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#21 Bex

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Posted 08 April 2009 - 08:41 PM

Many foods contain Vitamin C for us. It is contained in a wide variety of both fruits and vegetables. Though it can be reduced or even lost by cooking/storage etc. Which is why it is wise to eat enough foods in their natural state. Unfortunately due to early picking/storage/spraying, we have a degraded food.

But that is the results also of a fallen world and fallen mankind, NOT a broken gene.

God provided from the very beginning an abundent food supply containing everything we required. I always feel that food is one of the reminders of God's gifts to us and how reliant we are upon Him for our needs. It gives us yet another way of thanking and praising Him.

#22 falcone

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Posted 09 April 2009 - 01:54 AM

...this thread is about figuring out how this could have happened if evolution is false... *snip* ...We seek a creationist understanding of this phenomena.

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Exactly right, loveslife. Our starting point here is that evolution is false and that humans, chimps, bats, pigs, guinea pigs, hamsters, rats and mice were all created by God.

Adam and Bex have suggested that the non-functioning human GULO gene is a result of the fall. Perhaps we could explore this avenue of thought?

we would expect things to be going wrong and deteriorating because of the fall

But that is the results also of a fallen world and fallen mankind, NOT a broken gene.


Not being an expert on the fall, I have lots of questions about how and why it has impacted the structure of the GULO gene. One at a time though...

Bex, you threw me a little here by saying that the GULO gene is not broken but is a result of the fall. I'm struggling to correlate that with what Adam said about things going wrong and deteriorating becasue of the fall. Do you mean that it's not broken because its non-functioning is what God intended for it? Is it the use of the word 'broken' you're not keen on?

#23 CTD

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Posted 09 April 2009 - 02:25 AM

...this thread is about figuring out how this could have happened if evolution is false... *snip* ...We seek a creationist understanding of this phenomena.

Exactly right, loveslife. Our starting point here is that evolution is false and that humans, chimps, bats, pigs, guinea pigs, hamsters, rats and mice were all created by God.

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Not quite. The starting point included evohype, and said evohype is subject to discussion, as are the assumptions that it is correct.

Most other animals have a functioning GULO gene, so they don't need vitamin C in their diets.

The interesting thing is that humans have a very similar genetic code to old world monkeys, and our GULO genes are broken in pretty much the same way. Hamsters have their GULO gene broken in a different way, and fruitbats in yet another.

New world monkeys (South America) do not have a broken GULO gene. Nor do all old world monkeys. We appear to be more distantly related to those primates with functioning GULO genes than to those with the broken gene.

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Assuming the GULO(P) to be broken in spite of the fact that it performs a function is very much evohype and very much subject to discussion here. I don't consider it a good interpretation at all to say that producing pentose phosphate is not functioning, and I don't expect too many do.

#24 Richard Townsend

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Posted 09 April 2009 - 05:45 AM

Assuming the GULO(P) to be broken in spite of the fact that it performs a function is very much evohype and very much subject to discussion here. I don't consider it a good interpretation at all to say that producing pentose phosphate is not functioning, and I don't expect too many do.

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CTD, I think you've misinterpreted the ICR article here

In 1994, a group of Japanese scientists identified a DNA sequence in humans that had many similarities to the rat gene that codes for the enzyme (L-gulono-γ-lactone) that catalyzes the last step of vitamin C synthesis (Nishikimi et al. 1994). The human pseudogene sequence discovered has four of these 12 exons. (Exons are the modular coding regions of a gene.) These four human exon sequences have many characteristics of a pseudogene. There is a 70-80% sequence homology between the rat and human sequences depending on the exon, and two stop codons. Later analysis confirmed that these four exons are present in other primates as well (Inai, Ohta, and Nishikimi 2003). Humans are missing only the final enzyme for the last step in synthesizing vitamin C, but have all of the other enzymes necessary to convert glucose into vitamin C.


The GULO gene, according to this, only catalyses the final step in vitamin C synthesis. Other enzymes catalyse the earlier steps. The author's point, later in the article, is that the rest of the process still runs and has value for the organism. But it's not saying that the GULO gene is responsible for all those other steps as well.

