Four questions for YECs - (and a little history of creationism vs evolution)

[Retrobyter]

On 8/4/2023 at 8:20 AM, The Barbarian said:

And you were going to show us one of those "Achilles' Heels" from your guy's book so we could take a look and see if he's right.    Which one do you want to have us look at?

 

Shalom, The Barbarian.

Yes, I've been preparing one that I think will be right up your alley: Genetics. Chapter 2 of the book is entitled "Genetics and DNA," and it is from 18% to 29% of the book (Kindle edition), with the last 3% used for the 73 endnotes.  But, if I give this to you and you want to test it more, please read the book. In it, they provide all the references that one might need to confirm what is said.

First, we find Dr. Robert W. Carter Ph. D. Marine Biology, saying...

DNA fragility is one of many Achilles’ heels of evolutionary genetics, but it is an important one. In order for DNA to be useful, it needs a huge complement of repair enzymes to maintain it. There are many different ways DNA can be damaged and there are specific enzyme complexes that deal with each type of damage, but what is even more challenging to the evolutionary model is that those enzymes are also coded in the DNA, yet DNA cannot be sustained in the cell without them. This is a chicken-and-egg problem par excellence! These enzymes are also sensitive to changes. Mutations in the DNA repair and copying enzymes are often catastrophic. How, then, did they originate through the process of mutation and natural selection over time? Without them, life cannot exist, yet life had to originate without them and had to start using DNA to store information before the DNA toolkit evolved.

Evolution's Achilles' Heels . Kindle Edition. 

Dr. Carter also said,

The order of the nucleotides on the DNA molecule has all the characteristics of a message, laden with information. A message may be passed on, but in the real world, there can be no message without a message sender. The ultimate puzzle of life is not the complexity of the molecules upon which life depends (although this is a huge puzzle). It is not the complex arrangement of the parts living organisms use (although this is another huge puzzle). No, the ultimate puzzle of life is THE ORIGIN OF THE INFORMATION upon which life is based.

Evolution's Achilles' Heels . Kindle Edition. (emphasis mine)

I believe you've already said that you do not believe in 'junk' DNA, and that's good, for according to Dr. Carter, the term was coined by S. Ohno, in Brookhaven Symposia in Biology, no. 23 (Smith, H. H., ed.), pp 366-370, in 1972. And, the complexity of the genetic code since the Human Genome Project has been discovering more and more uses for the once-thought-to-be "junk."

But, he also said that one might still hear, though, a statement made like, “Only 2 to 3 percent of the human genome is functional. The rest is worthless, junk DNA—garbage left over from our evolutionary heritage.”

Evolution's Achilles' Heels . Kindle Edition. 

Then, he went on into a short history of Haldane's Dilemma back in the 1950s when Haldane showed that natural selection cannot possibly select for millions of beneficial mutations, even over the course of human evolutionary history. Instead, and despite several simplifying assumptions in favor of evolutionary theory, only a few hundred beneficial mutations could have been selected since our common ancestor with chimps. (Haldane, J.B.S., The cost of natural selection, Journal of Genetics 55:511-524, 1957.) And, then Dr. Carter said,

Haldane’s Dilemma was never solved. What happened instead was A FIGMENT OF EVOLUTIONARY IMAGINATION. In the late 1960s, Kimura developed the idea of neutral evolution. He reasoned that, if most of the DNA in a cell were non-functional, it would be free to mutate over time. Thus, there would be no cost to the organism to maintain the non-functional portions (‘cost’ is measured in terms of how many extra babies must be born in the population for natural selection to kill in order to eliminate the bad mutations and maintain fitness over time, given the assumption that natural selection can see the bad mutations it needs to eliminate, of course).

Evolution's Achilles' Heels . Kindle Edition. (emphasis mine)

I'll just mention this complexity here at the end as something else with which evolutionists must come to terms. After Carter explained the simple linear first dimension of the DNA chain to align "genes" with the proteins that they can make. Then, he went on...

We just learned about alternate splicing. Here, one part of the genome affects another part, either directly or through RNA and/or protein proxies. This is part of the second dimension of the genome. In order to draw these interactions, one would need to write out the genome and draw lots and lots of arrow from one place to another. To do this, you would need many sheets of paper, which have two dimensions (height and width). The second dimension of the genome is extremely complex and includes specificity factors, enhancers, repressors, activators, transcription factors, histone acetylization signals, DNA methylation signals, post-transciptional regulation of RNA, alternate splicing, and many other things. It plays a major role in the tight coordination and regulation of the vast network of events that occur both in the nucleus and throughout the cell. In this dimension, the order is not significantly important, for gene regulators have to float around in order to find their targets anyway. Having the target immediately next to the regulator is not necessary. It is at the next level that things get very interesting.

