genes are identical to the ancestral genes. But that can't be the case, because there were no large human brains 2 million years ago.

There were no human brains 1 million years ago, oh wait, there was Turkana Boy with a human body and a cranial capacity approaching 1,000cc (compared to apes ~400cc). One of the latest finds near Turkana found one of his fellow H erectus a million years later with a skull the size of a gorilla. What is more between 2 mya and 3 mya there are no hominid ancestors, just a few teeth fragments. To make it even more convoluted there are no chimpanzee ancestor fossils for the last 5 mya except for a few teeth found in 2005. There is a reason why we don't have any fossils for the chimpanzee, it's because everytime one is dug up it's automatically one of ours.

New Fossils Cast Evolutionary Lineage in New Light

Something he was wrong about. But if you did not get the limit of only two substitutions allowed from him, where did you get it from?

Oh that's right, there are no costs, just random mutations improving the form and function of genes like magic. He was pointing to real world problems with selective breeding and the consequences of even fixing a single mutation with a beneficial affect.

So if the original protein was shorter and a mutation lengthened it, you get the human ASPM gene and a large brain. Now when a mutation introduces a premature stop codon, it decreases the size of the brain. Why is this out of the question?

When the mutation causes a frameshift a stop codon is inserted and it produces a truncated protein, which results in a severely reduced brain size comparable to apes. I'm not saying that an improved sequence is not out of the question, I'm saying that there is only one known affect and it's a reduced size from a truncated protein. That's the known affects of mutations on the ASPM gene, in fact it gets it's name from the abnormal spindle the brain needs to develop normally.

Alternatively it could have been a different mutation, not just the reverse of a truncation, that allowed for brain size to increase. The question remains: if a single mutation can reduce brain size more than half, why can a single mutation, (either the reverse of this or a different independent mutation) why can such a mutation not increase brain size by the same amount?

Because it never does, not in brain related genes. The fact is that protein coding genes do not respond well to mutations if they respond at all. Maybe you would like to explore the possibility of changes in regulatory genes?

​

In case you can't make it out it's the:

* Prefrontal Cortex
* Frontal Pole
* Broca's Area
* Cerebellum
* Primary Visual Cortex
* Caludate Nucleus
* Anterior Cingulate Cortex

All you have shown me is a frameshift I already knew about. I have read Kimball's site too. It doesn't answer the question. We know that a single mutation produces microencephaly--a significant reduction in brain size. Why can a single mutation not have dramatically increased brain size 2 mya?

Because it's not that simple, the reduced brain size is still a human brain. There are a wide range of genes that are different between humans and chimpanzees that are extremely similar in other lineages. These are referred to as Human Accelerated Regions:

In order to focus on human-specific changes that have functional importance, we first identified a set of genomic regions which are at least 100 bp in length and identical between chimp (P. troglodytes), mouse (Mus musculus), and rat (Rattus norvegicus) in at least 96% of alignment columns...Bioinformatic analysis of the 34,498 predicted functional elements shows that they are very similar to previously described highly conserved elements in the human genome. Only 19.6% overlap coding regions of human genes, while the remaining non-coding regions are mostly intergenic (45.4%) and intronic (31.0%)...
Forces Shaping the Fastest Evolving Regions in the Human Genome


Including a regulatory gene that has allowed only 2 substitutions in over 300 million years getting 18 about 2 mya. All the substitutions are from weak to strong which means the changes are moving upstream.

The 118-bp HAR1 region showed the most dramatically accelerated change , with an estimated 18 substitutions in the human lineage since the human–chimpanzee ancestor, compared with the expected 0.27 substitutions on the basis of the slow rate of change in this region in other amniotes . Only two bases (out of 118) are changed between chimpanzee and chicken, indicating that the region was present and functional in our ancestor at least 310 million years (Myr) ago. No orthologue of HAR1 was detected in the frog , any of the available fish genomes, or in any invertebrate lineage, indicating that it originated no more than about 400 Myr ago​

An RNA gene expressed during cortical development evolved rapidly in humans

 

[birdan]

Your only tactic, at least the only one that I have ever seen you use. Just keep asking the same question no matter what the answer is. Never address the well researched and carefully prepared discussion, Oh no, just ask the question again, and again, and again ad infinitum, ad nauseum.



