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.

[Jose Fly]

[Replying to Jose Fly in post #162]

So now we're to the part where you ignore what's posted to you and just keep repeating yourself. I suppose I could repeat myself and keep reminding you that prezygotic reproductive isolation is one type of reproductive isolation, to which you would respond by ignoring that fact and repeating the above all over again.....but that's already gotten old so I'm not inclined to keep doing it.

Yes, because you are not even accepting what your own article is concluding. It is saying that speciation happens it is saying speciation may happen which is a big difference.

And yes you are ignoring what your own cited paper concludes. That speciation may happen not that it does happen.

I understand your not wanting to accept the fact that rapid speciation does not happen. Because I understand what it does to your worldview. I am sorry to be the one that disrupts your worldview in this way.

I'm trying to find the post where you made it clear that when you asked for examples of "experimental rapid speciation", you would only accept speciation that involved prezygotic reproductive isolation, but I can't find anything like that at all. All I see is your initial demand, me providing you with one example that you ignored, followed by me providing you the second example that you are now dismissing because it didn't involve prezygotic reproductive isolation.

I did ask for examples of "Rapid Speciation". This is not an example. Your own article that you cited and that I have repeatedly pointed out to you says that this is not an example of speciation. But that it may lead to speciation.

IOW, it's the standard creationist tactic of moving the goalposts.

What Goal post have I moved I am still looking for an example of rapid speciation.

And I suppose you're just going to completely ignore my question about why you're now arguing against rapid speciation when previously you claimed it supported your beliefs in the Biblical flood.

I did not see this question. I do not remember saying this. But I do support the Biblical flood model so yes there would have to be a rapid adaptation and speciation. I actually did expect you to find evidence of rapid speciation but nothing beyond the point of family. I am just saying that you have yet to show an example of rapid speciation.

In fact, 9 out of 10 species alive today have arisen in the last 200,000 years or less.

You should have gone to the creation site for your example. But rapid speciation happens within limits like the different breeds of dogs, cows, and pigs were made by humans. It also happens the same way that humans breed different domestic animals. Evidence of this is the different species of dogs that can breed. or the different species in the cat family that can mate. Or like the different members in the horse family that can mate like the Zebra and horse.

Are these different species if they can mate? Horses and Zebra's are considered to be different species but they can still mate. Ilama's and camels can also breed but are considered different species. This would fit a creationist model but not an evolutionary model but because the definition of species in evolutionary terms is.

• a group of living organisms consisting of similar individuals capable of exchanging genes or interbreeding.

So the creation model is outside that of evolutionary definition, but observations of interbreeding species do support it.

Here are some videos of the way that rapid speciation actually happens.

https://answersingenesis.org/natural-se ... peciation/
https://answersingenesis.org/natural-se ... nt-origin/

Increases in genetic information in the genome are limited by Haldane's dilemma. For example

• Imagine a population of 100,000 apes, the putative progenitors of humans. Suppose that a male and a female both received a mutation so beneficial that they out-survived everyone else; all the rest of the population died out—all 99,998 of them. And then the surviving pair had enough offspring to replenish the population in one generation. And this repeated every generation (every 20 years) for 10 million years, more than the supposed time since the last common ancestor of humans and apes. That would mean that 500,000 beneficial mutations could be added to the population (i.e., 10,000,000/20). Even with this completely unrealistic scenario, which maximizes evolutionary progress, only about 0.02% of the human genome could be generated. Considering that the difference between the DNA of a human and a chimp, our supposed closest living relative, is greater than 5%,2 evolution has an obvious problem in explaining the origin of the genetic information in a creature such as a human.
  
  However, with more realistic rates of fitness/selection and population replenishment, the number of beneficial mutations that can be accounted for plummets. Haldane calculated that no more than 1,667 beneficial substitutions could have occurred in the supposed 10 million years since the last common ancestor of apes and humans. This is a mere one substitution per 300 generations, on average. The origin of all that makes us uniquely human has to be explained within this limit.

Wow....this is unbelievable. In the same post, you actually say "rapid speciation does not happen" and "I do support the Biblical flood model so yes there would have to be a rapid adaptation and speciation".

You're scrambling so furiously, you can't even keep your own arguments straight, which is pretty darned funny to watch.

Then, as if the above wasn't absurd enough, you cite examples of different species that can mate and produce offspring as being examples of rapid speciation, apparently not realizing how they all involve the same type of reproductive isolation you just waved away (postzygotic reproductive isolation) in the bird lice experiment!

