How is there reality without God?

[EarthScienceguy]

Neils Bohr
"No Phenomenon is a phenomenon until it is an observed phenomenon." Or another way to say this is that a tree does not fall in a forest unless it is observed.

The only way for there to be an objective reality is if God is the constant observer everywhere.

Physicist John Archibald Wheeler: "It is wrong to think of the past as 'already existing' in all detail. The 'past' is theory. The past has no existence except as it is recorded in the present."

God is everywhere so He can observe everywhere and produce objective reality.

[The Barbarian]

If your hypothetical example is contrary to the way things work in reality, isn't that an important clue for you?

This is done all the time to find the maximized possibility.

I don't think you have given this much thought. Going from 2 individuals to 100,000 individuals in one generation seems pretty unlikely for apes. How did you think that was going to work?

It is not. It is called maximizing the possibility.

In fact, There is no way for a pair of primates to reproduce that way. I think the problem is that you've confused individuals with the population genome. If you learn nothing else from this, learn that evolution is a change in allele frequencies in a population over time. Evolution happens to populations; it does not happen to individuals.

Most of us have about 100 mutations that were not in either parent. If you were correct, we'd see a huge number of genetic disorders. But I'd be willing to look at your data for the ratio of neutral to harmful mutations. What do you have? BTW, remember that "neutral", "harmful" and "beneficial" only count in terms of the environment. So it changes as the environment changes. Would you like some examples? Meantime, show us your data for that 90% and 10%.

You were correct in pointing out that my 10% was off.

By a huge number. And using prokaryotes as a example for eukaryotes won't work.

The correct number is more like 42% deleterious.

If that were so, humans would have about 42 harmful mutations each. That would be a staggering amount of genetic disorders. We'd all have them.

Now let's look at how many beneficial mutations researchers have found.

Out of this high ratio of variants (one in eight bases shows variation, they said), there should be some proportion, even if small, that improves fitness. But we search the paper in vain for any mention of beneficial mutations. There’s plenty of talk about the disease. The authors only mention “neutral” variants twice. But there are no mentions of beneficial mutations. You can’t find one instance of any of these words: benefit, beneficial, fitness, advantage (in terms of mutation), improvement, innovation, invention, or positive selection. https://evolutionnews.org/2016/08/a_billion_genes/

And yet in a quick look at the literature, I pulled up over a dozen recent favorable mutations in humans. Your guys seem to have a real problem finding data. I think I know why.

The article in Nature involved 12 individuals. So about 1200 mutations. So maybe there would be one useful one in that bunch. But no one tested to see if any of them were actually useful changes. Most wouldn't be a lot different from the normal allele, of course.

Currently, there is a good number of favorable mutations going on in human populations right now. These include:
https://bigthink.com/surprising-science ... in-humans/

In Africa, a new mutation that provides very good immunity to malaria but does not kill homozygotes, is spreading rapidly. HbC is replacing HbS alleles because it protects people from malaria, but it does not kill a person who happens to get 2 copies of the mutation.

Another recent mutation is one that changes the myostatin gene to produce much greater strength.
https://www.dailymail.co.uk/sciencetech ... ities.html

What are you trying to prove by this statement?

Just noting that your anti-evolution website is stuffed with prunes. Lots of recent favorable mutations in humans.

Are you trying to say that these traits are going to become fixed in the the human genome?

Perhaps you don't know what "fixation" means in genetics. I'm merely showing you a few new favorable mutations in humans that are increasing in frequency in some populations. HbC would be predicted by evolutionary theory to increase in areas where malaria is endemic, And it is. But not in areas where the parasite is not endemic.

How is that going to work?

Natural selection; if you do the math, you'll see that humans who carry one or two HbC alleles will leave more viable offspring than those with normal hemoglobin or HbS. Would you like me to show you how that works?

Now back to your example if each of us has about 100 mutations that weren't present in either of our parents. That means that 1.4E-11 beneficial mutations will be expressed per generation. That means that in a population of 100,000 there will be 1.4E-6 beneficial mutations per generation. This means in 10 million years with 500,000 generations there would be 70 beneficial mutations expressed.

Again, if your assumptions don't match up with the reality, that's a pretty good sign that your assumptions are not very good.

So, if my assumptions which are not assumption match up with reality then that is a pretty good sign that my assumptions that are not assumptions are correct.

I showed you about a dozen that occurred within a few hundred years. Reality beats your assumptions.

