The strange case of John Sanford, creationist

[leroy]

By the evidence for evolution.





No fixation. The larger the population the larger the genetic diversity. The more ideal the environment the grater the genetic diversity in a population and the greater the rate of evolution.



The 35 M differences are meaningless, and a bogus creationist argument simply based on the direct observations of evolution. The greater the population the greater the genetic diversity in the population and the greater the rate of evolution.




No, it is a diverse interaction of the genetic diversity evolution of populations, and not specific step by step nonsense.



The mutations are not the cause of evolution. They only provide the diversity of genes in a population of organisms. The environment is the driving force and the cause of the variation in the rate of evolution over time.



It is relevant, because there are more types and factors involved in the genetics of evolution than your bogus statistical model not supported by actual evidence in the real world.




Contradiction big time. They are not fixed, because of the evidence of the diversity of differences throughout the history of evolution.

. . . because your use of statistics and numbers as limiting the timing of evolution is bogus. There is no evidence to support your bogus math.

No, evolution is a continuous process over time without specific beginnings involving tens of thousands individuals and between populations of tens of thousands of individuals.




Increasing population does not make fixation unlikely.

Your lack of knowledge in genetics, evolution and science in general makes your argument worse.

I have responded repeated to your flawed argument that genetic mutations are what cause or limit the timing of evolution. The statistical argument is unethically false, anote] bad math as has been demonstrated repeatedly in the past.. The numbers are rather meaningless, because first, genetic mutations are NOT random only the timing within the constraints of limited possibilities is random. You neglect that there are many types of over lapping types of mutation that contribute to the diversity By direct evidence the genetic diversity in populations of ideal environments is many times greater than less ideal environments.





As with all evolution and even abiogenesis it driven by environmental factors including the rate of evolution, and in the case of the post Cretaceous rapid evolution and the Cambrian explosion it was a void lack of competition accompanied by an ideal environment for the evolution of life,

Ok, feel free to present your model that explains how 35M nucleotide variations evolved in the human chimp line.

You can use any population size

The mutations are not the cause of evolution. They only provide the diversity of genes in a population of organisms. The environment is the driving force and the cause of the variation in the rate of evolution over time.

Sure and I would say that a big relevant portion of those mutations are non random. That our point of disagreement

 

[shunyadragon]

Ok, feel free to present your model that explains how 35M nucleotide variations evolved in the human chimp line.

Sure and I would say that a big relevant portion of those mutations are non random. That our point of disagreement

No, not a point of disagreement, but your misrepresentation of the evidence. The non-random nature mutations and their causes have been demonstrated a natural causes, governed by natural laws.

Your misrepresenting this phony 35M nucleotide variations. First of course they are not linear one after another mutations See the following for a beginning.

You can use any population size

. . . . the genetic diversity that is a result of mutations occur throughout populations not in a sequence of one after another in individuals. In other words the mutations can be massively parallel in large populations.

Comparing the human and chimpanzee genomes: Searching for needles in a haystack

Comparing the human and chimpanzee genomes: Searching for needles in a haystack

1. Ajit Varki1 and
2. Tasha K. Altheide

Conclusions
Sequencing of the chimpanzee genome signals not an end, but rather a beginning for researchers across diverse fields. The impressive array of data and analyses that have come from this sequencing has provided researchers with new and novel insights into rates and results of molecular processes such as nucleotide substitutions, gene duplications, insertions and deletions, retrotranspositions, and potential karyotypic changes. These data will provide the springboard for understanding the potential consequences of changes in these attributes between humans and chimpanzees. Over the years, scientists have proposed many theories about what makes humans different from the great apes, ranging from subtle changes in regulatory regions (King and Wilson 1975) all the way to the differential loss of gene activity in humans (Olson 1999; Olson and Varki 2003). In fact, given the rather complex series of events evident in the hominid fossil record (Wood and Collard 1999; Cela-Conde and Ayala 2003), every one of these hypothesized genetic mechanisms likely contributed to some degree to human-chimpanzee differences. Understanding what makes us evolutionarily, biomedically, and cognitively different from chimpanzees will require extensive comparative phenomics to complement the comparative genomics now possible using the chimpanzee genome. However, despite decades of research on wild and captive chimpanzees, our overall knowledge about the chimpanzee phenome is very incomplete (Gagneux 2004; Olson and Varki 2004; McConkey and Varki 2005). Studies of intra-specific variation among great apes are in their infancy, and biomedical and physiological data are few. This lack of comparative phenotypic data represents a serious knowledge imbalance. Better phenomic data would enhance our ability to make additional, focused choices for candidate gene studies, and also increase our understanding of the biochemical consequences of any genomic changes we do find. One step to extend the utility of the genome project is to have the phenome much better defined, not only through morphological and anatomical studies, but also via systematic collection of existing data in all fields relevant to understanding the human condition (practically speaking, most of the biological and social sciences). A recently initiated “Great Ape Phenome Project” will begin this process (Varki et al. 1998; Gagneux 2004; Olson and Varki 2004). Of course, the critically endangered status of great apes in the wild, and the fiscal, logistical, and ethical issues of studying great apes in captivity (Gagneux et al. 2005; McConkey and Varki 2005) create a situation wherein new data and resources will not be easy to come by. Regardless, for the purposes of comparison, there is no point in doing any study on a captive great ape that one would not also do on a human subject (Gagneux et al. 2005). Also, all studies on captive apes should try to financially contribute toward their conservation in the wild, e.g., via a proposed Great Apes Conservation Trust, which would receive a 10% overage on all grant funds awarded by various agencies for research projects on ape genomes, phenomes, or behavior (McConkey and Varki 2005).