Finally, to top it all off you return to making quantitative claims about "genetic information" even though we had earlier established that you have no idea how to define or measure "genetic information"!

Every once in a while I get asked why I keep doing this. Well, this latest post of yours is a great illustration of my answer to that....watching creationists tie themselves in knots, contradict themselves, and generally say some of the goofiest things you'll ever see is highly entertaining to me. I keep wondering...just how far will they go to deny reality? And almost every time y'all exceed my expectations.

[JoeyKnothead]

...Even with this completely unrealistic scenario...

"Even with this unrealistic scenario."

Chekmate evolutionists!

[The Barbarian]

I'm trying to find the post where you made it clear that when you asked for examples of "experimental rapid speciation", you would only accept speciation that involved prezygotic reproductive isolation, but I can't find anything like that at all. All I see is your initial demand, me providing you with one example that you ignored, followed by me providing you the second example that you are now dismissing because it didn't involve prezygotic reproductive isolation.

IOW, it's the standard creationist tactic of moving the goalposts.

And I suppose you're just going to completely ignore my question about why you're now arguing against rapid speciation, when previously you claimed it supported your beliefs in the Biblical flood.

Such is the fundamentally dishonest nature of creationism....

Most creationists today have conceded the fact of speciation. AIG, for example:

As creationists, we must frequently remind detractors that we do not deny that species vary, change, and even appear over time. The biodiversity represented in the 8.7 million or so species in the world is a testament, not to random chance processes, but to the genetic variability and potential for diversification within the created kinds.

Before the time of Charles Darwin, a false idea had crept into the church—the belief in the “fixity” or “immutability” of species. According to this view, each species was created in precisely the same form that we find it today. The Bible nowhere teaches that species are fixed and unchanging.

https://answersingenesis.org/natural-se ... peciation/

AIG simply redefines "evolution" to exclude the evolution of new species, genera, and occasionally families. In doing so, they ignore the meaning of biological evolution, which is "a change in allele frequencies in a population over time." Because such evolution, including speciation, is directly observed. I think Mr. Ham has confused evolution with common descent (which is a consequence of evolution, not evolution itself).

[The Barbarian]

Finally, to top it all off you return to making quantitative claims about "genetic information" even though we had earlier established that you have no idea how to define or measure "genetic information"!

Every once in a while I get asked why I keep doing this. Well, this latest post of yours is a great illustration of my answer to that....watching creationists tie themselves in knots, contradict themselves, and generally say some of the goofiest things you'll ever see is highly entertaining to me. I keep wondering...just how far will they go to deny reality? And almost every time y'all exceed my expectations.

Claude Shannon, who first showed how to quantify information, did much of his early work in biology. As he pointed out, any new mutation in a population increases the information in that population. By "new mutation" I mean the formation of a new gene (or allele of an existing gene). It is also possible for mutation to reduce information by deleting a functional gene.

I believe I offered to show how this works mathematically, but I don't remember any creationist interested in learning how information works in genetics.

[Jose Fly]

I'm trying to find the post where you made it clear that when you asked for examples of "experimental rapid speciation", you would only accept speciation that involved prezygotic reproductive isolation, but I can't find anything like that at all. All I see is your initial demand, me providing you with one example that you ignored, followed by me providing you the second example that you are now dismissing because it didn't involve prezygotic reproductive isolation.

IOW, it's the standard creationist tactic of moving the goalposts.

And I suppose you're just going to completely ignore my question about why you're now arguing against rapid speciation, when previously you claimed it supported your beliefs in the Biblical flood.

Such is the fundamentally dishonest nature of creationism....

Most creationists today have conceded the fact of speciation. AIG, for example:

As creationists, we must frequently remind detractors that we do not deny that species vary, change, and even appear over time. The biodiversity represented in the 8.7 million or so species in the world is a testament, not to random chance processes, but to the genetic variability and potential for diversification within the created kinds.

Before the time of Charles Darwin, a false idea had crept into the church—the belief in the “fixity” or “immutability” of species. According to this view, each species was created in precisely the same form that we find it today. The Bible nowhere teaches that species are fixed and unchanging.

https://answersingenesis.org/natural-se ... peciation/

AIG simply redefines "evolution" to exclude the evolution of new species, genera, and occasionally families. In doing so, they ignore the meaning of biological evolution, which is "a change in allele frequencies in a population over time." Because such evolution, including speciation, is directly observed. I think Mr. Ham has confused evolution with common descent (which is a consequence of evolution, not evolution itself).