Notice not a single substantive point addressed, not of the carefully prepared points made or even mentioned. Not a single one of the obvious problems is even considered and no to the inevitable ad hominem attack, which is the weapon of choice for TEs on this board.



See how this works, first the evidence and argument is ignored and then the argument goes, straight 'to the man':

An ad hominem argument, also known as argumentum ad hominem (Latin: "argument to the man", "argument against the man") consists of replying to an argument or factual claim by attacking or appealing to a characteristic or belief of the person making the argument or claim, rather than by addressing the substance of the argument or producing evidence against the claim. The process of proving or disproving the claim is thereby subverted, and the argumentum ad hominem works to change the subject. Wikipedia​

This is how they do it, they assume, a priori, that all living systems are related by lineage aka universal common ancestry. Never mind that the evidence only indicates many share a common ancestry you must assume all or you are assumed to be incredulous, which is a nice word for stupid. If you don't accept common ancestry as a self evident fact a priori then you are assumed ignorant and the focus is on proving that as a fact, not the specifics of the question being argued.



See what I mean, there were really only two choices, I am either ignorant, mentally incapable (same thing really) or I'm a liar by omission. This is stereotypical TE and evolutionist rhetoric and it has nothing to do with science, evolution are Christian thought. It is nothing more then an attack on traditional theistic reasoning.

Mark, I have to say that I don't think you've answered Gluadys' question either. Also, I don't think Gluadys has helped too much by asking the same question repeatedly - she should try re-framing the question in other ways.

But, I think the gist of it is that Gluadys is asking what effect these diseases have on the species, while Mark keeps answering about the effect on the individual. If I may extrapolate a bit, I think Gluadys' point is that a severely deleterious mutation will have no effect on the population because that individual will not produce offspring.

Mark, I would suggest that instead of reverting to "flame on" mode, that you might instead ask for clarification of the question or ask how your initial answer was unsatisfactory. And as I already mentioned, repeating the same question over and over doesn't do much good. If it was misunderstood the first time, chances are it will be the tenth time too.

[/Miss Manners]

 

[gluadys]

I noticed that you like to talk in circles endlessly, in generalities and blindly dismiss the substantive, specifics unconditionally.

On the contrary, I am saying your specifics are not specific enough. You do not make the necessary discrimination between figures which measure different things. You speak frequently of the percentage of genes which differ between human and chimp without noting that in many cases they only differ by one or two nucleotides.

But the number of nucleotides becomes important to you when talking of indels because you want to treat indels as if they were multiple instances of SNPs and not unique mutational events in themselves.

Until you show more responsibility in how you handle figures, your figures are not worth analyzing.

I don't like to play these little games, I am certainly not going to let you run me in circles while you ask the same rhetorical question again and again and again, no matter what the answer is.

Your only tactic, at least the only one that I have ever seen you use. Just keep asking the same question no matter what the answer is. Never address the well researched and carefully prepared discussion, Oh no, just ask the question again, and again, and again ad infinitum, ad nauseum.

It doesn't matter how carefully you research your data if the data is irrelevant to the question.

Notice not a single substantive point addressed, not of the carefully prepared points made or even mentioned. Not a single one of the obvious problems is even considered and no to the inevitable ad hominem attack, which is the weapon of choice for TEs on this board.

Because in terms of my question (the impact on the species) your "substantive points" are irrelevant.

But to make you happy, lets look at a few of your "obvious problems".

Neuroepithelial tumors
Epidemiology, and End Results (SEER) database for 1996 to 2000 indicate that the combined incidence of primary invasive CNS tumors in the United States is 6.6 per 100,000 persons per year with an estimated mortality of 4.7 per 100,000 persons per year.

Here and in all quotes, the emphasis is mine. I am using the links you provided.

To put it in layman's terms, that works out to 66 people per million or 396,000 people worldwide likely to suffer from such tumors per year and less than 50 per million dying of them per year.

What obvious problem is there with this from the perspective of the survival of the species? In fact, is there not a perfectly sound evolutionary explanation of why this disorder is so rare?