In the absence of adequate comparative phenomic data between humans and chimpanzees, genomic data provides only part of the blueprint for the phenotype. It is crucial, after identifying differences in the genomic data, to ascertain which ones are important by studying their biological consequences in the laboratory. For example, the relatively limited genomic differences between humans and chimpanzees mean that identifying statistically meaningful differences in rates of evolution are difficult. This limitation will hamper our ability to identify genes or regions of biological interest and importance. Additional primate outgroups will be important for detecting selection over longer time periods and for eliminating false positives. Also, genomic data alone cannot predict epistatic interactions between various loci, nor can it reveal the pleiotropic effects of changes that have occurred in a single gene. Comparative functional studies are necessary to reap the full potential of the genomic data, to translate the observed genetic changes into tangible quantitative differences. However, even such systematic functional studies may not capture the full magnitude of a difference's importance by examining only a single player in a multiplayer interaction. It is likely that, while there may be single-gene changes of large consequence, there will also be synergistic effects of many minor changes at multiple loci. That is, the human condition is likely to be the result of many small effect changes, not just a few large effect mutations. These smaller, subtle changes will be difficult to detect by genomic methods. On the other hand, even clearly identifiable genomic and phenomic differences between humans and chimpanzees may not be directly related to speciation nor to the question of “what makes us human.” Such differences may be a simple byproduct of neutral divergence or genetic drift.

Also, what might seem an important phenotypic difference between humans and great apes might not actually be the most critical factor in determining unique features of the human condition. For example, despite the frequent attention given to big brain size (Wood and Collard 1999; Preuss 2005), there is little evidence for causative connections between brain size and human cognitive abilities (Preuss 2005). Additionally, maximum brain size was achieved long before the emergence of modern human behaviors (Klein 1999; Wood and Collard 1999). Thus, while increased brain size is an impressively human-specific phenotypic difference from great apes, it may well have been just one step (like bipedalism) that occurred earlier, along the way to the emergence of uniquely human cognitive features. Conversely, apparently small phenotypic differences could turn out to play major roles. For example, a small (approximately twofold) difference in the level of a thyroid hormone-binding protein and associated differences in thyroid hormone metabolism between humans and apes (Gagneux et al. 2001) could turn out to be as important as brain-expressed genes in altering the trajectory and mechanisms of human brain development.

Explaining “humanness” is a vague and broadly philosophical question, not easily approached using the genome alone. We prefer to use the term “the human condition” to refer to the entire suite of characters that makes humans different from the great apes. What it means to be human involves quantitative aspects of biochemistry, physiology, and morphology, as well as more qualitative arenas such as cognition, behavior, symbolic communication, and culture. However, unlike typical biological questions, the great majority of experiments one might propose for studying the consequences of species-specific genetic changes are unethical and/or impractical to do, either in humans or in great apes (Gagneux et al. 2005; McConkey and Varki 2005). Meanwhile, studies in mice may not provide sufficient answers. Thus, we suggest that many answers must come from a logical inductive approach that synthesizes many various “clues” to arrive at the best possible “diagnosis”. Also, apparently minor differences between humans and great apes could turn out to be critical. For all of these reasons, we must keep an open mind, and leave no clue unattended to, even if it may appear trivial at first glance. It may well be that findings made from systems that are more ethically accessible and practical to study (such as the blood and the skin) will reveal clues that will eventually allow generation of testable hypotheses about organs like the brain. The other reason to take this type of broad approach to the “human condition” is that there are major biomedical lessons to be learned, which will benefit both humans and great apes, even though they may not be useful in explaining “humanness” in its philosophical sense.

Because of the many limitations mentioned above, we will have to arrive at many of our conclusions by considering all of the facts in aggregate, including some circumstantial evidence. In the final analysis, the best long-term approach to understanding human-chimpanzee differences is to ensure that the next generation of biologists interested in the evolution of the human phenotype is a cross-trained and collaborative one, with an interdisciplinary focus. Interactions among a great many disciplines, such as genomics, biochemistry, physiology, neurobiology, cognitive science, medicine, pathology, anthropology, ecology, primatology, and evolutionary biology, will be essential in dissecting out the key genetic features that contribute to making us human.

More to follow . . .