I think ESG is conflicted. He really wants to disagree with me and my position, but (as he recently posted) he needs rapid speciation for his flood beliefs.

It all started when he was trying to argue against PE, where he first challenged me to provide an example of rapid speciation. Of course the obvious question is, if he already accepted the concept, why challenge me to show an example?

I doubt even he knows.

[Jose Fly]

Finally, to top it all off you return to making quantitative claims about "genetic information" even though we had earlier established that you have no idea how to define or measure "genetic information"!

Every once in a while I get asked why I keep doing this. Well, this latest post of yours is a great illustration of my answer to that....watching creationists tie themselves in knots, contradict themselves, and generally say some of the goofiest things you'll ever see is highly entertaining to me. I keep wondering...just how far will they go to deny reality? And almost every time y'all exceed my expectations.

Claude Shannon, who first showed how to quantify information, did much of his early work in biology. As he pointed out, any new mutation in a population increases the information in that population. By "new mutation" I mean the formation of a new gene (or allele of an existing gene). It is also possible for mutation to reduce information by deleting a functional gene.

I believe I offered to show how this works mathematically, but I don't remember any creationist interested in learning how information works in genetics.

Well yeah....they're running so low on talking points, they can't risk losing one of their favorites! Better to ignore all that and just keep repeating the talking point.

One time I got a creationist to agree that functional nucleotide sequences are indeed "genetic information", but after I showed him how trivially easy it is to observe evolution generating them, he tried everything he could to go back on what he'd agreed to. Eventually he just declared it all to be pointless and left the thread.

Like I keep saying...I find that sort of behavior to be fascinating.

[The Barbarian]

Increases in genetic information in the genome are limited by Haldane's dilemma.

That's clearly wrong. Perhaps you don't know how information is measured in a population genome. How do you think it's measured?

• Imagine a population of 100,000 apes, the putative progenitors of humans. Suppose that a male and a female both received a mutation so beneficial that they out-survived everyone else; all the rest of the population died out—all 99,998 of them.[/quote]
  
  Genetic analysis shows that did not happen in the line that led to modern humans, and I can't think of a case where it has happened. You have an example?
  

  And then the surviving pair had enough offspring to replenish the population in one generation.

  
  
  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?
  

  And this repeated every generation (every 20 years) for 10 million years, more than the supposed time since the last common ancestor of humans and apes. That would mean that 500,000 beneficial mutations could be added to the population (i.e., 10,000,000/20).

  Each of us has about 100 mutations that weren't present in either of our parents. So let's say that 0.01percent of all mutations are favorable. In a population of 100,000 individuals, we'd then have about 1000 favorable mutations per generation. Since we observe that a mutation harmful enough to prevent one from leaving offspring is rather rare in humans (let's say 10%, a gross overestimate). So about 100 favorable mutations per generation.
  
  This would mean in ten million years, about 50,000,000 useful mutations.
  

  Even with this completely unrealistic scenario, which maximizes evolutionary progress, only about 0.02% of the human genome could be generated.

  
  
  Humans have about 30,000 genes. So this is why we have dozens of alleles for each gene locus. There's been a lot of evolution. Keep in mind that Adam and Eve could have had at most, 4 alleles for each gene locus. The rest evolved.
  

  Considering that the difference between the DNA of a human and a chimp, our supposed closest living relative, is greater than 5%,2 evolution has an obvious problem in explaining the origin of the genetic information in a creature such as a human.

  You realize that 50,000,000 is larger than 30,000, right?
  

  However, with more realistic rates of fitness/selection and population replenishment, the number of beneficial mutations that can be accounted for plummets. Haldane calculated that no more than 1,667 beneficial substitutions could have occurred in the supposed 10 million years since the last common ancestor of apes and humans. This is a mere one substitution per 300 generations, on average. The origin of all that makes us uniquely human has to be explained within this limit.

[/quote]

No. You're assuming that all the DNA differences between humans and chimps are functional. But that's demonstrably wrong.

Formation of human long intergenic non-coding RNA genes, pseudogenes, and protein genes: Ancestral sequences are key players
https://journals.plos.org/plosone/artic ... ne.0230236

And that's not the end of it. You see, it wasn't just humans evolving from a common ancestor; chimpanzees have been evolving just as long as we have from that ancestor. So each of us has evolved only about half of that difference. Leaving about 2.5% evolution over that time for each species.

I don't think you've thought this through very well.

