Is that Alleles there is?
New line of attack?
"From: Lenny Flank
Subject: Re: AiG nonsense about information increase (again)
Original Format
Newsgroups: talk.origins
Date: 2002-12-16 17:26:14 PST
Carl Wieland (MB BS) said
“However, it can be shown that in every situation where populations of living things change, they do so without increase (and often with a decrease) of information. Thus, it is completely illegitimate for anyone to claim that such changes show ‘evolution happening’.”
Creationism itself, of course, proves this silliness to be wrong. According to creationists, every human being alive today is descended from the 8 people that got off Noah’s Big Boat (actually, all of us are descended from 2 people who lived in the Really Nice Garden, but I will give the creationists the maximum benefit of the doubt here. …) Since I assume those 8 people on the Really Big Boat were diploid like all of us, that means they had a maximum possible of 16 different alleles for every genetic locus (actually they MUST ahve had less, since some on the Big Baot were descendents of others and therefore must have shared alleles, but again I will give the creationists the maximum possible benefit of the doubt). If Weyland’s [sic] drivel is right and ‘genetic information cannot increase’, then this means there can be NO human locus—none at all—that have more than 16 different alleles.
Hmmmm … there are over 200 known alleles for some of the hemoglobin genes, and over 400 allales for some of the HLA genes … Since there couldn’t have been more than 16 on the boat, and since there are well over 200 now, that means that genetic information has increased (after all, 200 is more than 16).
So I’d sure like to hear Weyland (or one of the creationist, uh, geniuses here) to tell me (1) how do we go from 16 alleles to over 200 alleles without a beneficial mutation, and (2) how does going from 16 alleles to over 200 represent a LOSS of genetic information. And please note than NONE of this—absolutely NONE of it, depends on any evolutionary assumptions. It is all straightforward CREATIONISM combined with fourth-grade-level genetics."
Dear D.W.,
Thanks for sending along that link. One despairs when one sees the many times that anti-creationists wax eloquent without ever having really read or carefully considered what the creationist arguments in question actually are. And we unfortunately know of this Flank person as one of the most abusive and ill-informed anticreationists and antiChristians on the Internet (for example, see Left Flank: Another Skeptic With the Same Old Canards).
I would believe that the various alleles of hemoglobin, for instance, could easily have arisen by mutation. But this is without any increase in information. The confusion in the critic’s mind comes because he clearly believes that ‘lots of varying copies’ means ‘lots of information’. That is as erroneous as the other commonly heard evolutionist claim that if you have doubling of chromosomes (polyploidy), that represents ‘more information’ (it would be like buying two copies of the same textbook and expecting to be able to learn twice as much!).
Information in the sense of ‘specified complexity’ is at stake. The specification involves function. No new functions have arisen for the hemoglobin alleles. The molecule in question actually has a part which is relatively fixed or invariant. This is the part that directly affects function (oxygen binding and release, primarily) and the variations that do not cause obvious disease all seem to take place in less critical portions, where quite a few changes can occur without impeding function. All these variant molecules function as either normal Hb (hemoglobin), or as defective Hb. Many blood diseases have been linked to mutations in the hemoglobin alleles.
Perhaps a simple analogy would help. Imagine you have a set of instructions in the form of a book for assembling an airplane. Imagine that in the set of instructions is a page specifying airline logos to be painted on the fuselage and tail. Now changes to this would be important to the airline, but it would not affect the airworthiness of the airplane. These are somewhat analogous to changes in a virus’s protein coat. They don’t alter any of the function of the virus, but like a change in an airplane’s logo, they might make it harder for the host immune system to recognize them. See Has AIDS evolved?.
In the course of copying, errors on this page of information would also not affect the airworthiness of the resulting airplanes. Many copies of the plans could end up in circulation, varying in their livery, but all having the same functionality. Copies of the instructions with changes to the core information would of course result in defective aircraft and would be discarded.
However, by using the logic of this critic, one would say that this shows that the original information in the assembly instructions for an airplane could easily have arisen by an accidental process whereby information gradually increases. I.e., he argues as if the random process that produced inconsequential variants of this airplane manual are the same processes that wrote the manual in the first place! This is not a perfect analogy, but I hope you get the picture.
The critic would do well to read Dr Lee Spetner’s book Not by Chance. Spetner is a biophysicist well versed in the whole issue of signal-noise relationships in DNA, and he explains the information issue carefully.
