Is the Human Brain the Null Hypothesis for Darwin's Theory?

mark kennedy · #21 20th July 2008, 12:02 PM

Originally Posted by Mallon

You keep accusing me of rhetorically asking you questions that you have already answered in the OP, but reading over this thread, I just don't see it, mark.

It's in the title of the thread Mallon. You never answered the question and then no matter how many times I answer yours you just going to ask it again. The problem with TEs is they use cookie cutter tactics. That means I have seen it a hundred times and I am not running in circles because you are feigning a fellowship post.

I've asked questions in earnest, and in each of your replies you've called me an "artful dodger", you've accused me of not being serious, you've
accused me of being dishonest and of subscribing to "modernist philosophy" (whatever that means). At this point, it's probably best that I drop out of this thread lest things become even more belligerent.

I called you the artful dodger because you circumvented the question in the title, not even the opening post but the title asks a direct question. Then you will ask the same question again and again pretending you didn't get an answer. It's not the creationist that bears the burden of proof, it's the evolutionists since they have dominated academics and natural science for 150 years. They didn't stop there, Liberal Theology has supplanted traditional Christian theism and theology with a philosophy that is essentially deist.

You want to know why I don't think it's possible for an organ as complex and highly conserved as the human brain to evolve from that of apes? Ok, here are the known effects of mutations on brain related genes.

renal cystic diseases
Colorectal carcinoma
Alzheimer's
Lissencephaly and microcephaly

Pick a chromosome, any chromosome and you will find diseases and disorders that are the direct effects of mutations on the human brain.

Landmark Poster

Edited to add:

This is the null hypothesis, how would you test it?

Darwin already indicated how this 'testable' null hypothesis would work.

1. An organ that could not have been formed by, 'numerous, successive, slight modifications.'
2. There has been little or no extinction.
3. Look to an organ common to all the members of a large class.
4. Discover the early transitional grades through which the organ has (or would have had to, emphasis mine) passed

Kyrisch · #22 20th July 2008, 10:00 PM

I can point to just as many deleterious mutations that cause skin disorders too, but it still wouldn't disprove the fact that the differences in skin colour in humans arise from different environments, not because God used different colour clay.

I don't think you understand that the only difference between our brains and the presumed brains of our common primate ancestor (assuming it's modeled after a chimps) is that our cerebral cortex has expanded. Like I said before, it's really not that hard to make something bigger; allow it to grow for a longer period of time and there it is. It really isn't a problem. All the intricacies have already been worked out. The lower brain's sections are physical, but they existed already. The upper brain's sections are purely emergent.

mark kennedy · #23 21st July 2008, 08:01 PM

Originally Posted by Kyrisch

I can point to just as many deleterious mutations that cause skin disorders too, but it still wouldn't disprove the fact that the differences in skin colour in humans arise from different environments, not because God used different colour clay.

Agreed:

During the last two decades the molecular basis of over 2000 inherited single gene disorders has been determined. More than 25% of these have a skin phenotype, making the inherited skin disorders one of the best characterized groups of genetic diseases. Advances in understanding the genetic basis of inherited single gene skin barrier disorders

But consider:

“By altering expression of this gene in one particular place in the body, the fish can fine tune the level of expression of that factor in some tissues but not others,” said Kingsley. “That lets evolution produce a big local effect on a trait like color while preserving the other functions of the gene.” Same Genetic Machinery Generates Skin Color Evolution in Fish and Humans

It takes regulatory genes with no massive overhauls of genes to accomplish skin pigmentation.

I don't think you understand that the only difference between our brains and the presumed brains of our common primate ancestor (assuming it's modeled after a chimps) is that our cerebral cortex has expanded. Like I said before, it's really not that hard to make something bigger; allow it to grow for a longer period of time and there it is. It really isn't a problem. All the intricacies have already been worked out. The lower brain's sections are physical, but they existed already. The upper brain's sections are purely emergent.

Emergent by what molecular mechanism? We are not talking about adding modules on, we are talking about a three fold expansion involving highly conserved genes. On regulatory gene in particular would not have allowed more then 2 substitutions in over 300 million years and then make weak to strong substitutions allowing 18. We are not talking about a rise in gene expression like we are when talking about skin pigmentation, we are talking about an evolutionary giant leap.

Kyrisch · #24 22nd July 2008, 12:35 AM

Emergent, as in non-physical. The sections just aren't there; the tissue of the cerebrum is largely homogenous. The apparent sections emerge because of where the sensory input is processed (which is worked out, already, too), and other environmental factors. In fact, it would be more fitting to describe it as specialisation as opposed to emergence.

birdan · #25 23rd July 2008, 08:39 AM

Originally Posted by mark kennedy

You say that despite the fact that it would require 18 substitutions in a regulatory gene that has only allowed 2 since the Cambrian. You say that despite the fact that the only effect of mutations on the ASPM gene is a reduced cranial capacity and it would have required ten insertions/deletions equal to or longer than 50 bp, all of them located within introns. All that despite the fact that there is not a single example of a beneficial effect from a mutation in a brain related gene known to modern science.

This will be my only post in this forum, and it is just to make a factual correction. There are variations in the ASPM gene (and other brain-associated genes) in the human population which are not deleterious. That is, people with physiologically and functionally normal brains have variations of these genes. I suggest you google 'Bruce Lahn' for his research on variations of the ASPM gene within the 'normal' human population. You can also google for the PDYN gene and the microcephalin gene for variations that are not deleterious.