[Diogenes]

[Replying to EarthScienceguy in post #170]
This is why I don't bother with people like Earth [fake] Science Guy. They don't even do their own work. An introductory sentence, then a paste from a pseudo science site, which is easily exposed by:

"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. Although neutral evolution remains the consensus theory among modern biologists,[3] and thus Kimura's resolution of Haldane's dilemma is widely regarded as correct, some biologists argue that adaptive evolution explains a large fraction of substitutions in protein coding sequence,[4] and they propose alternative solutions to Haldane's dilemma.
Contents

1 Substitution cost
2 Selection intensity
3 The cost
4 A mathematical model of the cost of diploids
5 Important number 300
6 Origin of the term "Haldane's dilemma"
7 Evolution above Haldane's limit
8 See also
9 References
10 Further reading

Substitution cost

In the introduction to The Cost of Natural Selection Haldane writes that it is difficult for breeders to simultaneously select all the desired qualities, partly because the required genes may not be found together in the stock; but, he writes,[5]

especially in slowly breeding animals such as cattle, one cannot cull even half the females, even though only one in a hundred of them combines the various qualities desired.[5]

That is, the problem for the cattle breeder is that keeping only the specimens with the desired qualities will lower the reproductive capability too much to keep a useful breeding stock.

Haldane states that this same problem arises with respect to natural selection. Characters that are positively correlated at one time may be negatively correlated at a later time, so simultaneous optimization of more than one character is a problem also in nature. And, as Haldane writes[5]

n this paper I shall try to make quantitative the fairly obvious statement that natural selection cannot occur with great intensity for a number of characters at once unless they happen to be controlled by the same genes.[5]

In faster breeding species there is less of a problem. Haldane mentions the peppered moth, Biston betularia, whose variation in pigmentation is determined by several alleles at a single gene.[5][6] One of these alleles, "C", is dominant to all the others, and any CC or Cx moths are dark (where "x" is any other allele). Another allele, "c", is recessive to all the others, and cc moths are light. Against the originally pale lichens the darker moths were easier for birds to pick out, but in areas, where pollution has darkened the lichens, the cc moths had become rare. Haldane mentions that in a single day the frequency of cc moths might be halved.

Another potential problem is that if "ten other independently inherited characters had been subject to selection of the same intensity as that for colour, only ( 1 / 2 ) 10 (1/2)^{{10}}, or one in 1024, of the original genotype would have survived." The species would most likely have become extinct; but it might well survive ten other selective periods of comparable selectivity, if they happened in different centuries.[5]
Selection intensity

Haldane proceeds to define the intensity of selection regarding "juvenile survival" (that is, survival to reproductive age) as I = ln ⁡ ( s 0 / S ) I=\ln(s_{0}/S), where s 0 s_{0} is the proportion of those with the optimal genotype (or genotypes) that survive to reproduce, and S S is the proportion of the entire population that similarly so survive. The proportion for the entire population that die without reproducing is thus 1 − S 1-S, and this would have been 1 − s 0 1-s_{0} if all genotypes had survived as well as the optimal. Hence s 0 − S s_{0}-S is the proportion of "genetic" deaths due to selection. As Haldane mentions, if s 0 ≈ S s_{0}\approx S, then I ≈ s 0 − S I\approx s_{0}-S.[7]
The cost

Haldane writes

I shall investigate the following case mathematically. A population is in equilibrium under selection and mutation. One or more genes are rare because their appearance by mutation is balanced by natural selection. A sudden change occurs in the environment, for example, pollution by smoke, a change of climate, the introduction of a new food source, predator, or pathogen, and above all migration to a new habitat. It will be shown later that the general conclusions are not affected if the change is slow. The species is less adapted to the new environment, and its reproductive capacity is lowered. It is gradually improved as a result of natural selection. But meanwhile, a number of deaths, or their equivalents in lowered fertility, have occurred. If selection at the i t h i^{th} selected locus is responsible for d i d_{i} of these deaths in any generation the reproductive capacity of the species will be ∏ ( 1 − d i ) \prod \left(1-d_{i}\right) of that of the optimal genotype, or exp ⁡ ( − ∑ d i ) \exp \left(-\sum d_{i}\right) nearly, if every d i d_{i} is small. Thus the intensity of selection approximates to ∑ d i \sum d_{i}.[5]

Comparing to the above, we have that d i = s 0 i − S d_{i}=s_{{0i}}-S, if we say that s 0 i s_{{0i}} is the quotient of deaths for the i t h i^{th} selected locus and S S is again the quotient of deaths for the entire population.