#25 CTD

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Posted 09 April 2009 - 05:00 PM

CTD, I think you've misinterpreted the ICR article here
The GULO gene, according to this, only catalyses the final step in vitamin C synthesis. Other enzymes catalyse the earlier steps. The author's point, later in the article, is that the rest of the process still runs and has value for the organism. But it's not saying that the GULO gene is responsible for all those other steps as well.

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I have to wonder how much attention you were paying. I don't see how the article can be honestly interpreted any other way. There is no dead end. Nothing is demonstrably broken.

There is no compelling reason why I should accept any of the assumptions the evolutionist argument requires. These are not assumptions I accept in other areas and reject as a matter of convenience. I grant that if one assumes evolution took place, etc. one could conclude something is probably wrong, depending on one's choice of selection goddess. One could alternatively posit tons of "parallel evolution" to account for the additional function found so commonly; so even an evolutionist isn't tied (as if!) to any single interpretation.

#26 falcone

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Posted 10 April 2009 - 02:14 AM

There is no dead end. Nothing is demonstrably broken.

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I've found some information that clearly explains why the GULO gene has absolutely nothing to do with pentose phosphate and is a dead end. I don't have time to post it right now, and I want to double check it in any case. I'll post it over the weekend.

In the meantime, could we get back to the OP please?

#27 scott

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Posted 10 April 2009 - 07:12 AM

I've found some information that clearly explains why the GULO gene has absolutely nothing to do with pentose phosphate and is a dead end. I don't have time to post it right now, and I want to double check it in any case. I'll post it over the weekend.

In the meantime, could we get back to the OP please?

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Sigh, just face it, you have to eat fruits to get Vitamin C, there is no broken gene, just a desire to not eat fruits.

#28 CTD

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Posted 12 April 2009 - 02:18 AM

I've found some information that clearly explains why the GULO gene has absolutely nothing to do with pentose phosphate and is a dead end. I don't have time to post it right now, and I want to double check it in any case. I'll post it over the weekend.

In the meantime, could we get back to the OP please?

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Well, it doesn't look like anyone's terribly interested in cobbling together what will surely amount to an argument from genetic "homology", I figure I'll share a little more of what I found out about this GULO(P) gene.

Found a chart
http://en.wikipedia....olism_790px.png

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or two
http://en.wikipedia....ki/File:Ppp.svg

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and a couple of wiki articles
http://en.wikipedia....osphate_pathway
http://en.wikipedia.org/wiki/Vitamin_C

Not the best sources, but we don't have to worry about accusations of creationist bias, at least. I don't intend to try to interpret the charts too much. In person, one can just point a finger at a place or two and explain. Our situation is not so convenient. Those who have the capacity will put it together if they apply themselves. Those who are gluttonous may even try to tackle the BIG chart.

I'm actually pretty content to wait & see what kind of "homology" argument comes. The most evolutionism can really hope for here is a draw, and that'd be the case if the inferred pattern(s) all held. They never do. Ad hoc nonsense always comes into play whenever "homology" is discussed; and the problem's so universal they've even named quite a few. "Convergent evolution", "parallel evolution", "co-evolution", and the rest are probably more widespread than the very similarities "homology" is supposedly based upon.

Once again, there is a barrier for the homologist, which can only be overcome at the cost of integrity. (from the second wiki article)

The vast majority of animals and plants are able to synthesize their own vitamin C, through a sequence of four enzyme-driven steps, which convert glucose to vitamin C.[6] The glucose needed to produce ascorbate in the liver (in mammals and perching birds) is extracted from glycogen; ascorbate synthesis is a glycogenolysis-dependent process.[13] In reptiles and birds the biosynthesis is carried out in the kidneys.


Perching birds should be more closely related in all things to other birds, if their designer hadn't decided otherwise. The evolutionists'd be crowing if it were the case, would they not? Boasting of the "successful prediction". But perhaps I assume too much. Perhaps our evolutionist posters will be man enough to look squarely at the evidence and admit to themselves that the pattern is broken; and in real science one cannot claim that both the following of the pattern and the breaking of the pattern conform.

Seriously, I could claim it rains in my hometown every day of my life if that were the case. Breaking the pattern doesn't matter, does it? So what if it's dry? It's still raining every day. Oh? Would it be better if I came up with an "impressive" name for the breaks in my pattern? Would I fool you if I got some PhD's in on it? TV? Textbooks? Clergy? What would it take? Maybe all of your friends? How about threatening you job? How about if believing this bunk let you believe what you want about God? Will any of those things help? Depends on the individual...