 

[leroy]

No, not a point of disagreement, but your misrepresentation of the evidence. The non-random nature mutations and their causes have been demonstrated a natural causes, governed by natural laws.

Your misrepresenting this phony 35M nucleotide variations. First of course they are not linear one after another mutations See the following for a beginning.





. . . . the genetic diversity that is a result of mutations occur throughout populations not in a sequence of one after another in individuals. In other words the mutations can be massively parallel in large populations.

Comparing the human and chimpanzee genomes: Searching for needles in a haystack

Comparing the human and chimpanzee genomes: Searching for needles in a haystack

1. Ajit Varki1 and
2. Tasha K. Altheide

Conclusions
Sequencing of the chimpanzee genome signals not an end, but rather a beginning for researchers across diverse fields. The impressive array of data and analyses that have come from this sequencing has provided researchers with new and novel insights into rates and results of molecular processes such as nucleotide substitutions, gene duplications, insertions and deletions, retrotranspositions, and potential karyotypic changes. These data will provide the springboard for understanding the potential consequences of changes in these attributes between humans and chimpanzees. Over the years, scientists have proposed many theories about what makes humans different from the great apes, ranging from subtle changes in regulatory regions (King and Wilson 1975) all the way to the differential loss of gene activity in humans (Olson 1999; Olson and Varki 2003). In fact, given the rather complex series of events evident in the hominid fossil record (Wood and Collard 1999; Cela-Conde and Ayala 2003), every one of these hypothesized genetic mechanisms likely contributed to some degree to human-chimpanzee differences. Understanding what makes us evolutionarily, biomedically, and cognitively different from chimpanzees will require extensive comparative phenomics to complement the comparative genomics now possible using the chimpanzee genome. However, despite decades of research on wild and captive chimpanzees, our overall knowledge about the chimpanzee phenome is very incomplete (Gagneux 2004; Olson and Varki 2004; McConkey and Varki 2005). Studies of intra-specific variation among great apes are in their infancy, and biomedical and physiological data are few. This lack of comparative phenotypic data represents a serious knowledge imbalance. Better phenomic data would enhance our ability to make additional, focused choices for candidate gene studies, and also increase our understanding of the biochemical consequences of any genomic changes we do find. One step to extend the utility of the genome project is to have the phenome much better defined, not only through morphological and anatomical studies, but also via systematic collection of existing data in all fields relevant to understanding the human condition (practically speaking, most of the biological and social sciences). A recently initiated “Great Ape Phenome Project” will begin this process (Varki et al. 1998; Gagneux 2004; Olson and Varki 2004). Of course, the critically endangered status of great apes in the wild, and the fiscal, logistical, and ethical issues of studying great apes in captivity (Gagneux et al. 2005; McConkey and Varki 2005) create a situation wherein new data and resources will not be easy to come by. Regardless, for the purposes of comparison, there is no point in doing any study on a captive great ape that one would not also do on a human subject (Gagneux et al. 2005). Also, all studies on captive apes should try to financially contribute toward their conservation in the wild, e.g., via a proposed Great Apes Conservation Trust, which would receive a 10% overage on all grant funds awarded by various agencies for research projects on ape genomes, phenomes, or behavior (McConkey and Varki 2005).

In the absence of adequate comparative phenomic data between humans and chimpanzees, genomic data provides only part of the blueprint for the phenotype. It is crucial, after identifying differences in the genomic data, to ascertain which ones are important by studying their biological consequences in the laboratory. For example, the relatively limited genomic differences between humans and chimpanzees mean that identifying statistically meaningful differences in rates of evolution are difficult. This limitation will hamper our ability to identify genes or regions of biological interest and importance. Additional primate outgroups will be important for detecting selection over longer time periods and for eliminating false positives. Also, genomic data alone cannot predict epistatic interactions between various loci, nor can it reveal the pleiotropic effects of changes that have occurred in a single gene. Comparative functional studies are necessary to reap the full potential of the genomic data, to translate the observed genetic changes into tangible quantitative differences. However, even such systematic functional studies may not capture the full magnitude of a difference's importance by examining only a single player in a multiplayer interaction. It is likely that, while there may be single-gene changes of large consequence, there will also be synergistic effects of many minor changes at multiple loci. That is, the human condition is likely to be the result of many small effect changes, not just a few large effect mutations. These smaller, subtle changes will be difficult to detect by genomic methods. On the other hand, even clearly identifiable genomic and phenomic differences between humans and chimpanzees may not be directly related to speciation nor to the question of “what makes us human.” Such differences may be a simple byproduct of neutral divergence or genetic drift.