The problem statement is therefore that the alleles in question are not particularly beneficial under the previous circumstances; but a change in environment favors these genes by natural selection. The individuals without the genes are therefore disfavored, and the favorable genes spread in the population by the death (or lowered fertility) of the individuals without the genes. Note that Haldane's model as stated here allows for more than one gene to move towards fixation at a time; but each such will add to the cost of substitution.

The total cost of substitution of the i t h i^{th} gene is the sum D i D_{i} of all values of d i d_{i} over all generations of selection; that is, until fixation of the gene. Haldane states that he will show that D i D_{i} depends mainly on p 0 p_{0}, the small frequency of the gene in question, as selection begins – that is, at the time that the environmental change occurs (or begins to occur).[5]
A mathematical model of the cost of diploids

Let A and a be two alleles with frequencies p n p_{n} and q n q_{n} in the n th n^{{\mbox{th}}} generation. Their relative fitness is given by[5]

Genotype AA Aa aa
Frequency p n 2 p_{n}^{2} 2 p n q n 2p_{n}q_{n} q n 2 q_{n}^{2}
Fitness 1 1 − λ K 1-\lambda K 1 − K 1-K

where 0 ≤ K K ≤ 1, and 0 ≤ λ ≤ 1.

If λ = 0, then Aa has the same fitness as AA, e.g. if Aa is phenotypically equivalent with AA (A dominant), and if λ = 1, then Aa has the same fitness as aa, e.g. if Aa is phenotypically equivalent with aa (A recessive). In general λ indicates how close in fitness Aa is to aa.

The fraction of selective deaths in the n th n^{{\mbox{th}}} generation then is

d n = 2 λ K p n q n + K q n 2 = K q n [ 2 λ + ( 1 − 2 λ ) q n ] d_{n}=2\lambda Kp_{n}q_{n}+Kq_{n}^{2}=Kq_{n}[2\lambda +(1-2\lambda )q_{n}]

and the total number of deaths is the population size multiplied by

D = K ∑ 0 ∞ q n [ 2 λ + ( 1 − 2 λ ) q n ] . D=K\sum _{0}^{\infty }q_{n}\;[2\lambda +(1-2\lambda )q_{n}].

Important number 300

Haldane approximates the above equation by taking the continuum limit of the above equation.[5] This is done by multiplying and dividing it by dq so that it is in integral form

d q n = − K p n q n [ λ + ( 1 − 2 λ ) q n ] dq_{n}=-Kp_{n}q_{n}[\lambda +(1-2\lambda )q_{n}]

substituting q=1-p, the cost (given by the total number of deaths, 'D', required to make a substitution) is given by

D = ∫ 0 q 0 [ 2 λ + ( 1 − 2 λ ) q ] ( 1 − q ) [ λ + ( 1 − 2 λ ) q ] d q = 1 1 − λ ∫ 0 q 0 [ 1 1 − q + λ ( 1 − 2 λ ) λ + ( 1 − 2 λ ) q ] d q . D=\int _{0}^{{q_{{_{0}}}}}{\frac {[2\lambda +(1-2\lambda )q]}{(1-q)[\lambda +(1-2\lambda )q]}}dq={\frac {1}{1-\lambda }}\int _{0}^{{q_{{_{0}}}}}\left[{\frac {1}{1-q}}+{\frac {\lambda (1-2\lambda )}{\lambda +(1-2\lambda )q}}\right]dq.

Assuming λ < 1, this gives

D = 1 1 − λ [ − ln p 0 + λ ln ( 1 − λ − ( 1 − 2 λ ) p 0 λ ) ] ≈ 1 1 − λ [ − ln p 0 + λ ln ( 1 − λ λ ) ] D={\frac {1}{1-\lambda }}\left[-{\mbox{ln }}p_{0}+\lambda {\mbox{ ln }}\left({\frac {1-\lambda -(1-2\lambda )p_{0}}{\lambda }}\right)\right]\approx {\frac {1}{1-\lambda }}\left[-{\mbox{ln }}p_{0}+\lambda {\mbox{ ln }}\left({\frac {1-\lambda }{\lambda }}\right)\right]

where the last approximation assumes p 0 p_{0} to be small.