Also, John Woodmorappe’s book Noah’s Ark: A Feasibility Study specifically addresses the question of multiple alleles generated after the Flood. Furthermore, Dr Jonathan Sarfati’s book Refuting Evolution 2 goes further into gene duplication, beneficial information-losing mutations etc. Actually, there is nothing in Flank’s diatribe that isn't covered in our Q&A pages on mutations and information theory.
Regards,
Carl Wieland
See also:
Variation and natural selection versus evolution
by Jonathan Sarfati, Ph.D., F.M.
Excerpt Below
"All (sexually reproducing) organisms contain their genetic information in paired form. Each offspring inherits half its genetic information from its mother, and half from its father. So there are two genes at a given position (locus, plural loci) coding for a particular characteristic. An organism can be heterozygous at a given locus, meaning it carries different forms (alleles) of this gene. For example, one allele can code for blue eyes, while the other one can code for brown eyes; or one can code for the A blood type and the other for the B type. Sometimes two alleles have a combined effect, while at other times only one allele (called dominant) has any effect on the organism, while the other does not (recessive). With humans, both the mother’s and father’s halves have 100,000 genes, the information equivalent to a thousand 500-page books (3 billion base pairs, as Teaching about Evolution correctly states on page 42). The ardent neo-Darwinist Francisco Ayala points out that humans today have an ‘average heterozygosity of 6.7 percent.’1 This means that for every thousand gene pairs coding for any trait, 67 of the pairs have different alleles, meaning 6,700 heterozygous loci overall. Thus, any single human could produce a vast number of different possible sperm or egg cells 26700 or 102017. The number of atoms in the whole known universe is ‘only’ 1080, extremely tiny by comparison. So there is no problem for creationists explaining that the original created kinds could each give rise to many different varieties. In fact, the original created kinds would have had much more heterozygosity than their modern, more specialized descendants. No wonder Ayala pointed out that most of the variation in populations arises from reshuffling of previously existing genes, not from mutations. Many varieties can arise simply by two previously hidden recessive alleles coming together. However, Ayala believes the genetic information came ultimately from mutations, not creation. His belief is contrary to information theory, as shown in chapter 9 on ‘Design.’"
Blood types and their origin
Excerpt below:
"Origin of the Blood Types
One aspect of the wide variety of humans is all the different blood types. The following explanation covers the main A, B and O blood types 2.
The A and B blood groups are caused by different antigens (substances which provoke immune responses) on the surface of the red blood cells. Their production is under the control of the DNA. The antigens develop from a red blood cell surface precursor called H substance, which is common to A, B and O. Type A results from the placement of N-acetylgalactosamine by the enzyme type A transferase on the H substance. Type B results from attachment of galactose to H by Type B transferase.
Type O is the result of a simple point mutation that greatly reduced or destroyed the ability of Type A transferase to attach N-acetylgalactosamine to H substance. Note that this is an example of loss of information, so is irrelevant to particles-to-people evolution. This ineffective Type A transferase is called circulating protein. The ineffectiveness of type O’s circulating protein depends on the point in the DNA where the mutation occurred, because some type Os attach more N-acetylgalactosamine to H than others. This sometimes causes discrepancies among blood banks. The mutations probably happened early in human history, since O is the most common blood group. Unattached H substance itself is an antigen which results in the rare blood type Bombay or Oh.
There is one gene in humans that controls the ABO blood type. There are three versions of the gene, or alleles: A, B, or O. Since the gene is always present as a pair of alleles, with one inherited from each parent, two alleles are always present, so that the possible genetic make-up of any individual is AA, BB, AB, AO, BO, or OO. The O allele is recessive to the A or B, meaning that in the presence of the A or B allele, the blood type is determined by the A or B allele. That is, an AO person has A-type blood; a BO person has B-type blood, whereas only an OO person has O-type blood. Anyone with O-type blood is called a universal donor because their blood lacks the A or B proteins so that O-type blood can be given to a person with A, B or AB type blood. If, for example, A-type blood is given to a person with B-type blood, an allergic reaction can result in death of the recipient."
There is a world of information about Alleles and blood types and what we know about them. One thing we know is that 4500 years was plenty of time for the races and types of people that we have now to come forth. In fact, the difference in all the human race is 0.1 percent in this area, an amazing similarity unless we are all descended from fairly recent ancestors.
Professor of genetics says 'No!' to evolution
by Maciej Giertych
Me, too! But then we knew that already...