The above are not assumptions but they come from actual EXPERIMENTAL EVIDENCE.

The actual count of such mutations is more persuasive than you anti-evolution site's interpretation of research. Sorry.

Saying that some people have beneficial mutations is not experimental evidence of beneficial mutation rate.

But the actual existence of such mutations is. Reality wins.

Adam and Eve could have had at most 4 alleles for each gene locus. Yet most human gene have dozens of alleles. From 4 to about 50 in a few thousand years seem like a lot, doesn't it?

Dorit et al.8 examined a 729-base pair intron (the DNA in the genome that is not read to make proteins) from a worldwide sample of 38 human males and reported no sequence variation. This sort of invariance Dorit, R.L., Akashi, H. and Gilbert, W., Absence of polymorphism at the ZFY locus on the human Y chromosome, Science 268(5214):1183–1185, 1995.

You might not be aware of the fact that non-coding DNA (what creationists call "junk DNA") often has other functions. And such functional introns are understandably not very likely to change. In fact, that's one of the ways that we can find those that are functional. Thought you knew. Not surprisingly, the stuff that's highly variable between individuals and species, tends to be the stuff for which we can find no function.

Again your belief system simply does not support experimental evidence.

Well, let's take a look at that belief...

Front Genet 2012 Apr 13;3:55.
The function of introns
ABSTRACT
The intron-exon architecture of many eukaryotic genes raises the intriguing question of whether this unique organization serves any function, or is it simply a result of the spread of functionless introns in eukaryotic genomes. In this review, we show that introns in contemporary species fulfill a broad spectrum of functions, and are involved in virtually every step of mRNA processing. We propose that this great diversity of intronic functions supports the notion that introns were indeed selfish elements in early eukaryotes, but then independently gained numerous functions in different eukaryotic lineages. We suggest a novel criterion of evolutionary conservation, dubbed intron positional conservation, which can identify functional introns.

There is more evidence for this. Would you like me to show you some more?

The above evidence shows that the human race went through a bottle neck less than 10K years ago.

That would be pretty hard to sell to anyone familiar with the evidence. There were populations in Africa, Asia, Europe, Australia and the Americas about 13,000 years ago. They all have descendants living today. Doesn't seem like much of a bottleneck, does it? Would you like to see some details?

[JoeyKnothead]

If your hypothetical example is contrary to the way things work in reality, isn't that an important clue for you?

This is done all the time to find the maximized possibility.

I don't think you have given this much thought. Going from 2 individuals to 100,000 individuals in one generation seems pretty unlikely for apes. How did you think that was going to work?

My data suggests a little wine and some old Barry White records'll help, if not completely fulfill the prophesy. YMMV

[The Barbarian]

I don't think you have given this much thought. Going from 2 individuals to 100,000 individuals in one generation seems pretty unlikely for apes. How did you think that was going to work?

data suggests a little wine and some old Barry White records'll help, if not completely fulfill the prophesy. YMMV

[EarthScienceguy]

[Replying to The Barbarian in post #191]

How is that going to work?
Natural selection; if you do the math, you'll see that humans who carry one or two HbC alleles will leave more viable offspring than those with normal hemoglobin or HbS. Would you like me to show you how that works?

Back we are again to Haldane's Dilemma.

Haldane's Dilemma puts a time limit on the number of mutations that can be passed on by natural selection because of the cost of natural selection. Cost of natural selection is the number of different ways that an animal can die or that a positive trait can be selected out of a population.

This is also supported in more recent papers.

• Lynch doesn’t believe natural selection is up to the task. In a 2007 paper in Proceedings of the U.S. National Academy of Sciences titled “The frailty of adaptive hypotheses for the origins of organismal complexity,” he explains that among evolutionary biologists, “What is in question is whether natural selection is a necessary or sufficient force to explain the emergence of the genomic and cellular features central to the building of complex organisms.”54 Using similar language, a paper in the journal Theoretical Biology and Medical Modelling concludes that “it is important for biologists to realistically appraise what selection can and cannot do under various circumstances. Selection may neither be necessary nor sufficient to explain numerous genomic or cellular features of complex organisms.”55 Lynch is clear in his views: “there is no compelling empirical or theoretical evidence that complexity, modularity, redundancy or other features of genetic pathways are promoted by natural selection.”56 https://evolutionnews.org/2015/01/problem_4_natur/