If λ = 1, then we have

D = ∫ 0 q 0 2 − q ( 1 − q ) 2 = ∫ 0 q 0 [ 1 1 − q + 1 ( 1 − q ) 2 ] d q = p 0 − 1 − ln p 0 + O ( λ K ) . D=\int _{0}^{{q_{{_{0}}}}}{\frac {2-q}{(1-q)^{2}}}=\int _{0}^{{q_{{_{0}}}}}\left[{\frac {1}{1-q}}+{\frac {1}{(1-q)^{2}}}\right]dq=p_{0}^{{-1}}-{\mbox{ ln }}p_{0}+O(\lambda K).

In his discussion Haldane writes that the substitution cost, if it is paid by juvenile deaths, "usually involves a number of deaths equal to about 10 or 20 times the number in a generation" – the minimum being the population size (= "the number in a generation") and rarely being 100 times that number. Haldane assumes 30 to be the mean value.[5]

Assuming substitution of genes to take place slowly, one gene at a time over n generations, the fitness of the species will fall below the optimum (achieved when the substitution is complete) by a factor of about 30/n, so long as this is small – small enough to prevent extinction. Haldane doubts that high intensities – such as in the case of the peppered moth – have occurred frequently and estimates that a value of n = 300 is a probable number of generations. This gives a selection intensity of I = 30 / 300 = 0.1 I=30/300=0.1.

Haldane then continues:[5]

The number of loci in a vertebrate species has been estimated at about 40,000. 'Good' species, even when closely related, may differ at several thousand loci, even if the differences at most of them are very slight. But it takes as many deaths, or their equivalents, to replace a gene by one producing a barely distinguishable phenotype as by one producing a very different one. If two species differ at 1000 loci, and the mean rate of gene substitution, as has been suggested, is one per 300 generations, it will take 300,000 generations to generate an interspecific difference. It may take a good deal more, for if an allele a1 is replaced by a10, the population may pass through stages where the commonest genotype is a1a1, a2a2, a3a3, and so on, successively, the various alleles in turn giving maximal fitness in the existing environment and the residual environment.[5]

The number 300 of generations is a conservative estimate for a slowly evolving species not at the brink of extinction by Haldane's calculation. For a difference of at least 1,000 genes, 300,000 generations might be needed – maybe more, if some gene runs through more than one optimisation.
Origin of the term "Haldane's dilemma"

Apparently the first use of the term "Haldane's dilemma" was by paleontologist Leigh Van Valen in his 1963 paper "Haldane's Dilemma, Evolutionary Rates, and Heterosis".

Van Valen writes:[8]

Haldane (1957 [= The Cost of Natural Selection]) drew attention to the fact that in the process of the evolutionary substitution of one allele for another, at any intensity of selection and no matter how slight the importance of the locus, a substantial number of individuals would usually be lost because they did not already possess the new allele. Kimura (1960, 1961) has referred to this loss as the substitutional (or evolutional) load, but because it necessarily involves either a completely new mutation or (more usually) previous change in the environment or the genome, I like to think of it as a dilemma for the population: for most organisms, rapid turnover in a few genes precludes rapid turnover in the others. A corollary of this is that, if an environmental change occurs that necessitates the rather rapid replacement of several genes if a population is to survive, the population becomes extinct.[8]

That is, since a high number of deaths are required to fix one gene rapidly, and dead organisms do not reproduce, fixation of more than one gene simultaneously would conflict. Note that Haldane's model assumes independence of genes at different loci; if the selection intensity is 0.1 for each gene moving towards fixation, and there are N such genes, then the reproductive capacity of the species will be lowered to 0.9N times the original capacity. Therefore, if it is necessary for the population to fix more than one gene, it may not have reproductive capacity to counter the deaths.
Evolution above Haldane's limit

Various models evolve at rates above Haldane's limit.

J. A. Sved[9] showed that a threshold model of selection, where individuals with a phenotype less than the threshold die and individuals with a phenotype above the threshold are all equally fit, allows for a greater substitution rate than Haldane's model (though no obvious upper limit was found, though tentative paths to calculate one were examined e.g. the death rate). John Maynard Smith[10] and Peter O'Donald[11] followed on the same track.