Also, what might seem an important phenotypic difference between humans and great apes might not actually be the most critical factor in determining unique features of the human condition. For example, despite the frequent attention given to big brain size (Wood and Collard 1999; Preuss 2005), there is little evidence for causative connections between brain size and human cognitive abilities (Preuss 2005). Additionally, maximum brain size was achieved long before the emergence of modern human behaviors (Klein 1999; Wood and Collard 1999). Thus, while increased brain size is an impressively human-specific phenotypic difference from great apes, it may well have been just one step (like bipedalism) that occurred earlier, along the way to the emergence of uniquely human cognitive features. Conversely, apparently small phenotypic differences could turn out to play major roles. For example, a small (approximately twofold) difference in the level of a thyroid hormone-binding protein and associated differences in thyroid hormone metabolism between humans and apes (Gagneux et al. 2001) could turn out to be as important as brain-expressed genes in altering the trajectory and mechanisms of human brain development.

Explaining “humanness” is a vague and broadly philosophical question, not easily approached using the genome alone. We prefer to use the term “the human condition” to refer to the entire suite of characters that makes humans different from the great apes. What it means to be human involves quantitative aspects of biochemistry, physiology, and morphology, as well as more qualitative arenas such as cognition, behavior, symbolic communication, and culture. However, unlike typical biological questions, the great majority of experiments one might propose for studying the consequences of species-specific genetic changes are unethical and/or impractical to do, either in humans or in great apes (Gagneux et al. 2005; McConkey and Varki 2005). Meanwhile, studies in mice may not provide sufficient answers. Thus, we suggest that many answers must come from a logical inductive approach that synthesizes many various “clues” to arrive at the best possible “diagnosis”. Also, apparently minor differences between humans and great apes could turn out to be critical. For all of these reasons, we must keep an open mind, and leave no clue unattended to, even if it may appear trivial at first glance. It may well be that findings made from systems that are more ethically accessible and practical to study (such as the blood and the skin) will reveal clues that will eventually allow generation of testable hypotheses about organs like the brain. The other reason to take this type of broad approach to the “human condition” is that there are major biomedical lessons to be learned, which will benefit both humans and great apes, even though they may not be useful in explaining “humanness” in its philosophical sense.

Because of the many limitations mentioned above, we will have to arrive at many of our conclusions by considering all of the facts in aggregate, including some circumstantial evidence. In the final analysis, the best long-term approach to understanding human-chimpanzee differences is to ensure that the next generation of biologists interested in the evolution of the human phenotype is a cross-trained and collaborative one, with an interdisciplinary focus. Interactions among a great many disciplines, such as genomics, biochemistry, physiology, neurobiology, cognitive science, medicine, pathology, anthropology, ecology, primatology, and evolutionary biology, will be essential in dissecting out the key genetic features that contribute to making us human.

More to follow . . .

Granted I am not arguing for supernatural mutations

All I am saying is that non random natural mechanisms such as trasposons, NGE, epigenetics likely played a mayor role the our evolutionary past.

Is there any point of disagreement?

Can you explain the relevance of the article that you are quoting?

 

[shunyadragon]

Granted I am not arguing for supernatural mutations

All I am saying is that non random natural mechanisms such as trasposons, NGE, epigenetics likely played a mayor role the our evolutionary past.

If you are arguing fro anything other than a natural explanation for the cause of abiogensis and evolution, then we do not agree.

Is there any point of disagreement?

Can you explain the relevance of the article that you are quoting?

It explains that the bogus 35 M nucleotide differences are meaningless to the argument. The article explains what is meaningful concerning the differences in terms of evolution. It also, and the references, goes into the timing of evolution.

 

[leroy]

If you are arguing fro anything other than a natural explanation for the cause of abiogensis and evolution, then we do not agree.



It explains that the bogus 35 M nucleotide differences are meaningless to the argument. The article explains what is meaningful concerning the differences in terms of evolution. It also, and the references, goes into the timing of evolution.

Again, I am arguing that non random mutations likelly played a mayor role in supplying the diversity of genetic material in the human line evolution

Is there any point of disagreement?



Can you quote a portion of your article that is in conflict with anything that I have said?...

 

[tas8831]

Never did get any kind of straight-forward answer to any of this. That is the creationist way...

Yes, pretty sure it is you, unless I plugged in the wrong number..
View attachment 40276
The mutation rate is in mutations per site per year. Multiply the rate times the number of sites times the years. The number of sites and the number of years came from YOU, so if the numbers are out of whack (as I already indicated they could well be), it is likely due to my use of YOUR numbers.


Please show your work as I did. Because that seems utterly nonsensical.

Not a yes or no question - what do you mean "evolved" - what is your measure?

Entirely possible, as you never really seem to make one.

Darwinism contained drift? huh...

Wow, OK...

The mechanism of random mutation is primarily replication error during DNA replication/synthesis:

Mutations arise spontaneously at low frequency owing to the chemical instability of purine and pyrimidine bases and to errors during DNA replication. Natural exposure of an organism to certain environmental factors, such as ultraviolet light and chemical carcinogens (e.g., aflatoxin B1), also can cause mutations.