Fragile X syndrome
Fragile X syndrome is the most common inherited form of mental disability, world-wide. Main clinical features are cognitive deficit, speech difficulties, delayed development, autism, and particular physical characteristics. The syndrome can be cytogenetically diagnosed by the expression of chromosome X fragile site at band Xq27.3. At molecular level, the cause of the syndrome is defined as an abnormal expansion of CGG trinucleotide repeats in the 5'UTR of the FMR-1 gene as well as hypermethylation at the proximal CpG island. Study of fragile X syndrome at Songklanagarind Hospital during May 1991-June 1996 was herein reported. A total of 287 blood samples of 260 unrelated families were cytogenetically examined by using lymphocyte culture method with 2-4 different treatments. Frequency of positive fragile X cases was found to be 7 in 260 (2.7%).

So a "common" inherited disorder is found to affect 2.7% of the sampled population. Is this a significant threat to the survival of the species?

Burkitt's lymphoma
Germline mutations of the p53 gene have been reported in cancer-prone families. The Li-Fraumeni syndrome (LFS) is a rare autosomal dominantly inherited syndrome with the following familial characteristics: a proband with either acute lymphocytic leukemia, sarcoma, breast cancer, brain tumor and/or adrenocortical carcinoma before the age of 45; a first-degree relative with a cancer in this group; and a first- or second-degree relative with sarcoma at any age or any cancer before age 45. The affected individuals have a germline mutation of p53 (12-16). The prevalence of a germline p53 mutation is approximately 0.01% in the general population, but is 5-10% among young patients with multiple cancers.

Do you get the picture yet? Yes, these diseases are genetic in origin. Yes, they are traumatic when they occur. But they all occur rarely. And they probably occur rarely because they are deleterious.

Hence they really tell us nothing at all about the evolution of the human brain. The evolution of the human brain requires changes that are adaptive and that spread through the population to become the norm. You are fixated on the abnormal.

This is how they do it, they assume, a priori, that all living systems are related by lineage aka universal common ancestry. Never mind that the evidence only indicates many share a common ancestry you must assume all or you are assumed to be incredulous, which is a nice word for stupid. If you don't accept common ancestry as a self evident fact a priori then you are assumed ignorant and the focus is on proving that as a fact, not the specifics of the question being argued.

When it comes to the human brain, all we need to consider is the common ancestry of chimpanzees and humans, not the whole standard phylogeny.

I expect, however, that that is precisely the sticking point. Accept the common ancestry of chimpanzees and humans and there is no theological reason to reject universal common ancestry.

Now, a much better question would be what are the actually differences in brain anatomy when comparing the human and chimpanzee brain. I say that in all seriousness since the MRCA would have had a brain the same size 2 mya.

Indeed, that would be a much better question, and I hope you follow up on it. The focus on brain size is much too narrow. As you noted, a microcephalic human brain is still a human brain (and it is not even clear that this has serious impacts on intellect). By the same token, an enlarged chimpanzee brain with no other changes would still be a chimpanzee brain

That's the known affects of mutations on the ASPM gene, in fact it gets it's name from the abnormal spindle the brain needs to develop normally.

And the homologous gene in other species directs the spindle-formation in cell division. Sounds like a case of an older gene developing a new function. Isn't that evolution?

Because it never does, not in brain related genes.

Do we really know that? But what about when the human brain was first developing? Are you not committing an inductive fallacy here? What happens when one beneficial mutation is discovered? Your whole thesis is falsified. What if the difference between human ASPM and its homologues in other species was due to such a beneficial mutation?

Maybe you would like to explore the possibility of changes in regulatory genes?

That is an excellent idea. This is where a lot of new research is focussed. btw have your read Sean Carroll's Endless Forms Most Beautiful yet?

Including a regulatory gene that has allowed only 2 substitutions in over 300 million years getting 18 about 2 mya. All the substitutions are from weak to strong which means the changes are moving upstream.