• Unfortunately, the public is rarely made aware of these problems or this debate. According to Lynch, natural selection is typically portrayed as an “all powerful (without any direct evidence)”63 mechanism that can build complex biological features. He warns that “the myth that all of evolution can be explained by adaptation continues to be perpetuated by our continued homage to Darwin’s treatise in the popular literature.”64 The reality is that neither non-random forces like natural selection, nor random forces like genetic drift, can explain the origin of many complex biological features. https://evolutionnews.org/2015/01/problem_4_natur/

Saying that some people have beneficial mutations is not experimental evidence of beneficial mutation rate.
But the actual existence of such mutations is. Reality wins.

Saying that they exist is not a rate. But 12 mutations in "a couple of hundred years" is a mutation rate of about .06 mutations per year. In humans, that means that the "evolution between man to ape would have taken 1.7E8 years not 6E6 years. That is only off by a couple of orders of magnitude.

[Miles]

[Replying to The Barbarian in post #191]

How is that going to work?
Natural selection; if you do the math, you'll see that humans who carry one or two HbC alleles will leave more viable offspring than those with normal hemoglobin or HbS. Would you like me to show you how that works?

Back we are again to Haldane's Dilemma.

Haldane's Dilemma puts a time limit on the number of mutations that can be passed on by natural selection because of the cost of natural selection. Cost of natural selection is the number of different ways that an animal can die or that a positive trait can be selected out of a population.

This is also supported in more recent papers.

• Lynch doesn’t believe natural selection is up to the task. In a 2007 paper in Proceedings of the U.S. National Academy of Sciences titled “The frailty of adaptive hypotheses for the origins of organismal complexity,” he explains that among evolutionary biologists, “What is in question is whether natural selection is a necessary or sufficient force to explain the emergence of the genomic and cellular features central to the building of complex organisms.”54 Using similar language, a paper in the journal Theoretical Biology and Medical Modelling concludes that “it is important for biologists to realistically appraise what selection can and cannot do under various circumstances. Selection may neither be necessary nor sufficient to explain numerous genomic or cellular features of complex organisms.”55 Lynch is clear in his views: “there is no compelling empirical or theoretical evidence that complexity, modularity, redundancy or other features of genetic pathways are promoted by natural selection.”56 https://evolutionnews.org/2015/01/problem_4_natur/

• Unfortunately, the public is rarely made aware of these problems or this debate. According to Lynch, natural selection is typically portrayed as an “all powerful (without any direct evidence)”63 mechanism that can build complex biological features. He warns that “the myth that all of evolution can be explained by adaptation continues to be perpetuated by our continued homage to Darwin’s treatise in the popular literature.”64 The reality is that neither non-random forces like natural selection, nor random forces like genetic drift, can explain the origin of many complex biological features. https://evolutionnews.org/2015/01/problem_4_natur/

Saying that some people have beneficial mutations is not experimental evidence of beneficial mutation rate.
But the actual existence of such mutations is. Reality wins.

Saying that they exist is not a rate. But 12 mutations in "a couple of hundred years" is a mutation rate of about .06 mutations per year. In humans, that means that the "evolution between man to ape would have taken 1.7E8 years not 6E6 years. That is only off by a couple of orders of magnitude.

How about an even more recent finding (2019)

"Sex solves Haldane's dilemma

Abstract
The cumulative reproductive cost of multi-locus selection has been considered to be a potentially limiting factor on the rate of adaptive evolution. In this paper, we show that Haldane's arguments for the accumulation of reproductive costs over multiple loci are valid only for a clonally reproducing population of asexual genotypes. We show that a sexually reproducing population avoids this accumulation of costs. Thus, sex removes a perceived reproductive constraint on the rate of adaptive evolution. The significance of our results is twofold. First, the results demonstrate that adaptation based on multiple genes-such as selection acting on the standing genetic variation-does not entail a huge reproductive cost as suggested by Haldane, provided of course that the population is reproducing sexually. Second, this reduction in the cost of natural selection provides a simple biological explanation for the advantage of sex. Specifically, Haldane's calculations illustrate the evolutionary disadvantage of asexuality; sexual reproduction frees the population from this disadvantage."
Source
Full article

.

[The Barbarian]

How is that going to work?
Natural selection; if you do the math, you'll see that humans who carry one or two HbC alleles will leave more viable offspring than those with normal hemoglobin or HbS. Would you like me to show you how that works?