Additionally, the effects of density-dependent processes, epistasis, and soft selective sweeps on the maximum rate of substitution have been examined.[12]

By looking at the polymorphisms within species and divergence between species an estimate can be obtained for the fraction of substitutions that occur due to selection. This parameter is generally called alpha (hence DFE-alpha), and appears to be large in some species, although almost all approaches suggest that the human-chimp divergence was primarily neutral. However, if divergence between Drosophila species was as adaptive as the alpha parameter suggests, then it would exceed Haldane's limit.
See also

Error catastrophe
Genetic drift
Genetic load
Muller's ratchet

References

Sanford J, Brewer W, Smith F, Baumgardner J (September 2015). "The waiting time problem in a model hominin population". Theoretical Biology & Medical Modelling. 12 (1): 18. doi:10.1186/s12976-015-0016-z. PMC 4573302. PMID 26376851.
Kimura M (February 1968). "Evolutionary rate at the molecular level". Nature. 217 (5129): 624–6. Bibcode:1968Natur.217..624K. doi:10.1038/217624a0. PMID 5637732. S2CID 4161261.
Jensen JD, Payseur BA, Stephan W, Aquadro CF, Lynch M, Charlesworth D, Charlesworth B (January 2019). "The importance of the Neutral Theory in 1968 and 50 years on: A response to Kern and Hahn 2018". Evolution; International Journal of Organic Evolution. 73 (1): 111–114. doi:10.1111/evo.13650. PMC 6496948. PMID 30460993.
Kern AD, Hahn MW (June 2018). "The Neutral Theory in Light of Natural Selection". Molecular Biology and Evolution. 35 (6): 1366–1371. doi:10.1093/molbev/msy092. PMC 5967545. PMID 29722831.
Haldane JB. "The Cost of Natural Selection" (PDF). J. Genet. 55 (511–524): 1957.
Majerus ME (1998). Melanism: Evolution in Action. New York: Oxford University Press.
See Haldane.[5] If a = 1 − s 0 {\displaystyle a=1-s_{0}} and b = 1 − S {\displaystyle b=1-S}, then I = ln ⁡ ( 1 − a ) − ln ⁡ ( 1 − b ) ≈ − a + b = s 0 − S {\displaystyle I=\ln(1-a)-\ln(1-b)\approx -a+b=s_{0}-S} .
Van Valen L (1963). "Haldane's Dilemma, evolutionary rates, and heterosis". Am. Nat. 47 (894): 185–190. doi:10.1086/282267. S2CID 222327449.
Sved JA (June 1968). "Possible Rates of Gene Substitution in Evolution". American Naturalist. 102 (925): 283–93. doi:10.1086/282542. S2CID 84618125.
Maynard Smith J (September 1968). ""Haldane's dilemma" and the rate of evolution". Nature. 219 (5159): 1114–6. Bibcode:1968Natur.219.1114S. doi:10.1038/2191114a0. PMID 5675622. S2CID 864709.
O'Donald P (March 1969). ""Haldane's dilemma" and the Rate of Natural Selection". Nature. 221 (5183): 815–6. Bibcode:1969Natur.221..815O. doi:10.1038/221815a0. PMID 5765051. S2CID 4288246.

Nunney L (January 2003). "The cost of natural selection revisited" (PDF). Annales Zoologici Fennici. Finnish Zoological and Botanical Publishing Board. 40: 185–194.

Further reading

Grant V, Flake RH (October 1974). "Solutions to the cost-of-selection dilemma". Proceedings of the National Academy of Sciences of the United States of America. 71 (10): 3863–5. Bibcode:1974PNAS...71.3863G. doi:10.1073/pnas.71.10.3863. PMC 434284. PMID 4530266.
Nunney L (January 2003). "The cost of natural selection revisited" (PDF). Annales Zoologici Fennici. Finnish Zoological and Botanical Publishing Board. 40: 185–194. (This paper describes computer simulations of small populations with variations in mutation rate and other factors, and produces results that are dramatically different from Haldane's low substitution limit except in certain limited situations).
https://en.wikipedia.org/wiki/Haldane%2 ... ne's_limit"

[EarthScienceguy]

[Replying to The Barbarian in post #0]

Imagine a population of 100,000 apes, the putative progenitors of humans. Suppose that a male and a female both received a mutation so beneficial that they out-survived everyone else; all the rest of the population died out—all 99,998 of them.

Genetic analysis shows that did not happen in the line that led to modern humans, and I can't think of a case where it has happened. You have an example?

No this is a hypothetical example.

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?

Again it is not going to work it is a hypothetical situation to produce the best possible outcome.

And this repeated every generation (every 20 years) for 10 million years, more than the supposed time since the last common ancestor of humans and apes. That would mean that 500,000 beneficial mutations could be added to the population (i.e., 10,000,000/20).

Each of us has about 100 mutations that weren't present in either of our parents. So let's say that 0.01percent of all mutations are favorable. In a population of 100,000 individuals, we'd then have about 1000 favorable mutations per generation. Since we observe that a mutation harmful enough to prevent one from leaving offspring is rather rare in humans (let's say 10%, a gross overestimate). So about 100 favorable mutations per generation.