The 118-bp HAR1 region showed the most dramatically accelerated change , with an estimated 18 substitutions in the human lineage since the human–chimpanzee ancestor, compared with the expected 0.27 substitutions on the basis of the slow rate of change in this region in other amniotes . Only two bases (out of 118) are changed between chimpanzee and chicken, indicating that the region was present and functional in our ancestor at least 310 million years (Myr) ago. No orthologue of HAR1 was detected in the frog , any of the available fish genomes, or in any invertebrate lineage, indicating that it originated no more than about 400 Myr ago​

Ah, so that is where the figure came from. So, what is the problem with this?
Why do you find rapid evolution so incredible?

 

[gluadys]

But, I think the gist of it is that Gluadys is asking what effect these diseases have on the species, while Mark keeps answering about the effect on the individual. If I may extrapolate a bit, I think Gluadys' point is that a severely deleterious mutation will have no effect on the population because that individual will not produce offspring.

Exactly right. And this HAS been explained to Mark many times over. I don't think he is really so dense that he does not understand the question. But it is either that or he is deliberately ignoring the implications.

After all, his position is that natural selection is mysticism.

 

[mark kennedy]

Mark, I have to say that I don't think you've answered Gluadys' question either. Also, I don't think Gluadys has helped too much by asking the same question repeatedly - she should try re-framing the question in other ways.

Right and this goes on why the OP lies untouched. I have seen this debate tactic used too many times to take it seriously.

But, I think the gist of it is that Gluadys is asking what effect these diseases have on the species, while Mark keeps answering about the effect on the individual. If I may extrapolate a bit, I think Gluadys' point is that a severely deleterious mutation will have no effect on the population because that individual will not produce offspring.

No I'm not, I'm talking about the known affect of mutations on the human brain and the deleterious affects are legion and affect populations in profound ways. Just because you have a disease or disorder does not mean you will not produce. Odds are that is it's a lethal mutation they won't even get out of the womb but beneficial affects from mutations in brain related genes are unknown to modern science. So how do the changes in these highly conserved genes get there in the first place?

Mark, I would suggest that instead of reverting to "flame on" mode, that you might instead ask for clarification of the question or ask how your initial answer was unsatisfactory. And as I already mentioned, repeating the same question over and over doesn't do much good. If it was misunderstood the first time, chances are it will be the tenth time too.

[/Miss Manners]

I have answered the question repeatedly and I'm not running in circles because I know that's all that's going to happen. You guys have at least three detailed and substantive posts laying essentially untouched. That does not encourage me to spend hours preparing another that will be ignored as well.

I don't appreciate being called a liar or ignorant buddy. Not when I have made every effort to offer a detailed exposition of the relevant scientific literature. I'm not the one turning this into a flame thread, the TEs are notorious for it. That's why by and large these debates are shunned by creationists.

 

[mark kennedy]

On the contrary, I am saying your specifics are not specific enough. You do not make the necessary discrimination between figures which measure different things. You speak frequently of the percentage of genes which differ between human and chimp without noting that in many cases they only differ by one or two nucleotides.

That's a deceptive statistic, the number of know differences in vitally important genes are growing as we speak. No explanation for how they get there except for the mantra of random mutations plus selection. It just doesn't work that way.

But the number of nucleotides becomes important to you when talking of indels because you want to treat indels as if they were multiple instances of SNPs and not unique mutational events in themselves.

No I don't

Until you show more responsibility in how you handle figures, your figures are not worth analyzing

.

At least I have them.

It doesn't matter how carefully you research your data if the data is irrelevant to the question.

Ok, now I'm ignorant and irrelevant and I should jump through hoops for you why?

Because in terms of my question (the impact on the species) your "substantive points" are irrelevant.

See, no matter how the question is answered it just keeps getting asked again, and again, and again...

But to make you happy, lets look at a few of your "obvious problems".

My problem is the fallacious debate tactics of my opponents.

Here and in all quotes, the emphasis is mine. I am using the links you provided.

To put it in layman's terms, that works out to 66 people per million or 396,000 people worldwide likely to suffer from such tumors per year and less than 50 per million dying of them per year.

What obvious problem is there with this from the perspective of the survival of the species? In fact, is there not a perfectly sound evolutionary explanation of why this disorder is so rare?