#29 falcone

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Posted 12 April 2009 - 02:52 AM

I don't intend to try to interpret the charts too much.

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That's a shame. I've no idea what point you're trying to make with them

#30 falcone

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Posted 28 April 2009 - 03:46 AM

Attached File  pentosephosphate3aa.jpg   118.76KB   21 downloads
This is quite a useful diagram in explaining why the GULO gene is irrelevant to the Pentose Phosphate Pathway (PPP). Here's how I understand it:

The GULO gene is part of the Glucoronic Acid Pathway (GAP), and while there are is a link between the GAP and the PPP, GULO isn't part of it. See point 2 below.

1. At this point in the GAP, Glucuronides, Proteoglycans , and Glycosaminoglycans are produced. All of these have an important function, and this looks to me like the main job of the GAP, at least in animals with nonfunctional GULO genes.
2. Glucoronic acid is converted to xylulose-5-phosphate (X-5-P) and 'feeds' into the PPP. However, this feeding process normally isn't necessary since the PPP creates its own X-5-P from ribulose-5-phosphate (R-5-P). If there is a defect in the PPP and X-5-P can't be made, then the X-5-P generated by conversion of glucuronic acid can substitute.
3. The remaining steps in the GAP are only there to produce vitamin C. There is no 'feeding' or 'lnking' to any other pathway from this point on. So, a nonfunctioning GULO gene renders these remaing steps useless for us, fruitbats, guinea pigs and so on. It's a dead end.

I suspect it's unlikely that the GAP and nonfunctional GULO gene are the result of deliberate design because that would make it either a mistake or bad design. There has been extensive research into the GULO gene and to argue that it has some other as yet unknown function is unsupported speculation.

So as as already been suggested, this must be a result of the Fall. But how? What processes were/are at work to reach this state of affairs?

#31 falcone

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Posted 15 May 2009 - 07:51 AM

I was disappointed that this thread went quiet, so thought I'd bump it up again.

I don't intend to argue that the GAP and in particular the GULO gene evolved, rather I'd like to hear an alternative explanation as to how it came to be.

It had been suggested that the "broken" GULO gene is a result of the Fall, so I'm interested in pursuing this line of discussion. Adam previously said that after the Fall things started to go wrong and deteriorate. In what way? What directs this deterioration?

It makes no sense to think that the GAP was deliberately designed in it's current form. What Fall processes were/are at work and how can these be used to demonstrate the current structure of the GAP / GULO gene?

#32 Adam Nagy

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Posted 15 May 2009 - 08:33 AM

I was disappointed that this thread went quiet, so thought I'd bump it up again.

I don't intend to argue that the GAP and in particular the GULO gene evolved, rather I'd like to hear an alternative explanation as to how it came to be.

It had been suggested that the "broken" GULO gene is a result of the Fall, so I'm interested in pursuing this line of discussion. Adam previously said that after the Fall things started to go wrong and deteriorate. In what way? What directs this deterioration?

It makes no sense to think that the GAP was deliberately designed in it's current form. What Fall processes were/are at work and how can these be used to demonstrate the current structure of the GAP / GULO gene?

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You do understand that this is all highly speculative in the first place, right? It's a guessing game either way. I wouldn't be surprised to detect biological effects from the fall and flood but it's all speculation.

Something I've been thinking through is how animals became carnivorous after the fall and primarily after the flood. I believe diets were severely altered both at the removal of Gods perfect light and the altered state of the planet after the flood. We can demonstrate the change by looking at the fossil record and how much more robust plant life seemed to be before the flood and animals and even insects were more robust before the flood.

I have a hypothesis that certain vegetation couldn't survive in the post flood environment. The vegetation that was more hearty was also less nutritious. If you think about it this applies well to what we see today. The more robust and useful fruits and vegetables grow in tropical climates and the more hearty but less nutritious plants grow in temperate climates. I believe the shift in the quality of vegetation also caused a shift in diet. The most resilient and well suited animals remained vegetarians, being able to consume and use the degraded quality of plant life, while animals that thrived on plants that existed pre-flood, but existed no more, where driven to eat other animals for those life sustaining nutrients. I believe this is why God told Noah and his family to eat meat, not because God enjoyed watching man eat his beautiful creatures. It was because the new environment put our physical needs in a position where we were going to be healthiest with a diet of both meat and vegetation.