The third dimension of the genome is the 3-D structure of the DNA in the nucleus. At this level, genes are not randomly distributed in the nucleus, but are ordered and clustered according to need. Genes that are used together in series may not be found next to each other on the chromosomes, but when the chromosomes fold, they are often found next to each other in 3-D space, and are also often clustered near a nuclear pore or close to a center of transcription. Thus, something is holding them in place. Since the DNA is equivalent to a huge bundle of string, the parts of that bundle that are buried are difficult to access while other parts are exposed on the outside or in internal pockets.36,37 Part of the code imbedded within the first dimension affects the 3-D folding of the DNA, which, in turn, affects gene expression patterns. This third dimension is extremely important. 

The fourth dimension of the genome involves changes to the first, second, and third dimensions over time. The chromosomes are in a particular shape in the nucleus, but that shape changes during development because different cell types need different complements of genes and other genetic instructions. The shape can change in the short term as cells respond to stimuli and unwrap portions of DNA in order to get at buried genes, only to re-wrap that section when the gene is no longer needed.

Evolution's Achilles' Heels . Kindle Edition. 

This is just a short introduction to the complexity within the genetic structure they've found ... SO FAR!

That's just a START of the Achilles' Heels found in evolution.

[The Barbarian]

2 hours ago, Retrobyter said:

First, we find Dr. Robert W. Carter Ph. D. Marine Biology, saying...

DNA fragility is one of many Achilles’ heels of evolutionary genetics, but it is an important one. In order for DNA to be useful, it needs a huge complement of repair enzymes to maintain it. There are many different ways DNA can be damaged and there are specific enzyme complexes that deal with each type of damage, but what is even more challenging to the evolutionary model is that those enzymes are also coded in the DNA, yet DNA cannot be sustained in the cell without them. This is a chicken-and-egg problem par excellence! These enzymes are also sensitive to changes. Mutations in the DNA repair and copying enzymes are often catastrophic. How, then, did they originate through the process of mutation and natural selection over time? Without them, life cannot exist, yet life had to originate without them and had to start using DNA to store information before the DNA toolkit evolved.

Evolution's Achilles' Heels . Kindle Edition. 

Dr. Robert is simply confused about what evolutionary theory is.   Evolutionary theory is not about how life started.   It's about how living populations change over time.   If God had magically poofed the first living things into existence (Darwin, for example thought that God just created the first living things) evolution would work exactly as we see it working today.  

A clue about this is the fact that prokaryotes have simpler repair systems:

DNA Damage Responses in Prokaryotes: Regulating Gene Expression, Modulating Growth Patterns, and Manipulating Replication Forks

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3809575/

No doubt earlier forms of life had even simpler processes.   But not a concern for evolutionary theory at all.

Let's go on...

2 hours ago, Retrobyter said:

Then, he went on into a short history of Haldane's Dilemma back in the 1950s when Haldane showed that natural selection cannot possibly select for millions of beneficial mutations, even over the course of human evolutionary history.

Well, that wasn't Haldane's conclusion...

Journal of Genetics

Published: December 1957

The cost of natural selection

J. B. S. Haldane 

Unless selection is very intense, the number of deaths needed to secure the substitution, by natural selection, of one gene for another at a locus, is independent of the intensity of selection. It is often about 30 times the number of organisms in a generation. It is suggested that, in horotelic evolution, the mean time taken for each gene substitution is . about 300 generations. This accords with the observed slowness of evolution.

In fact Haldane is talking about the time it would take for one gene to completely replace another at a given gene locus.    Which is not how most evolution proceeds.    But even if it did, Haldane notes that it works about as fast as evolution proceeds in the fossil record.

2 hours ago, Retrobyter said:

Haldane’s Dilemma was never solved. What happened instead was A FIGMENT OF EVOLUTIONARY IMAGINATION. In the late 1960s, Kimura developed the idea of neutral evolution. He reasoned that, if most of the DNA in a cell were non-functional, it would be free to mutate over time.

That's a fact, but here's what really throws a wrench into Dr. Rob's claims:

A radical form of genetic novelty

The emergence of new genes from non-coding DNA is common across eukaryotes — how they contribute to adaptive evolutionary novelties is fascinating.

https://www.nature.com/articles/s41559-017-0180.pdf

Before this, new genes were assumed to have developed by gene duplication, followed by mutation.   And they often do.  But it turns out that a large number of genes have come about by mutation of non-coding DNA.   Dr. Rob seems unaware of these findings.