Back we are again to Haldane's Dilemma.

Haldane's Dilemma puts a time limit on the number of mutations that can be passed on by natural selection because of the cost of natural selection. Cost of natural selection is the number of different ways that an animal can die or that a positive trait can be selected out of a population.

Well, that's one of the problems with your theory. You see, HbC is becoming more common in malaria areas. Which is precisely what your interpretation of Haldane's Dilemma says is impossible. Would you like to learn about some more "impossible cases?"

Most of us have about 100 mutations that were not in either parent. If you were correct, we'd see a huge number of genetic disorders. But I'd be willing to look at your data for the ratio of neutral to harmful mutations. What do you have?

The correct number is more like 42% deleterious.

If so, then most humans would have about 42 harmful mutations. Yet few of us have any genetic disorders. So your assumptions don't fit reality. In science, when the theory doesn't fit the evidence, the theory is discarded and new theories that are consistent with the evidence are accepted:

Haldane's dilemma, also known as "the waiting time problem",[1] is a limit on the speed of beneficial evolution, calculated by J. B. S. Haldane in 1957. Before the invention of DNA sequencing technologies, it was not known how much polymorphism DNA harbored, although alloenzymes (variant forms of an enzyme which differ structurally but not functionally from other alloenzymes coded for by different alleles at the same locus) were beginning to make it clear that substantial polymorphism existed. This was puzzling because the amount of polymorphism known to exist seemed to exceed the theoretical limits that Haldane calculated, that is, the limits imposed if polymorphisms present in the population generally influence an organism's fitness. Motoo Kimura's landmark paper on neutral theory in 1968[2] built on Haldane's work to suggest that most molecular evolution is neutral, resolving the dilemma.
https://en.wikipedia.org/wiki/Haldane%27s_dilemma

More recently, some scientists have looked to other possible ways to explain the reality of a large number of beneficial mutations, although none of these have replaced Kimura's theory, which still fits the evidence better than anything else.

Saying that some people have beneficial mutations is not experimental evidence of beneficial mutation rate.

Showing that they have beneficial mutations is experimental proof that there is a beneficial mutation rate. What that rate is, would depend on the population and environment. What you're missing is that "beneficial" only counts in terms of environment. The less fit a population is in a particular environment the greater the beneficial mutation rate. Hence the observation that pioneering populations in new environments tend to evolve rapidly. Would you like me to show you more evidence?

And in many cases balancing selection (as in the ratio of sickle cell alleles in malaria areas with normal alleles) makes this far more interesting and complicated than Haldane thought. There even may be a cost to balancing selection:

Molecular Biology and Evolution, Volume 33, Issue 10, October 2016
Excess of Deleterious Mutations around HLA Genes Reveals Evolutionary Cost of Balancing Selection
Abstract
Deleterious mutations are expected to evolve under negative selection and are usually purged from the population. However, deleterious alleles segregate in the human population and some disease-associated variants are maintained at considerable frequencies. Here, we test the hypothesis that balancing selection may counteract purifying selection in neighboring regions and thus maintain deleterious variants at higher frequency than expected from their detrimental fitness effect. We first show in realistic simulations that balancing selection reduces the density of polymorphic sites surrounding a locus under balancing selection, but at the same time markedly increases the population frequency of the remaining variants, including even substantially deleterious alleles. To test the predictions of our simulations empirically, we then use whole-exome sequencing data from 6,500 human individuals and focus on the most established example for balancing selection in the human genome, the major histocompatibility complex (MHC). Our analysis shows an elevated frequency of putatively deleterious coding variants in nonhuman leukocyte antigen (non-HLA) genes localized in the MHC region. The mean frequency of these variants declined with physical distance from the classical HLA genes, indicating dependency on genetic linkage. These results reveal an indirect cost of the genetic diversity maintained by balancing selection, which has hitherto been perceived as mostly advantageous, and have implications both for the evolution of recombination and also for the epidemiology of various MHC-associated diseases.

[EarthScienceguy]

[Replying to The Barbarian in post #0]

Well, that's one of the problems with your theory. You see, HbC is becoming more common in malaria areas. This is precisely what your interpretation of Haldane's Dilemma says is impossible. Would you like to learn about some more "impossible cases?"