So, the part of your argument that I bolded above is not factually correct.

busterdog · #26 23rd July 2008, 10:24 AM

Originally Posted by birdan

This will be my only post in this forum, and it is just to make a factual correction. There are variations in the ASPM gene (and other brain-associated genes) in the human population which are not deleterious. That is, people with physiologically and functionally normal brains have variations of these genes. I suggest you google 'Bruce Lahn' for his research on variations of the ASPM gene within the 'normal' human population. You can also google for the PDYN gene and the microcephalin gene for variations that are not deleterious.

So, the part of your argument that I bolded above is not factually correct.

Why should he assume that all genetic variations represent "mutations?"

How do we know that any of these expressions were not found in Adam OR Eve or the sons of Noah or their wives? I am not sure how many genes you are talking about.

By way of analogy, you can get a camry with four cyl. or six. In the factory of meiosis, things are created that are not "mutations", but are a different options packages.

How do we know that the information that is optional did not reside in our ancestors and is not carried? That is a question, not a rhetorical question, since I don't know the answer.

And Mark, what is the latest on where such information would be stored. One thing that research seems to show is that our simplistic notion of what the genetic code is seems to have a less defined boundary that was taught 20 years ago. Does the fact that you don't see the information in the strands of the 46 base pairs mean that the information isn't otherwise there? Remember that geneticists must rely upon notions like "self organizing", which implies that the information is present somewhere that we have no idea about.

birdan · #27 23rd July 2008, 11:39 PM

Originally Posted by busterdog

Why should he assume that all genetic variations represent "mutations?"

How do we know that any of these expressions were not found in Adam OR Eve or the sons of Noah or their wives? I am not sure how many genes you are talking about.

By way of analogy, you can get a camry with four cyl. or six. In the factory of meiosis, things are created that are not "mutations", but are a different options packages.

How do we know that the information that is optional did not reside in our ancestors and is not carried? That is a question, not a rhetorical question, since I don't know the answer.

And Mark, what is the latest on where such information would be stored. One thing that research seems to show is that our simplistic notion of what the genetic code is seems to have a less defined boundary that was taught 20 years ago. Does the fact that you don't see the information in the strands of the 46 base pairs mean that the information isn't otherwise there? Remember that geneticists must rely upon notions like "self organizing", which implies that the information is present somewhere that we have no idea about.

OK, since you asked so nice I'll venture a second post here. I was adressing MK's contention that there are no 'healthy' variations of the ASPM gene. And since we're talking about a specific sequence of base pairs on chromosome 1, it doesn't matter what other nucleic components come into play.

While I'm here ..... Mark, here's a thought. We know that a baby can be born with microcephaly from two normal parents. This is caused by a mutation to the ASPM gene and results in a decrease of brain size by up to 70%, or a 1 lb brain instead of a normal 3 lb brain. One mutation, one generation, 70% change in brain size.

So here's a 'thought experiment' - assume the mutated ASPM gene that causes microcephaly was the 'normal' ASPM gene several million years ago. Then a single mutation (the reverse of the mutation that causes microcephaly), in a single generation, would increase brain size by up 2 lbs. You do understand that genes today that are 'normal' were at one time variants? If the variant produced a selective advantage it became fixed and thus became the 'normal' version?

Anyway, there's that 'molecular mechanism' that you've been asking for that can produce a 70% increase in brain size in a single generation. I'm not saying that this actually happened, which is why I call it a 'thought experiment'. But given that an ASPM -> ASPM' mutation currently produces a 70% reduction in brain size, why couldn't it be possible that in the distant past there was an ASPM' -> ASPM mutation that produced a 300% increase in brain size?

shernren · #28 25th July 2008, 02:46 AM

Here's a brief mathematical quibble: the proper meaning of the term "null hypothesis" as used in statistics has absolutely nothing to do with what mark is trying to argue. Having said that, I doubt anybody here actually cares what a real null hypothesis is, so I shall save my pedantry for some other time.

Just tagging so that I can keep up with what happens in this thread. ^^

mark kennedy · #29 25th July 2008, 09:09 AM

Originally Posted by Kyrisch

Emergent, as in non-physical. The sections just aren't there; the tissue of the cerebrum is largely homogenous. The apparent sections emerge because of where the sensory input is processed (which is worked out, already, too), and other environmental factors. In fact, it would be more fitting to describe it as specialisation as opposed to emergence.

Skulls are there, in fact there are an abundance of them. Just one problem though, we don't have chimpanzee ancestors to compare our to. You can know a lot about the brain by looking at the skull. We do have the soft parts, they are in your head, we have what our ancestors brains would have looked like, it would look almost exactly like a Chimpanzee brain. We know what would have been involved on a molecular level and I think it's wrong to pretend that special creation in not a possibility or that genes are as mutable as they would have had to be.

mark kennedy · #30 25th July 2008, 09:23 AM

Originally Posted by shernren

Here's a brief mathematical quibble: the proper meaning of the term "null hypothesis" as used in statistics has absolutely nothing to do with what mark is trying to argue. Having said that, I doubt anybody here actually cares what a real null hypothesis is, so I shall save my pedantry for some other time.

Just tagging so that I can keep up with what happens in this thread. ^^

Playing with the semantics again I see. One of the things that were not expected is the divergence being as high as it is. The obvious reason is the pleiotropy of mutations:

One critical parameter that affects the relative contribution of different genetic mechanisms to anatomical variation is the pleiotropy of mutations. In general, it is expected that mutations with greater pleiotropic effects will have more deleterious effects on organismal fitness and will be a less common source of variation in form than mutations with less widespread effects.Evolution at Two Levels: On Genes and Form