Yea, but beneficial affects are rarer still, if they exist at all in brain related genes. Look, my answers are irrelevant and your posts are simply insulting so were even. I only posted the thread because Mallon suggested he might be interested in pursuing the discussion in the open forum.

So a "common" inherited disorder is found to affect 2.7% of the sampled population. Is this a significant threat to the survival of the species?


Do you get the picture yet? Yes, these diseases are genetic in origin. Yes, they are traumatic when they occur. But they all occur rarely. And they probably occur rarely because they are deleterious.

And you call my posts irrelevant.

Hence they really tell us nothing at all about the evolution of the human brain. The evolution of the human brain requires changes that are adaptive and that spread through the population to become the norm. You are fixated on the abnormal.

Because the beneficial affects you are assuming happened don't happen.

When it comes to the human brain, all we need to consider is the common ancestry of chimpanzees and humans, not the whole standard phylogeny.

It's a common practice in genetics research to have out groups. Now you are dismissing the cutting edge research of Pollard as irrelevant as well.

I expect, however, that that is precisely the sticking point. Accept the common ancestry of chimpanzees and humans and there is no theological reason to reject universal common ancestry.

That's the whole point isn't it, dispense with creation and you can dispense with traditional Christian theism entirely. This isn't about science, it's about attacking a Biblical worldview. My theology could endure, virtually untouched, if I woke up tomorrow and decided we were just evolved apes.The sticking point is that I am expected to assume common ancestry whatever the evidence or I am assumed to be ignorant, deceitful or something worse.

Sorry, just not buying into that kind of a Faustian bargain.

Indeed, that would be a much better question, and I hope you follow up on it. The focus on brain size is much too narrow. As you noted, a microcephalic human brain is still a human brain (and it is not even clear that this has serious impacts on intellect). By the same token, an enlarged chimpanzee brain with no other changes would still be a chimpanzee brain

It results in mild to sever mental retardation. We don't just have a large chimpanzee brain, the differences are extensive, measurable and inexplicable apart from a directly observed or demonstrated mechanism and random mutations are not it. It's impossible.

And the homologous gene in other species directs the spindle-formation in cell division. Sounds like a case of an older gene developing a new function. Isn't that evolution?

Sounds like a very if/then proposition to me.

Do we really know that? But what about when the human brain was first developing? Are you not committing an inductive fallacy here? What happens when one beneficial mutation is discovered? Your whole thesis is falsified. What if the difference between human ASPM and its homologues in other species was due to such a beneficial mutation?

If we were talking about an accumulation of alleles over millions of years I would not have a problem. This would have had to be accelerated evolution starting for no apparent reason 2 mya with the cranial capacity, metabolic overhaul, and the requisite skeletal reorganization fully in tact in an unprecedented time frame.

Now if a beneficial effect is discovered I'll cross that bridge when I come to it because I have yet to see single one.

That is an excellent idea. This is where a lot of new research is focussed. btw have your read Sean Carroll's Endless Forms Most Beautiful yet?

It doesn't ring a bell, sorry.

Ah, so that is where the figure came from. So, what is the problem with this?
Why do you find rapid evolution so incredible?

The human brain had neither the time nor the means, it's as simple as that.

Hominid Brain Evolution: Looks Can Be Deceiving

You know what I have a problem with and why, that's not the problem. You just think it's no problem and I have a problem with that. This does not happen in reality by any measure of rational, explicable or otherwise demonstrative evidence available and yet it must be accepted unconditionally. I simply refuse because the evidence is indicating brain related genes don't evolve like this and because the academic and scientific community has determined that making sport of my particular religious views is acceptable, encouraged and necessary. Why would I ever take their word over the testimony of Scripture when they don't accept traditional theism as even rational?

No thank you, I'm not having any of that.

 

[birdan]

Right and this goes on why the OP lies untouched. I have seen this debate tactic used too many times to take it seriously.


No I'm not, I'm talking about the known affect of mutations on the human brain and the deleterious affects are legion and affect populations in profound ways. Just because you have a disease or disorder does not mean you will not produce. Odds are that is it's a lethal mutation they won't even get out of the womb but beneficial affects from mutations in brain related genes are unknown to modern science. So how do the changes in these highly conserved genes get there in the first place?