1. This is one trait. You still have not given me a beneficial mutation rate. So this would be one in how many years.
2. Haldane's Dilemma does not say that this is impossible. In fact, this is exactly how Haldane's dilemma says that a beneficial trait can be fixed in a population. There must be a massive death that kills off all of those organisms that do not have the beneficial trait. In regards to Malaria half of all humans that have ever existed have been killed by malaria. I would call that massive death.

Most of us have about 100 mutations that were not in either parent. If you were correct, we'd see a huge number of genetic disorders. But I'd be willing to look at your data for the ratio of neutral to harmful mutations. What do you have?

• Mutations can be neutral, harmful, or beneficial, though the neutral theory of molecular evolution predicts that most mutations are “nearly” neutral or only slightly deleterious, while beneficial mutations—which confer a survival advantage on an organism and, if it reproduces, on its progeny—are quite rare. As a whole, mutations occur at the rate of approximately five substitutions per billion nucleotide sites per year.

• Then they quantified the “fitness” of each mutant strain by measuring how quickly it reproduced relative to the nonmutant strain. Darwinian fitness, simply put, refers to the number of offspring an individual has. In this case, measuring the reproductive rates of the yeast strains showed whether the mutations were beneficial, harmful or neutral.
  
  To their surprise, the researchers found that 75.9% of synonymous mutations were significantly deleterious, while 1.3% were significantly beneficial. https://news.umich.edu/study-most-silen ... lications/

More recently, some scientists have looked to other possible ways to explain the reality of a large number of beneficial mutations, although none of these have replaced Kimura's theory, which still fits the evidence better than anything else.

Yea, Kimura's theory, right? Kimura wrote his theory when the scientific consensus was that most of the genome was junk and had no function. Which is no longer the case. Kimura also believed that most mutations were neutral and not harmful which from the paper above also does not seem to be the case.

Kimura's theory falls apart if most of the genome is not junk. Because in Kimura's theory only like 25% of the genome was actually functional. (the 25% is off the top of my head, I have the actual number in a book I have somewhere, I believe it is lower than 25%.)

And in many cases balancing selection (as in the ratio of sickle cell alleles in malaria areas with normal alleles) makes this far more interesting and complicated than Haldane thought. There even may be a cost to balancing selection:

This totally fits Haldane cost analysis. You have an increase in sickle cell alleles because of the drastic increase in deaths. Death is the cost of Haldane's dilemma. Death from malaria is much higher than death from sickle cell this is totally what Haldane's cost analysis would predict.

[EarthScienceguy]

[Replying to Miles in post #195]

Abstract
The cumulative reproductive cost of multi-locus selection has been considered to be a potentially limiting factor on the rate of adaptive evolution. In this paper, we show that Haldane's arguments for the accumulation of reproductive costs over multiple loci are valid only for a clonally reproducing population of asexual genotypes. We show that a sexually reproducing population avoids this accumulation of costs. Thus, sex removes a perceived reproductive constraint on the rate of adaptive evolution. The significance of our results is twofold. First, the results demonstrate that adaptation based on multiple genes-such as selection acting on the standing genetic variation-does not entail a huge reproductive cost as suggested by Haldane, provided of course that the population is reproducing sexually. Second, this reduction in the cost of natural selection provides a simple biological explanation for the advantage of sex. Specifically, Haldane's calculations illustrate the evolutionary disadvantage of asexuality; sexual reproduction frees the population from this disadvantage."

1. This study is based on a simulation, not on actual observations. The problem with simulations are the parameters or assumptions that are input into the simulations. For example in this simulations they make the following assumption. "the fittest individuals had the highest probability of survival from zygote to adult."

• This is making no distinction it seems if it is a dominant trait or a recessive trait. This is highly important in Haldane's dilemma. A recessive trait takes much longer and a lot more death than a dominant trait. This simulation seems to be programmed to assume all traits are dominant

• It is highly probable that a recessive trait even if it is beneficial will be selected out of the population.

2. This study assumes that natural selection will always pick the most advantageous trait.

• Natural selection as a means to produce complexity, modularity, and redundancy is promoted by natural selection.