And there's this:
Nature volume 221, pages 815–816 (1969)

“Haldane's Dilemma” and the Rate of Natural Selection

Abstract

The conclusion that most new genes must be more or less without selective effect can be supported in the face of recent criticism.

 

3 hours ago, Retrobyter said:

We just learned about alternate splicing. Here, one part of the genome affects another part, either directly or through RNA and/or protein proxies. This is part of the second dimension of the genome.

This is well-known to geneticists.  It's called "epistasis."   And it's a major driver in evolution...

Types of Epistasis

There are six common types of epistasis gene interactions: dominant, dominant inhibitory, duplicate dominant, duplicate recessive, polymeric gene interaction, and recessive. When a dominant allele masks the expression of both dominant and recessive alleles at another locus, it is referred to as dominant epistasis or simple epistasis. When it is a recessive allele that masks the expression, it is called recessive epistasis. Some genes can also mask other genes by suppression. This is referred to as dominant inhibitory or suppression epistasis because the gene is acting as a suppressor, or a factor that prevents the expression of another allele.

Duplicate types of epistasis depend on two loci. When there is a dominant allele masking the expression of recessive alleles at two loci, this is known as duplicate dominant epistasis or duplicate gene action. When there is a recessive allele masking the expression of dominant alleles at two loci, this is known as duplicate recessive epistasis. It is also known as complementary gene action because both genes are required in order for the correct phenotype to be present.

Polymeric gene interaction is the combination of two dominant alleles that intensifies the phenotype or creates a median variation. Alone, each dominant allele produces a physical trait different from the combined dominant alleles. Therefore, this creates three phenotypes for only two dominant alleles. This shows that neither dominant allele is prevailing over the other dominant allele.

Examples of Epistasis

The plant Primula produces a chemical called malvidin. Synthesis of the chemical is influenced by the K gene, while suppression of synthesis is controlled by the D gene. Both are considered to be dominant traits. If a dominant D allele is present, there will be no expression regardless of whether there is a dominant K allele present. This interaction between alleles is then classified as dominant inhibitory epistasis, since the dominant D allele is inhibiting the K allele.

Summer squash can have three different colors: white, yellow, and green. The white color is determined by the dominant gene W, yellow by the dominant gene G, and green by the recessive genes w and g. The white color is dominant over yellow and green. Since the white is dominant, it is called epistatic to the dominant and recessive G/g alleles. This interaction is then classified as simple or dominant epistasis.

https://biologydictionary.net/epistasis/

Your guy seems a little behind on what's going on in genetics.

3 hours ago, Retrobyter said:

That's just a START of the Achilles' Heels found in evolution.

So far, nothing.   Just misunderstandings of what evolution, new genes, and epistasis are about.

[The Barbarian]

On 8/9/2023 at 3:48 PM, SavedOnebyGrace said:

As an OEC, I wrote a topic some time ago that Noah's Flood was a large local flood, not a global flood. This view agreed with the Bible and the Science of the natural world, e.g. Geology. To make it a global flood, you would have to add a number of additional miracles to the biblical text. There are knowledgeable Christians and Theologians who share this view which explains the copious amount of flood stories worldwide.

It appears that there was a great regional flood in the Middle East, just about the right time, when the Mediterranean Sea broke through and created the Black Sea.  

 

[Retrobyter]

17 minutes ago, The Barbarian said:

Dr. Robert is simply confused about what evolutionary theory is.   Evolutionary theory is not about how life started.   It's about how living populations change over time. 

Shabbat shalom, The Barbarian.

Well, you're very good about denial, but you're not so good at keeping on track. I'm not talking about the Special Theory of Evolution (STE); I'm talking about the GENERAL Theory of Evolution (GTE). GTE IS talking about how life started.

17 minutes ago, The Barbarian said:

If God had magically poofed the first living things into existence (Darwin, for example thought that God just created the first living things) evolution would work exactly as we see it working today.  

And, again, you've switched to STE.

17 minutes ago, The Barbarian said:

A clue about this is the fact that prokaryotes have simpler repair systems:

DNA Damage Responses in Prokaryotes: Regulating Gene Expression, Modulating Growth Patterns, and Manipulating Replication Forks

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3809575/

No doubt earlier forms of life had even simpler processes.   But not a concern for evolutionary theory at all.