A common cause of spontaneous point mutations is the deamination of cytosine to uracil in the DNA double helix. Subsequent replication leads to a mutant daughter cell in which a T·A base pair replaces the wild-type C·G base pair. Another cause of spontaneous mutations is copying errors during DNA replication. Although replication generally is carried out with high fidelity, errors occasionally occur. Figure 8-5 illustrates how one type of copying error can produce a mutation. In the example shown, the mutant DNA contains nine additional base pairs.​

There are other factors as well, but the bulk of mutations are produced by errors. They are random with respect to fitness. That is, any given mutation can be neutral, beneficial, or deleterious. Most mutations are neutral. Of the rest, most are bad. But more are beneficial than previously believed.

The statement that mutations are random is both profoundly true and profoundly untrue at the same time. The true aspect of this statement stems from the fact that, to the best of our knowledge, the consequences of a mutation have no influence whatsoever on the probability that this mutation will or will not occur. In other words, mutations occur randomly with respect to whether their effects are useful. Thus, beneficial DNA changes do not happen more often simply because an organism could benefit from them. Moreover, even if an organism has acquired a beneficial mutation during its lifetime, the corresponding information will not flow back into the DNA in the organism's germline. This is a fundamental insight that Jean-Baptiste Lamarck got wrong and Charles Darwin got right.

However, the idea that mutations are random can be regarded as untrue if one considers the fact that not all types of mutations occur with equal probability. Rather, some occur more frequently than others because they are favored by low-level biochemical reactions. These reactions are also the main reason why mutations are an inescapable property of any system that is capable of reproduction in the real world. Mutation rates are usually very low, and biological systems go to extraordinary lengths to keep them as low as possible, mostly because many mutational effects are harmful. Nonetheless, mutation rates never reach zero, even despite both low-level protective mechanisms, like DNA repair or proofreading during DNA replication, and high-level mechanisms, like melanin deposition in skin cells to reduce radiation damage. Beyond a certain point, avoiding mutation simply becomes too costly to cells. Thus, mutation will always be present as a powerful force in evolution.​

I should have thought that someone so well-versed in evolution and genetics - such as yourself - might have taken the time to learn some of this stuff. Regarding selection and drift:

Genetic drift

Natural Selection


So yet again I address your demands, you still run off when challenged.

Is that your point? Odd then that you seem incapable of presenting any actual rationale, much less supporting evidence, for your "point." That is standard - Sanford and ReMine didn't either. They think assertions and made-up stories work. They don't.

So now it s your turn - present your model that accounts for this mysterious, unnamed, 'additional factor', supported by evidence, of course.
I just did - using YOUR numbers.

But please do explain what is so 'fast' - what is the evidence, other than your zany heroes pulling numbers out of thin air and arguing via personal disbelief.

You say it is 'too fast', but you can never explain why that is (eagerly awaiting some inaccurate paraphrasing or creationist/fringe sources). The ONLY way it seems "too fast" is if you are still clinging to the mere assertion-based claim that 500,000 or now 30 million 'beneficial mutations' are too few, which not even the professional creationists can seem to explain or support. It is mere assertion.



Your point? You've never mentioned transposons to me before. But I did find this from you from November:

Non random mechanisms like NGE, epigenetics, transposons etc. can create brand new functional and selectively positive proteins in 1 generation, this makes some scientists wonder that perhaps some of these non-random mechanism play a more important role than the process of random mutations and natural selection. Other scientists would argue that random mutations and natural selection play the most important role and that these other mechanisms provide a minor contribution.​

Isn't it precious that you have glommed onto "non-random". Yes, this causes some fringey-types that are out for name recognition to make all kinds of wild extrapolations.
But do tell me about how this "non-randomness" works in this context - tell us all how transposons are non-random, for example.



Really? Odd - all I can ever remember from you are paraphrasings of creationists like ReMine. That is where your earlier 500,000 mutation nonsense came from. And if that was really your point all along, one has to wonder why you expended so much energy NOT clearly indicating this, and instead spent most of your time demanding we address ReMine/Sanford's fantasies and disinformation.

Major role, according to you.

Interesting thing - part of my graduate research was on the evolution of a gene family in mammals. There are multiple genes in the family, all mutated copies of each other. One of the major duplication events was facilitated by the insertion of a LINE between 2 of the genes.
The most common LINE in mammals is L1, and it is able to recognize the hexanucleotide "TTAAAA"
and use that to insert itself into a genome. In that sense, it is non-random, since it uses a specific DNA sequence.

Would you like to guess how frequently that sequence shows up in genomes? Just for kicks, I searched GENBANK for the sequence for human chromosome 3. It is about 200 million BP, and my browser kept crashing, so I only downloaded 20 MB of it ( quick back of the envelope calculation indicates that 20 MB = only about 10 million 'letters' representing nucleotides, or about 1/20 of the chromosome in question). Once it loaded, I did a simple search for TTAAAA...........................
How many times do you think TTAAAA showed up?

22,679 times.

That is, there are potentially 22,679 insertion sites for the L1 LINE in about 1/20 of just 1 chromosome.
But sure, transposon insertion is totally 'non-random'....wrt fitness....