• Lynch doesn’t believe natural selection is up to the task. In a 2007 paper in Proceedings of the U.S. National Academy of Sciences titled “The frailty of adaptive hypotheses for the origins of organismal complexity,” he explains that among evolutionary biologists, “What is in question is whether natural selection is a necessary or sufficient force to explain the emergence of the genomic and cellular features central to the building of complex organisms.”54 Using similar language, a paper in the journal Theoretical Biology and Medical Modelling concludes that “it is important for biologists to realistically appraise what selection can and cannot do under various circumstances. Selection may neither be necessary nor sufficient to explain numerous genomic or cellular features of complex organisms.”55 Lynch is clear in his views: “there is no compelling empirical or theoretical evidence that complexity, modularity, redundancy or other features of genetic pathways are promoted by natural selection.”56

Try a paper that makes actual observations, I do not believe you will find one.

[The Barbarian]

Well, that's one of the problems with your theory. You see, HbC is becoming more common in malaria areas. This is precisely what your interpretation of Haldane's Dilemma says is impossible. Would you like to learn about some more "impossible cases?"

[Replying to The Barbarian in post #0]
1. This is one trait.

Yes. Precisely what your interpretation of Haldane's Dilemma holds to be impossible. That should be a clue for you.

You still have not given me a beneficial mutation rate.

That's another odd idea creationists have invented. You see, "beneficial" only counts in terms of a specific population and environment. As Darwin pointed out, a well-fitted population in a constant environment would have fewer possible new beneficial traits, and evolution would be slowed greatly by natural selection. Likewise, a population entering a new environment will have many possible favorable traits and so the rate of beneficial mutations would be much greater. This is what we see in nature; Mayr noted a long time ago, that atypical species of any genus tend to be found in unusual environments.

You're looking for a number that will always depend on environment and population. It's actually more interesting than that; mutation rates of different taxa vary.

Genetics 2016 Nov;204(3):1249-1266
Evolution of Mutation Rates in Rapidly Adapting Asexual Populations
When deleterious mutations are included, natural selection pushes the population toward a stable mutation rate that can be suboptimal for the adaptation of the population as a whole. The approach to this stable mutation rate is not necessarily monotonic: even in the absence of epistasis, selection can favor mutator and antimutator alleles that "overshoot" the stable mutation rate by substantial amounts.

So this would be one in how many years.

This is like asking "what is the ideal size for an animal?" It's much, much more involved than most creationists imagine. This is why they keep thinking that there must be a single "beneficial mutation rate" for all organisms. Notice too, that this is another reason that Haldane's Dilemma is not a dilemma at all. I think you can see why if you think about it.

Haldane's Dilemma does not say that this is impossible. In fact, this is exactly how Haldane's dilemma says that a beneficial trait can be fixed in a population. There must be a massive death that kills off all of those organisms that do not have the beneficial trait.

No. Your interpretation of Haldane's Dilemma says it's impossible. And BTW, most alleles for any gene locus eventually become fixed in a population by random factors. Would you like me to show you how? That's the first realized reason why Haldane's Dilemma doesn't rule out evolutionary change.

In regards to Malaria half of all humans that have ever existed have been killed by malaria. I would call that massive death.

Sounds interesting. Since roughly 6.8 percent of all humans who have ever lived, were alive in 2022, I'd like to see your numbers on that. What do you have?

Most of us have about 100 mutations that were not in either parent. If you were correct, we'd see a huge number of genetic disorders. But I'd be willing to look at your data for the ratio of neutral to harmful mutations. What do you have?

Mutations can be neutral, harmful, or beneficial, though the neutral theory of molecular evolution predicts that most mutations are “nearly” neutral or only slightly deleterious, while beneficial mutations—which confer a survival advantage on an organism and, if it reproduces, on its progeny—are quite rare.

So your number is...?

To their surprise, the researchers found that 75.9% of synonymous mutations were significantly deleterious, while 1.3% were significantly beneficial.
https://news.umich.edu/study-most-silen ... lications/

Perhaps you don't know what synonymous mutations are. They are only a subset of all mutations. There are some amino acids that can be coded by more than one sequence of nucleotides. But your source considers 1.3% of those to be significantly beneficial. Now, since we all have about 100 mutations, if even half of them significantly reduced our likelihood of surviving long enough to reproduce, we'd be extinct. So natural selection takes care of this rather effectively. Part of this is because so many of them are recessive. But there are vertebrates that inbreed as a rule and (no surprise) they have few if any harmful recessives. If you thought it over, it is easy to see why.

More recently, some scientists have looked to other possible ways to explain the reality of a large number of beneficial mutations, although none of these have replaced Kimura's theory, which still fits the evidence better than anything else.