Well, that's all interesting, but again, you're missing the point. How did the prokaryotes even get started?! It doesn't matter that they have "simpler repair systems." The fact still remains that they need repair systems, TOO, as well as the code for replication! It's like bees and the flowers that they frequent. If each needs the other, how did the system even get its start?

17 minutes ago, The Barbarian said:

Let's go on...

Well, that wasn't Haldane's conclusion...

Journal of Genetics

Published: December 1957

The cost of natural selection

J. B. S. Haldane 

Unless selection is very intense, the number of deaths needed to secure the substitution, by natural selection, of one gene for another at a locus, is independent of the intensity of selection. It is often about 30 times the number of organisms in a generation. It is suggested that, in horotelic evolution, the mean time taken for each gene substitution is . about 300 generations. This accords with the observed slowness of evolution.

In fact Haldane is talking about the time it would take for one gene to completely replace another at a given gene locus.    Which is not how most evolution proceeds.    But even if it did, Haldane notes that it works about as fast as evolution proceeds in the fossil record.

That's a fact, but here's what really throws a wrench into Dr. Rob's claims:

A radical form of genetic novelty

The emergence of new genes from non-coding DNA is common across eukaryotes — how they contribute to adaptive evolutionary novelties is fascinating.

https://www.nature.com/articles/s41559-017-0180.pdf

Before this, new genes were assumed to have developed by gene duplication, followed by mutation.   And they often do.  But it turns out that a large number of genes have come about by mutation of non-coding DNA.   Dr. Rob seems unaware of these findings.

READ THE BOOK! Or, just stop talking. Perhaps, I didn't communicate it well enough for your needs, but you should really "hear" it from him, rather than relying on me to give a "summary" of what he said! Turns out he DID talk about these findings.

17 minutes ago, The Barbarian said:

And there's this:
Nature volume 221, pages 815–816 (1969)

“Haldane's Dilemma” and the Rate of Natural Selection

Abstract

The conclusion that most new genes must be more or less without selective effect can be supported in the face of recent criticism.

This is well-known to geneticists.  It's called "epistasis."   And it's a major driver in evolution...

Types of Epistasis

There are six common types of epistasis gene interactions: dominant, dominant inhibitory, duplicate dominant, duplicate recessive, polymeric gene interaction, and recessive. When a dominant allele masks the expression of both dominant and recessive alleles at another locus, it is referred to as dominant epistasis or simple epistasis. When it is a recessive allele that masks the expression, it is called recessive epistasis. Some genes can also mask other genes by suppression. This is referred to as dominant inhibitory or suppression epistasis because the gene is acting as a suppressor, or a factor that prevents the expression of another allele.

Duplicate types of epistasis depend on two loci. When there is a dominant allele masking the expression of recessive alleles at two loci, this is known as duplicate dominant epistasis or duplicate gene action. When there is a recessive allele masking the expression of dominant alleles at two loci, this is known as duplicate recessive epistasis. It is also known as complementary gene action because both genes are required in order for the correct phenotype to be present.

Polymeric gene interaction is the combination of two dominant alleles that intensifies the phenotype or creates a median variation. Alone, each dominant allele produces a physical trait different from the combined dominant alleles. Therefore, this creates three phenotypes for only two dominant alleles. This shows that neither dominant allele is prevailing over the other dominant allele.

Examples of Epistasis

The plant Primula produces a chemical called malvidin. Synthesis of the chemical is influenced by the K gene, while suppression of synthesis is controlled by the D gene. Both are considered to be dominant traits. If a dominant D allele is present, there will be no expression regardless of whether there is a dominant K allele present. This interaction between alleles is then classified as dominant inhibitory epistasis, since the dominant D allele is inhibiting the K allele.

Summer squash can have three different colors: white, yellow, and green. The white color is determined by the dominant gene W, yellow by the dominant gene G, and green by the recessive genes w and g. The white color is dominant over yellow and green. Since the white is dominant, it is called epistatic to the dominant and recessive G/g alleles. This interaction is then classified as simple or dominant epistasis.

https://biologydictionary.net/epistasis/

Your guy seems a little behind on what's going on in genetics.

So far, nothing.   Just misunderstandings of what evolution, new genes, and epistasis are about.

Brush-offs and disrespecting the writer. Nothing new here.

[The Barbarian]

21 hours ago, Retrobyter said:

Well, you're very good about denial, but you're not so good at keeping on track. I'm not talking about the Special Theory of Evolution (STE); I'm talking about the GENERAL Theory of Evolution (GTE). GTE IS talking about how life started.