I have answered the question repeatedly and I'm not running in circles because I know that's all that's going to happen. You guys have at least three detailed and substantive posts laying essentially untouched. That does not encourage me to spend hours preparing another that will be ignored as well.

I don't appreciate being called a liar or ignorant buddy. Not when I have made every effort to offer a detailed exposition of the relevant scientific literature. I'm not the one turning this into a flame thread, the TEs are notorious for it. That's why by and large these debates are shunned by creationists.

I've been trying to address some of the points in your posts, but don't seem to be conveying my thoughts well. So I'll try again....

No I'm not, I'm talking about the known affect of mutations on the human brain and the deleterious affects are legion and affect populations in profound ways. Just because you have a disease or disorder does not mean you will not produce. Odds are that is it's a lethal mutation they won't even get out of the womb but beneficial affects from mutations in brain related genes are unknown to modern science. So how do the changes in these highly conserved genes get there in the first place?

1. There are known variations for genes associated with brain development. In the case of ASPM and microcephalin, these have recently spread through the population rapidly enough to strongly suggest positive selection. (c.f., Bruce Lahn's research.) But the fact that there are variations of brain-related genes (i.e., mutations) shows that mutations to these genes do not have to be deleterious.

2. Frameshifting has nothing to do with the mutations you've noted for the ASPM gene. Those mutations all occurred at intron portions of the gene and thus would have no effect on the protein building. The mutations that result in microcephaly occur on the exon portions and do effect the structure of the protein.

3. If in the past an individual had a severe neural development mutation, I would say that in most cases their reproduction rate would be lower (if not zero) than the population at large, and thus would be negatively selected.

4. The increase in brain mass and/or brain functioning does not have to have been accomplished via mutations to the protein encoding DNA. It could have occurred via changes in the regulatory portions controlling neural development. If that control was changed to express neural development genes longer or stronger, the goal would be accomplished. I'm not talking about regulatory genes here (though they could also be candidates), but cis-regulatory regions controlling gene expression. To my knowledge, this is a fairly new research area and I don't know if there are any results for neural genes yet. So it may not matter much how many mutations have occurred to protein coding neural genes.


Edit: Here's a fairly detailed look at the ASPM gene across several primates:
http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pbio.0020126

And an abstract on cis-regulatory changes in human neural development (I'm not a member of AAAS):
http://www.sciencemag.org/cgi/content/abstract/314/5800/786?etoc

 

[theIdi0t]

See what I mean, there were really only two choices, I am either ignorant, mentally incapable (same thing really) or I'm a liar by omission. This is stereotypical TE and evolutionist rhetoric and it has nothing to do with science, evolution are Christian thought. It is nothing more then an attack on traditional theistic reasoning.

Mark I don't see as to why it is so difficult for you to answer the question, rather than resorting to "stereotypical TE rhetoric", if you didn't agree with the three scenarios Gluadys painted for you, why not just paint a scenario that you do agree with. When I read your initial response to Gluadys, it read as if you didn't understand Gluadys question. In may have been that I was wrong in this. Though you haven't shown that I was.

And also Gluadys didn't offer you two choices, but three. You didn't provide an answer to the question, and she provided you an option "A.) you know the answer but refuse to state it.", which doesn't imply that you are ignorant, or mentally incapable, but that you just chose to not to answer the question.

I was looking forward to hearing you actually respond to her question, and I'm saddened that you still haven't.

It's quite natural for us to have a sense of pride that won't allow us to ask an opponent (particularly those we are in strong disagreement with) for clarification, or even to educate us on a certain point, but that's not a good quality, especially for Christian, who see humility as a virtue.

 

[gluadys]

Ok, now I'm ignorant and irrelevant and I should jump through hoops for you why?

You are the one who is trying to make a point about the evolution of the human brain and common ancestry yet your posts are only about the deleterious effects of some mutations in the modern human brain which are clearly not relevant to the point you are trying to make.

It's a common practice in genetics research to have out groups.