So to postulate that we could see some genetic blip because our environment has changed both post fall and post flood is perfectly reasonable to me. It's still speculative so I don't think we could nail any conclusions down with certainty regarding how much past events effected present gene expressions.

#33 jason777

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Posted 15 May 2009 - 08:39 AM

I was disappointed that this thread went quiet, so thought I'd bump it up again.

I don't intend to argue that the GAP and in particular the GULO gene evolved, rather I'd like to hear an alternative explanation as to how it came to be.

It had been suggested that the "broken" GULO gene is a result of the Fall, so I'm interested in pursuing this line of discussion. Adam previously said that after the Fall things started to go wrong and deteriorate. In what way? What directs this deterioration?

It makes no sense to think that the GAP was deliberately designed in it's current form. What Fall processes were/are at work and how can these be used to demonstrate the current structure of the GAP / GULO gene?

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Genetic mutation.

Do you know of any mutation that fixes anything?

I don't know of any mechanic that works on car with a hammer.But if your an evolutionists,then i guess thats what your stuck with.



Thanks.

#34 Adam Nagy

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Posted 15 May 2009 - 08:46 AM

I don't know of any mechanic that works on car with a hammer.But if your an evolutionists,then i guess thats what your stuck with.
Thanks.

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The evolution mechanic pounds the car with a hammer hoping to manipulate the hammer into the form of a wrench. :) Anything is possible... :D

#35 falcone

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Posted 15 May 2009 - 08:47 AM

Genetic mutation.

I agree. Was the genetic mutation of the GULO gene intelligently directed?

#36 jason777

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Posted 15 May 2009 - 08:51 AM

I agree. Was the genetic mutation of the GULO gene intelligently directed?

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I was speeking "tongue in cheek",falcone.

Honestly,i have no idea.

#37 Guest_Keith C_*

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Posted 17 May 2009 - 09:38 AM

That was quick - pigs share the trait also.

Not quite.
Some pigs, because they carry 2 copies of a mutated GULO gene, can not make vitamin C.
[URL]http://www.ncbi.nlm....pubmed/15112110[URL]
"Clinical cases of scurvy were described in a family of Danish pigs. This trait is controlled by a single autosomal recessive allele designated od (osteogenic disorder). Here we demonstrate that the absence of GULO activity and the associated vitamin C deficiency in od/od pigs is due to the occurrence of a 4.2-kbp deletion in the GULO gene. "
Normal pigs have at least one functional gene for this step.

What you have found is probably another case of evolution in action. Some domesticated pigs, fed scraps of human food, may have less need to make vitamin C than their wild ancestors.

#38 scott

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Posted 17 May 2009 - 04:40 PM

The Gulo gene proves absolutely nothing. It is what it is. Nothing more, and nothing less. End of discussion.

#39 Ron

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Posted 17 May 2009 - 05:47 PM

Not quite.
Some pigs, because they carry 2 copies of a mutated GULO gene, can not make vitamin C. 
[URL]http://www.ncbi.nlm....pubmed/15112110[URL]
"Clinical cases of scurvy were described in a family of Danish pigs. This trait is controlled by a single autosomal recessive allele designated od (osteogenic disorder). Here we demonstrate that the absence of GULO activity and the associated vitamin C deficiency in od/od pigs is due to the occurrence of a 4.2-kbp deletion in the GULO gene. "
Normal pigs have at least one functional gene for this step.

What you have found is probably another case of evolution in action.  Some domesticated pigs, fed scraps of human food, may have less need to make vitamin C than their wild ancestors.

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So the gene is still a gene right? I mean, it didn’t evolve into a pig or anything, isn’t that correct?

By the way, there's something wrong with your link.

#40 Guest_Keith C_*

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Posted 17 May 2009 - 06:40 PM

So the gene is still a gene right? I mean, it didn’t evolve into a pig or anything, isn’t that correct?

By the way, there's something wrong with your link.

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This should work better. Sorry
http://www.ncbi.nlm....pubmed/15112110

My point was that the GULO gene in pigs has not mutated.
Some pigs do have a GULO mutation which prevents vitamin C synthesis when two copies are present.
Incidentally, this mutation is different from the mutations in the human pseudogene.




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