Sorry, no such animal.   That's just a fairy tale made up by creationists.     There is a theory of stellar evolution, and a theory of biological evolution, but what you're talking about is the theory of abiogenesis.    

21 hours ago, Retrobyter said:

Well, that's all interesting, but again, you're missing the point. How did the prokaryotes even get started?!

That's the theory of abiogenesis, remember?       I get it; there's really not much to criticize in the theory of biological evolution, so Professor Rob decided to criticize something else and pretend it is evolution.

21 hours ago, Retrobyter said:

If each needs the other, how did the system even get its start?

Evolutionary theory merely assumes life began, and describes how it changes.    It makes no claims about how that happened.  As I showed you, Darwin just thought  God made the first living things.

(Regarding "Haldane's Dilemma")

Well, that wasn't Haldane's conclusion...

Journal of Genetics

Published: December 1957

The cost of natural selection

J. B. S. Haldane 

Unless selection is very intense, the number of deaths needed to secure the substitution, by natural selection, of one gene for another at a locus, is independent of the intensity of selection. It is often about 30 times the number of organisms in a generation. It is suggested that, in horotelic evolution, the mean time taken for each gene substitution is . about 300 generations. This accords with the observed slowness of evolution.

In fact Haldane is talking about the time it would take for one gene to completely replace another at a given gene locus.    Which is not how most evolution proceeds.    But even if it did, Haldane notes that it works about as fast as evolution proceeds in the fossil record.

21 hours ago, Retrobyter said:

READ THE BOOK!

Seems pointless.   Professor Rob seems to know very little about evolutionary theory at all.

21 hours ago, Retrobyter said:

didn't communicate it well enough for your needs, but you should really "hear" it from him, rather than relying on me to give a "summary" of what he said!

If you don't understand it well enough to show it to us, what makes you think it's right?  I already showed you a number of major goofs he made.  

That's a fact, but here's what really throws a wrench into Dr. Rob's claims:

A radical form of genetic novelty

The emergence of new genes from non-coding DNA is common across eukaryotes — how they contribute to adaptive evolutionary novelties is fascinating.

https://www.nature.com/articles/s41559-017-0180.pdf

Before this, new genes were assumed to have developed by gene duplication, followed by mutation.   And they often do.  But it turns out that a large number of genes have come about by mutation of non-coding DNA.   Dr. Rob seems unaware of these findings.

21 hours ago, Retrobyter said:

Brush-offs and disrespecting the writer. Nothing new here.

I'm just showing you some facts, and wondering why Dr. Rob didn't know about this.

Edited August 13, 2023 by The Barbarian

[Michael37]

Some insulting rhetoric has been reported. Some posts have been withheld. Those at fault please note:

[Daniel Marsh]

On 7/27/2023 at 9:13 PM, The Barbarian said:

He said that Adam had become like him.   But as you know, scripture never said that Adam was immortal, and God acknowledges that he was not. 

I know how much you want scripture to say that Adam was immortal.   But it doesn't.   Find a way to accept God's word as it is.

 

I always understood that as Adam and Eve gained knowledge of right and wrong like G_d has. 

[Daniel Marsh]

On 7/27/2023 at 9:13 PM, The Barbarian said:

He said that Adam had become like him.   But as you know, scripture never said that Adam was immortal, and God acknowledges that he was not. 

I know how much you want scripture to say that Adam was immortal.   But it doesn't.   Find a way to accept God's word as it is.

 

I always understood that as Adam and Eve gained knowledge of right and wrong like G_d has.   Oh no, too far behind to catch up.  https://encrypted-tbn0.gstatic.com/images?q=tbn:ANd9GcRZsQgcosyg25CCqr761FulnNGDjCHqbiQR6A&usqp=CAU

[The Barbarian]

31 minutes ago, Daniel Marsh said:

I always understood that as Adam and Eve gained knowledge of right and wrong like G_d has.

That's what He said.

Genesis 3:22 And the Lord God said, “The man has now become like one of us, knowing good and evil.

Of course he didn't become like God in other ways.

The serpent deceived by telling part of the truth.

 

[Retrobyter]

12 hours ago, The Barbarian said:

That's what He said.

Genesis 3:22 And the Lord God said, “The man has now become like one of us, knowing good and evil.

Of course he didn't become like God in other ways.

The serpent deceived by telling part of the truth.

 

Shalom, The Barbarian.

I agree with you on this point.