It is not that I do not think they play a role in evolution or fitness or selection - they clearly do (I have referred to one such insertion that conferred DDT resistance to fruit flies), but this genotype STILL has to spread throughout a population for it to become fixed, just like plain old SNPs. So your "speed" issue... isn't.


I have done this repeatedly, even using YOUR numbers.

That you keep re-asking me to do this for you - even as you seem 100% incapable of providing your rationale for asking over and over, and seem 100% incapable of providing any kind of counter model or rationale for whatever it is your actually think about it - and that tells everyone that you are amazingly disingenuous/dishonest about this whole subject. You seem unable or unwilling to explain or answer simple questions related to your anti-'Darwinism' claims, such as how many mutations would have been required if evolution were true according to your claims - again, dishonest.

 

[tas8831]

Well then show that random mutations (rather than othe rmechanisms) where mainly responsible for larger brains, upright posture, cooperative behavior etc.

Darn it, I can't find your evidence that you presented to support you implication that transposons (rather than other mechanisms) where mainly responsible for larger brains, upright posture, cooperative behavior etc..

Surely you must have some that consists of more than just claiming 'standard population genetics' cannot explain it. Because that isn't evidence.

 

[shunyadragon]

Granted I am not arguing for supernatural mutations

All I am saying is that non random natural mechanisms such as trasposons, NGE, epigenetics likely played a mayor role the our evolutionary past.

Is there any point of disagreement?

Can you explain the relevance of the article that you are quoting?

It is only the occurance of individual cause and effect events, such as a genetic mutation where the outcome is timitied by Natural Laws and processes which are random...

Transposons is not a Natural Law nor a ntural process like those that determine the outcome organic and other chemical reaction. Transposons is a descriptive term for a type of non-random mutation where segments move around in a predictable pattern, and not the natural laws and processes that cause transposons. .

NGE? Please explain.

Epigenetics is not the natural processes I refer to. Epigenetics represents the 'study of heritable phenotype changes that do not involve alterations in the DNA sequence.' It is the Natural LAws and natural processes that determine epignetics that I am referring to.

 

[tas8831]

@leroy wrote:

"Just think about it in the last 30 years (since the genome project started) not a single mutation has been observed to become fixed in the human population, and you are supposed to average 6.6 per year"


I am eagerly waiting for you to provide the evidence for this assertion of fact.

 

[leroy]

@leroy wrote:

"Just think about it in the last 30 years (since the genome project started) not a single mutation has been observed to become fixed in the human population, and you are supposed to average 6.6 per year"


I am eagerly waiting for you to provide the evidence for this assertion of fact.

Exactly what claim are you talking about?

1 that not a single mutations has been observed to become fixed and dominant in the human population in the last 30 years.

2 or that you need and average rate of 6.6 mutations per year to examplain the differences between chimps and humans?

 

[Subduction Zone]

Exactly what claim are you talking about?

1 that not a single mutations has been observed to become fixed and dominant in the human population in the last 30 years.

So what? Why would anyone expect to observe such an event over such a short time period? When one forms unrealistic demands not getting an answer is not a confirmation of being right. Try to ask reasonable questions. Not ones that demonstrate that you do not know what you are talking about.

2 or that you need and average rate of 6.6 mutations per year to examplain the differences between chimps and humans?

Do you think that this is a problem? With a population of a million people and twenty year generations and 100 mutations per generation, and a birth rate of two person per couple that grows to adulthood. (all reasonably rough, if not overly conservative estimations) . Over a twenty year span there would be 100 million mutations. That is 5 million mutations per year. Let's say that I was just a tad conservative and round up to 6.6 million mutations. That means only one out of a million mutations need to become fixed for evolution to occur. That does not seem to be out of the question at all.

 

[leroy]

So what? Why would anyone expect to observe such an event over such a short time period? When one forms unrealistic demands not getting an answer is not a confirmation of being right. Try to ask reasonable questions. Not ones that demonstrate that you do not know what you are talking about.



Do you think that this is a problem? With a population of a million people and twenty year generations and 100 mutations per generation, and a birth rate of two person per couple that grows to adulthood. (all reasonably rough, if not overly conservative estimations) . Over a twenty year span there would be 100 million mutations. That is 5 million mutations per year. Let's say that I was just a tad conservative and round up to 6.6 million mutations. That means only one out of a million mutations need to become fixed for evolution to occur. That does not seem to be out of the question at all.

Ok , if one out of every million mutations become fixed and dominant, why is it that not a single one was observed in the last 30 years in humans? According to your own math this would be 150 million mutations…….and 150 that become fixed and dominant.

 

[Subduction Zone]

Ok , if one out of every million mutations become fixed and dominant, why is it that not a single one was observed in the last 30 years in humans? According to your own math this would be 150 million mutations…….and 150 that become fixed and dominant.

Because that is far too short of a time span. That is all. It appears that you do not even understand what "become fixed and dominant" would entail.