"From: Lenny Flank
Subject: Re: AiG nonsense about information increase (again)
Original Format
Newsgroups: talk.origins
Date: 2002-12-16 17:26:14 PST
Carl Wieland (MB BS) said
“However, it can be shown that in every situation where populations of living things change, they do so without increase (and often with a decrease) of information. Thus, it is completely illegitimate for anyone to claim that such changes show ‘evolution happening’.”
Creationism itself, of course, proves this silliness to be wrong. According to creationists, every human being alive today is descended from the 8 people that got off Noah’s Big Boat (actually, all of us are descended from 2 people who lived in the Really Nice Garden, but I will give the creationists the maximum benefit of the doubt here. …) Since I assume those 8 people on the Really Big Boat were diploid like all of us, that means they had a maximum possible of 16 different alleles for every genetic locus (actually they MUST ahve had less, since some on the Big Baot were descendents of others and therefore must have shared alleles, but again I will give the creationists the maximum possible benefit of the doubt). If Weyland’s [sic] drivel is right and ‘genetic information cannot increase’, then this means there can be NO human locus—none at all—that have more than 16 different alleles.
Hmmmm … there are over 200 known alleles for some of the hemoglobin genes, and over 400 allales for some of the HLA genes … Since there couldn’t have been more than 16 on the boat, and since there are well over 200 now, that means that genetic information has increased (after all, 200 is more than 16).
So I’d sure like to hear Weyland (or one of the creationist, uh, geniuses here) to tell me (1) how do we go from 16 alleles to over 200 alleles without a beneficial mutation, and (2) how does going from 16 alleles to over 200 represent a LOSS of genetic information. And please note than NONE of this—absolutely NONE of it, depends on any evolutionary assumptions. It is all straightforward CREATIONISM combined with fourth-grade-level genetics."
Dear D.W.,
Thanks for sending along that link. One despairs when one sees the many times that anti-creationists wax eloquent without ever having really read or carefully considered what the creationist arguments in question actually are. And we unfortunately know of this Flank person as one of the most abusive and ill-informed anticreationists and antiChristians on the Internet (for example, see Left Flank: Another Skeptic With the Same Old Canards).
I would believe that the various alleles of hemoglobin, for instance, could easily have arisen by mutation. But this is without any increase in information. The confusion in the critic’s mind comes because he clearly believes that ‘lots of varying copies’ means ‘lots of information’. That is as erroneous as the other commonly heard evolutionist claim that if you have doubling of chromosomes (polyploidy), that represents ‘more information’ (it would be like buying two copies of the same textbook and expecting to be able to learn twice as much!).
Information in the sense of ‘specified complexity’ is at stake. The specification involves function. No new functions have arisen for the hemoglobin alleles. The molecule in question actually has a part which is relatively fixed or invariant. This is the part that directly affects function (oxygen binding and release, primarily) and the variations that do not cause obvious disease all seem to take place in less critical portions, where quite a few changes can occur without impeding function. All these variant molecules function as either normal Hb (hemoglobin), or as defective Hb. Many blood diseases have been linked to mutations in the hemoglobin alleles.
Perhaps a simple analogy would help. Imagine you have a set of instructions in the form of a book for assembling an airplane. Imagine that in the set of instructions is a page specifying airline logos to be painted on the fuselage and tail. Now changes to this would be important to the airline, but it would not affect the airworthiness of the airplane. These are somewhat analogous to changes in a virus’s protein coat. They don’t alter any of the function of the virus, but like a change in an airplane’s logo, they might make it harder for the host immune system to recognize them. See Has AIDS evolved?.
In the course of copying, errors on this page of information would also not affect the airworthiness of the resulting airplanes. Many copies of the plans could end up in circulation, varying in their livery, but all having the same functionality. Copies of the instructions with changes to the core information would of course result in defective aircraft and would be discarded.
However, by using the logic of this critic, one would say that this shows that the original information in the assembly instructions for an airplane could easily have arisen by an accidental process whereby information gradually increases. I.e., he argues as if the random process that produced inconsequential variants of this airplane manual are the same processes that wrote the manual in the first place! This is not a perfect analogy, but I hope you get the picture.
The critic would do well to read Dr Lee Spetner’s book Not by Chance. Spetner is a biophysicist well versed in the whole issue of signal-noise relationships in DNA, and he explains the information issue carefully.