Yea, Kimura's theory, right? Kimura wrote his theory when the scientific consensus was that most of the genome was junk and had no function.

No, that's wrong, too. When I was an undergraduate in the 1960s, there were numerous articles in the literature about the functions of non-coding DNA (what creationists call "junk DNA") Creationists aren't entirely wrong; some of it is junk. But much of it has important functions. Moreover, it has been noted that non-coding DNA is a major source of new genes by mutation. Would you like to learn about that?

Kimura also believed that most mutations were neutral and not harmful which from the paper above also does not seem to be the case.

You've merely assumed that synonymous mutations represent all mutations. That's not the case.

Kimura's theory falls apart if most of the genome is not junk. Because in Kimura's theory only like 25% of the genome was actually functional.

Rather only 25% of it is coding DNA. He was quite aware that non-coding DNA often had other functions. Sometimes, it's just a confusion of terms:

[In 2012, scientists with the ENCODE project, a huge catalog of all noncoding DNA in the human genome, declared that 80 percent of our DNA was active and performing some function. Now scientists at Oxford have analyzed the human genome and claim that less than 10 percent of our DNA is functional.

Who’s correct? It’s possible–in fact, it’s likely–that both groups are. It depends on what is meant by the word “functional.” The explanation seems to be that, while some 80 percent of our DNA is doing stuff, less than 10 percent of it is doing such important stuff that natural selection has preserved it largely intact in the mammal line for 100 million years. (Anatomically modern humans — that’s all 7 billion of us, the last Homo standing — have only been around for a couple of hundred thousand years.)

The ENCODE scientists (ENCODE stands for Encyclopedia of DNA Elements), defined “functional” as meaning the DNA has some specific biochemical activity. For example, activity that makes copies of DNA during cell division is functional–essential, in fact–because cells must divide in order for life to go on.

But that activity is not functional in the way the new paper, published in PLOS Genetics July 24, uses that term. The Oxford researchers want to count as “functional” only DNA involved in shaping a person’s body and behavior–the phenotype, DNA that is acted upon by natural selection.

And in many cases balancing selection (as in the ratio of sickle cell alleles in malaria areas with normal alleles) makes this far more interesting and complicated than Haldane thought. There even may be a cost to balancing selection:

This totally fits Haldane cost analysis.

But not your interpretation of it. Hence the relatively new HbC is replacing HbS in malaria areas because it is somewhat more beneficial than HbS. And both are disappearing in the population of Americans who are of West African descent, because both of those alleles are harmful in the American environment. By now, you understand why your imagined beneficial/harmful mutation ratio does not exist as an absolute number.

You have an increase in sickle cell alleles because of the drastic increase in deaths. Death is the cost of Haldane's dilemma. Death from malaria is much higher than death from sickle cell

This is totally what evolutionary theory predicts. And seeing as populations in areas were malaria is endemic tend to be stable with the relative percent of alleles matching evolutionary predictions, we can only observe that Darwin was right.

[The Barbarian]

[Replying to Miles in post #195]
Lynch is clear in his views: “there is no compelling empirical or theoretical evidence that complexity, modularity, redundancy or other features of genetic pathways are promoted by natural selection.”56[/list]

Try a paper that makes actual observations, I do not believe you will find one.

Genetics 1982 Jul-Aug;101(3-4):335-44
Evolution of a regulated operon in the laboratory
The evolution of new metabolic functions is being studied in the laboratory using the EBG system of E. coli as a model system. It is demonstrated that the evolution of lactose utilization by lacZ deletion strains requires a series of structural and regulatory gene mutations. Two structural gene mutations act to increase the activity of ebg enzyme toward lactose, and to permit ebg enzyme to convert lactose into allolactose, and inducer of the lac operon. A regulatory mutation increases the sensitivity of the ebg repressor of lactose, and permits sufficient ebg enzyme activity for growth. The resulting fully evolved ebg operon regulates its own expression, and also regulates the synthesis of the lactose permease.

Here, an irreducibly complex enzyme system evolved over a relatively short time. It is irreducibly complex because the system will not work with unless both the enzyme and the regulator are present. Yet it evolved. A strain of bacteria that could not utilize lactose was given a lactose-rich environment. A series of mutations and natural selection led to the evolution of a strain that could utilize lactose. But it also evolved a regulator, such that the system would not work unless lactose was actually present (this reduces metabolic costs when there is not much lactose present).