There are millions upon millions of genetic "experiments" running simultaneously. They take generations to come to a solution.

 

[leroy]

Because that is far too short of a time span. That is all. It appears that you do not even understand what "become fixed and dominant" would entail.

There are millions upon millions of genetic "experiments" running simultaneously. They take generations to come to a solution.

Ok and what would be the correct time span?


It will also be nice to have a source that supports you 1 in 1 million mutstions get fixed and dominant....... Or is it an other case where "you are an atheist therefore you don't have to support any of your asertions

 

[shunyadragon]

Ok and what would be the correct time span?

Variable depending on the beneficial nature and the nature of the mutations. Time span from hundreds to hundreds of thousands of years depending on the demands on the populations of animals to adapt to change. Changes in the environment are the main deriving force for evolution, and process of diversification of species and the adaptation to the new environment results in beneficial mutations becoming fixed and dominant.

The problem is your anti-science religious combative agenda against evolution results in your failure to make any effort to understand the science of evolution, and get a decent science education.

It will also be nice to have a source that supports you 1 in 1 million mutations get fixed and dominant....... Or is it an other case where "you are an atheist therefore you don't have to support any of your assertions

Examples of mutations in humans:

4 beneficial evolutionary mutations that humans are undergoing right now

4 beneficial evolutionary mutations that humans are undergoing right now
The genetic mutation that drives evolution is random. But here's a list of some beneficial mutations that are known to exist in human beings

Most random genetic changes caused by evolution are neutral, and some are harmful, but a few turn out to be positive improvements. These beneficial mutations are the raw material that may, in time, be taken up by natural selection and spread through the population. In this post, I'll list some examples of beneficial mutations that are known to exist in human beings.

Beneficial mutation #1: Apolipoprotein AI-Milano

Heart disease is one of the scourges of industrialized countries. It's the legacy of an evolutionary past which programmed us to crave energy-dense fats, once a rare and valuable source of calories, now a source of clogged arteries. But there's evidence that evolution has the potential to deal with it.

All humans have a gene for a protein called Apolipoprotein AI, which is part of the system that transports cholesterol through the bloodstream. Apo-AI is one of the HDLs, already known to be beneficial because they remove cholesterol from artery walls. But a small community in Italy is known to have a mutant version of this protein, named Apolipoprotein AI-Milano, or Apo-AIM for short. Apo-AIM is even more effective than Apo-AI at removing cholesterol from cells and dissolving arterial plaques, and additionally functions as an antioxidant, preventing some of the damage from inflammation that normally occurs in arteriosclerosis. People with the Apo-AIM gene have significantly lower levels of risk than the general population for heart attack and stroke, and pharmaceutical companies are looking into marketing an artificial version of the protein as a cardioprotective drug.

There are also drugs in the pipeline based on a different mutation, in a gene called PCSK9, which has a similar effect. People with this mutation have as much as an 88% lower risk of heart disease.

Beneficial mutation #2: Increased bone density

One of the genes that governs bone density in human beings is called low-density lipoprotein receptor-related protein 5, or LRP5 for short. Mutations which impair the function of LRP5 are known to cause osteoporosis. But a different kind of mutation can amplify its function, causing one of the most unusual human mutations known.

This mutation was first discovered fortuitously, when a young person from a Midwest family was in a serious car crash from which they walked away with no broken bones. X-rays found that they, as well as other members of the same family, had bones significantly stronger and denser than average. (One doctor who's studied the condition said, "None of those people, ranging in age from 3 to 93, had ever had a broken bone.") In fact, they seem resistant not just to injury, but to normal age-related skeletal degeneration. Some of them have benign bony growths on the roof of their mouths, but other than that, the condition has no side effects - although, as the article notes dryly, it does make it more difficult to float. As with Apo-AIM, some drug companies are researching how to use this as the basis for a therapy that could help people with osteoporosis and other skeletal diseases.

Beneficial mutation #3: Malaria resistance

The classic example of evolutionary change in humans is the hemoglobin mutation named HbS that makes red blood cells take on a curved, sickle-like shape. With one copy, it confers resistance to malaria, but with two copies, it causes the illness of sickle-cell anemia. This is not about that mutation.

As reported in 2001 (see also), Italian researchers studying the population of the African country of Burkina Faso found a protective effect associated with a different variant of hemoglobin, named HbC. People with just one copy of this gene are 29% less likely to get malaria, while people with two copies enjoy a 93% reduction in risk. And this gene variant causes, at worst, a mild anemia, nowhere near as debilitating as sickle-cell disease.

Beneficial mutation #4: Tetrachromatic vision

Most mammals have poor color vision because they have only two kinds of cones, the retinal cells that discriminate different colors of light. Humans, like other primates, have three kinds, the legacy of a past where good color vision for finding ripe, brightly colored fruit was a survival advantage.

The gene for one kind of cone, which responds most strongly to blue, is found on chromosome 7. The two other kinds, which are sensitive to red and green, are both on the X chromosome. Since men have only one X, a mutation which disables either the red or the green gene will produce red-green colorblindness, while women have a backup copy. This explains why this is almost exclusively a male condition.