Also, John Woodmorappe’s book Noah’s Ark: A Feasibility Study specifically addresses the question of multiple alleles generated after the Flood. Furthermore, Dr Jonathan Sarfati’s book Refuting Evolution 2 goes further into gene duplication, beneficial information-losing mutations etc. Actually, there is nothing in Flank’s diatribe that isn't covered in our Q&A pages on mutations and information theory.
Regards,
Carl Wieland
See also:
Variation and natural selection versus evolution
by Jonathan Sarfati, Ph.D., F.M.
Excerpt Below
"All (sexually reproducing) organisms contain their genetic information in paired form. Each offspring inherits half its genetic information from its mother, and half from its father. So there are two genes at a given position (locus, plural loci) coding for a particular characteristic. An organism can be heterozygous at a given locus, meaning it carries different forms (alleles) of this gene. For example, one allele can code for blue eyes, while the other one can code for brown eyes; or one can code for the A blood type and the other for the B type. Sometimes two alleles have a combined effect, while at other times only one allele (called dominant) has any effect on the organism, while the other does not (recessive). With humans, both the mother’s and father’s halves have 100,000 genes, the information equivalent to a thousand 500-page books (3 billion base pairs, as Teaching about Evolution correctly states on page 42). The ardent neo-Darwinist Francisco Ayala points out that humans today have an ‘average heterozygosity of 6.7 percent.’1 This means that for every thousand gene pairs coding for any trait, 67 of the pairs have different alleles, meaning 6,700 heterozygous loci overall. Thus, any single human could produce a vast number of different possible sperm or egg cells 26700 or 102017. The number of atoms in the whole known universe is ‘only’ 1080, extremely tiny by comparison. So there is no problem for creationists explaining that the original created kinds could each give rise to many different varieties. In fact, the original created kinds would have had much more heterozygosity than their modern, more specialized descendants. No wonder Ayala pointed out that most of the variation in populations arises from reshuffling of previously existing genes, not from mutations. Many varieties can arise simply by two previously hidden recessive alleles coming together. However, Ayala believes the genetic information came ultimately from mutations, not creation. His belief is contrary to information theory, as shown in chapter 9 on ‘Design.’"
Blood types and their origin
Excerpt below:
"Origin of the Blood Types
One aspect of the wide variety of humans is all the different blood types. The following explanation covers the main A, B and O blood types 2.
The A and B blood groups are caused by different antigens (substances which provoke immune responses) on the surface of the red blood cells. Their production is under the control of the DNA. The antigens develop from a red blood cell surface precursor called H substance, which is common to A, B and O. Type A results from the placement of N-acetylgalactosamine by the enzyme type A transferase on the H substance. Type B results from attachment of galactose to H by Type B transferase.
Type O is the result of a simple point mutation that greatly reduced or destroyed the ability of Type A transferase to attach N-acetylgalactosamine to H substance. Note that this is an example of loss of information, so is irrelevant to particles-to-people evolution. This ineffective Type A transferase is called circulating protein. The ineffectiveness of type O’s circulating protein depends on the point in the DNA where the mutation occurred, because some type Os attach more N-acetylgalactosamine to H than others. This sometimes causes discrepancies among blood banks. The mutations probably happened early in human history, since O is the most common blood group. Unattached H substance itself is an antigen which results in the rare blood type Bombay or Oh.
There is one gene in humans that controls the ABO blood type. There are three versions of the gene, or alleles: A, B, or O. Since the gene is always present as a pair of alleles, with one inherited from each parent, two alleles are always present, so that the possible genetic make-up of any individual is AA, BB, AB, AO, BO, or OO. The O allele is recessive to the A or B, meaning that in the presence of the A or B allele, the blood type is determined by the A or B allele. That is, an AO person has A-type blood; a BO person has B-type blood, whereas only an OO person has O-type blood. Anyone with O-type blood is called a universal donor because their blood lacks the A or B proteins so that O-type blood can be given to a person with A, B or AB type blood. If, for example, A-type blood is given to a person with B-type blood, an allergic reaction can result in death of the recipient."
There is a world of information about Alleles and blood types and what we know about them. One thing we know is that 4500 years was plenty of time for the races and types of people that we have now to come forth. In fact, the difference in all the human race is 0.1 percent in this area, an amazing similarity unless we are all descended from fairly recent ancestors.
Professor of genetics says 'No!' to evolution
by Maciej Giertych
Me, too! But then we knew that already...