Of course it is, but one generally tests what one believes to be a clade, not the whole standard phylogeny. Nor is it necessary to even believe in universal common ancestry. Creationists generally hold to the common ancestry of a Genesis "kind" while denying universal common ancestry.

The question relevant to the evolution of the human brain is whether or not humans and chimps are part of the same clade or separately created kinds. Neither answer requires universal common ancestry.

But theologically, if it is established that humans and chimps are part of the same clade, there is not much point in insisting that whales and hippos are not.

Now you are dismissing the cutting edge research of Pollard as irrelevant as well.

The name doesn't ring a bell. And a quick google turned up a musician, a jockey, a basketball player and a comedian, none of whom are likely the Pollard you are referring to.

That's the whole point isn't it, dispense with creation and you can dispense with traditional Christian theism entirely.

You can, but you don't have to. I certainly don't.

My theology could endure, virtually untouched, if I woke up tomorrow and decided we were just evolved apes.

Just as mine has..

The sticking point is that I am expected to assume common ancestry whatever the evidence

No, but you are expected to take all relevant evidence into account. You point to evidence that is not relevant but you never discuss evidence that is e.g. ERVs

We don't just have a large chimpanzee brain, the differences are extensive, measurable and inexplicable apart from a directly observed or demonstrated mechanism and random mutations are not it. It's impossible.

But of course you dismiss natural selection as a demonstrated mechanism. However, I would encourage you to focus on some of the other differences between human and other hominid brains. The focus on size is getting you nowhere, nor does the focus on disease.

It doesn't ring a bell, sorry.

Look it up, or if you prefer check out his original papers as I know you prefer them. The work he is doing on the evolution of embryological development, on the role of Hox genes, tool-kit genes and other regulators of development could be the mechanism you have thought missing.

The human brain had neither the time nor the means, it's as simple as that.
Hominid Brain Evolution: Looks Can Be Deceiving

I had to smile when I read this article. You state there was not time for the evolution of the human brain and refer me to a paper which suggests there may have been more time than contemporary thinking has proposed.

For example, what now of the received wisdom that cranial capacity took off in early Homo relative to australopithecines somewhere around 2 million years ago (see figure) (6, 7)? Is this true, or did cranial capacity begin its sharp increase much earlier in (some) australopithecines and simply continue in their Homo descendants?​

Bolding added.

 

[SLP]

Seems Kennedy has regurgiposted this not only here on two forums, but on a couple other forums as well, such as CARM.

Apparently he hopes/believes that if he spams enough boards with his long-ago refuted non-arguments, someone somewhere will agree with him.

He's been making the exact same error-filled claims for years, and every time he gets shot down, he just whines about how rude everyone is, and re-states the same nonsense over and over again. Oh, and he of course claims that nobody will 'debate' him.

By the way, Glad - Kennedy claims that he mopped the floor with you in your debate.

Rest assured, he is the ONLY person to come to such a bizarre conclusion.

 

[SLP]

That's a deceptive statistic, the number of know differences in vitally important genes are growing as we speak.

Really? Tell us al labout it, Mark.

No explanation for how they get there except for the mantra of random mutations plus selection. It just doesn't work that way.

Right - it works by Yahweh willing it so.

But the number of nucleotides becomes important to you when talking of indels because you want to treat indels as if they were multiple instances of SNPs and not unique mutational events in themselves.

Indels are single events, regardless of thier length.

See, no matter how the question is answered it just keeps getting asked again, and again, and again...

Ironic that YOU of all people would write that...

Yea, but beneficial affects are rarer still, if they exist at all in brain related genes.

So you keep saying, so yo never can support.

If we were talking about an accumulation of alleles over millions of years I would not have a problem. This would have had to be accelerated evolution starting for no apparent reason 2 mya with the cranial capacity, metabolic overhaul, and the requisite skeletal reorganization fully in tact in an unprecedented time frame.

Wow... are you saying that the ancestral skeleton was not "intact"?

The human brain had neither the time nor the means, it's as simple as that.

Gee - an unsupported assertion presented as show-stopping evidence for the YEC. I am SHOCKED!

Please, for once, explain WHY there was neither the time nor the means.