But here's a question: What happens if a mutation to the red or the green gene, rather than disabling it, shifts the range of colors to which it responds? (The red and green genes arose in just this way, from duplication and divergence of a single ancestral cone gene.)

To a man, this would make no real difference. He'd still have three color receptors, just a different set than the rest of us. But if this happened to one of a woman's cone genes, she'd have the blue, the red and the green on one X chromosome, and a mutated fourth one on the other... which means she'd have four different color receptors. She would be, like birds and turtles, a natural "tetrachromat", theoretically capable of discriminating shades of color the rest of us can't tell apart. (Does this mean she'd see brand-new colors the rest of us could never experience? That's an open question.)

And we have evidence that just this has happened on rare occasions. In one study of color discrimination, at least one woman showed exactly the results we would expect from a true tetrachromat.[/QUOTE]

 

[shunyadragon]

Again, I am arguing that non random mutations likelly played a mayor role in supplying the diversity of genetic material in the human line evolution

Is there any point of disagreement?



Can you quote a portion of your article that is in conflict with anything that I have said?...

If you need glasses, and most likely a better education in science to understand references than please do so. The bottom line remains that the occurrence of individual mutations are random as with fractal outcomes of cause and effect events in nature. The natural processes of evolution are naturally NOT random that determine changes in genetics and the genetic shift that results in diversification and speciation of life to environmental change.

Randomness and non-randomness of cause and effect outcomes in the natural processes of all our physical existence have adequate natural explanations determined in science. You need to get a better education in science instead of pushing an anti-science agenda.

 

[Subduction Zone]

Ok and what would be the correct time span?


It will also be nice to have a source that supports you 1 in 1 million mutstions get fixed and dominant....... Or is it an other case where "you are an atheist therefore you don't have to support any of your asertions

What do you mean "correct time span"? Scientists can estimate how long ago the split between man and chimp occurred. Your question does not make much sense.

And you tried to change my claim. Why did you do that? That appears to be dishonest. There are no papers needed for a claim that I did not make.

 

[shunyadragon]

Ok, feel free to present your model that explains how 35M nucleotide variations evolved in the human chimp line.

You can use any population size.

No. It has been objectively determined that species with too low a genetic diversity and numbers have gone extinct.

Sure and I would say that a big relevant portion of those mutations are non random. That our point of disagreement

Randomness nor non-randomness in natural process is not remotely an issue in the science of evolution nor any othe science concerning the nature of our physical existence. Science has an adequate natural explanation of the nature of cause and effect outcomes of natural events regardless.

The bottom line the natural processes that determine the nature of evolution over the past billions of years are not naturally random, regardless of whether mutations are random or non-random.

 

[leroy]

What do you mean "correct time span"? Scientists can estimate how long ago the split between man and chimp occurred. Your question does not make much sense.

And you tried to change my claim. Why did you do that? That appears to be dishonest. There are no papers needed for a claim that I did not make.

yes you did claimed that 1 out of 1 million mutations get fixed and dominant*

That is 5 million mutations per year. Let's say that I was just a tad conservative and round up to 6.6 million mutations. That means only one out of a million mutations need to become fixed for evolution to occur. That does not seem to be out of the question at all.

well I am questioning that claim.(in blue)..... where did you get that data? based on what you made that assertion?

1 130 million babies are born every year

2 The mutation rate is around 100 base substitutions per generation

3 So we have 13,000,000,000 mutations to work with

4 You said that 1 mutation per million becomes fixed and dominant

….So according to your math 13,000 mutations per year should become fixed and dominat.

Since this is not what we observe, there most be something wrong with your math...I suggest that point 4 is wrong,…….do you have any other suggestion?

...
I would also like you to notice and appreciate the fact that I am pointing to you exactly where my point of disagreement is (in blue letters above), so that you can defend your position, I hope to have the same courtesy from you in the future,

Scientists can estimate how long ago the split between man and chimp occurred. Your question does not make much sense.

Yes and my point is that the mechanism of random mutation + natural selection is too slow and cant account for the differences between chimps and humans , given that we only have 5M years

The argument is very simple

1 the difference between humans and chimps is around 30,000,000 base pairs substitutions

2 this give us an average of 6 mutations per year (divide 30 million by 5 million)

3 based on what we can observe today….we don’t observe such a fast rate of mutations that become fixed and dominant

Therefore the mechanism of random mutation + natural selection is not sufficient to explain the differences between humans and chimps.

Please show the same courtesy that I had with you and explain exactly where is your point of disagreement?

 

[leroy]

..... regardless of whether mutations are random or non-random.

Ok can we agree on that we don’t know if mutations that caused evolution were mainly random or non random ? (random with respect to fitness)…this is simply an open area of reaserch where scientists are working on and nobody claims to have a definitive answer…………(any disagreement from your part)?