You have a couple of issues here.

• 1st. You are not reading the hypothetical situation correctly. Every 20 years all of the offspring die off but 2. This would mean there would be 500,000 beneficial mutations.

• 2nd. In your example where does the 0.01 percent mutations that are favorable come from? Most mutations are neutral like 90% and 10% are deleterious. Beneficial mutations are almost nonexistent. For example in Lenski's experiment of e-coli there were 12 so-called beneficial mutations in 70,000 generations. That would mean that 1.4E-4 beneficial mutations/generation. That would be 12 beneficial mutations in population size of trillions. But let's say it was only a population of 1 billion. That means that 1.4 E-13 beneficial mutation*Individual/generation.
  
  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.

Humans have about 30,000 genes. So this is why we have dozens of alleles for each gene locus. There's been a lot of evolution. Keep in mind that Adam and Eve could have had at most, 4 alleles for each gene locus. The rest evolved.

Experimental evidence shows that there is very little variation actually only a few thousand years worth.

• 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.

• Knight et al.9 have had similar research results: ‘We obtained over 55 kilobases of sequence from three autosomal loci encompassing Alu repeats for representatives of diverse human populations as well as orthologous sequences for other hominoid species at one of these loci. Nucleotide diversity was exceedingly low. Most individuals and populations were identical. Only a single nucleotide difference distinguished presumed ancestral alleles from descendants. These results differ from those expected if alleles from divergent archaic populations were maintained through multiregional continuity. The observed virtual lack of sequence polymorphism is the signature of a recent single origin for modern humans, with general replacement of archaic populations.’ Knight, A., Batzer, M.A., Stoneking, M., Tiwari, H.K., Scheer, W.D., Herrera, R.J. and Deininger, P.L., DNA sequences of Alu elements indicate a recent replacement of the human autosomal genetic complement, Proc. Nat. Acad. Sci. USA 93(9):4360–4364, 1996.

This would mean in ten million years, about 50,000,000 useful mutations.

Even if that was true only 70 would be expressed. Although I am not sure where your 0.01% comes from.

You realize that 50,000,000 is larger than 30,000, right?

You do realize that 30,000 is much larger than 70 and that experimental evidence suggest very little variation in the human genome.

No. You're assuming that all the DNA differences between humans and chimps are functional. But that's demonstrably wrong.

Are you trying to make the case that Junk DNA is not used?

But it is being found that pseudogenes do have functions.

• Our findings demonstrate a specific regulatory role of an expressed pseudogene, and point to the functional significance of non-coding RNAs.’ Hirotsune, S., Yoshida, N., et al., An expressed pseudogene regulates the messenger-RNA stability of its homologous coding gene, Nature 423:91–96, 2003.

• The functional Makorin1-p1 pseudogene is described as the first known instance of a biological function for any pseudogene. Actually, this is not correct. The two earlier-described snail pseudogenes, antiNOS-1 and antiNOS-2, are also examples of functional pseudogenes.18,19
  Lee, J.T., Complicity of gene and pseudogene, Nature 423:26–28, 2003.
  Woodmorappe, J., Unconventional gene behavior and its relationship to pseudogenes, Proceedings of the Fifth International Conference on Creationism: Technical Symposium Sessions, pp. 505–514, 2003.

• With respect to the evolution of regulatory functions of pseudogenes, we must now conclude that transcribed pseudogenes are not necessarily without function. Indeed, they would appear to be especially suited to roles involving the antisense regulation of the active genes to which they are related.’Korneev, S. and O‘Shea, M., Evolution of nitric oxide synthase regulatory genes by DNA inversion, Molecular Biology and Evolution 19:1228–1233, 200

• A pseudogene arises when a gene loses the ability to produce a protein, which can be due to mutation or inaccurate duplication. Previous dogma has dictated that because the pseudogene no longer produces a protein it becomes functionless and evolutionarily inert, being neither conserved nor removed. However, recent evidence has forced a re-evaluation of this view. Some pseudogenes, although not translated into protein, are at least transcribed into RNA. In some cases, these pseudogene transcripts are capable of influencing the activity of other genes that code for proteins, thereby altering expression and in turn affecting the phenotype of the organism. In the present chapter, we will define pseudogenes, describe the evidence that they are transcribed into non-coding RNAs and outline the mechanisms by which they are able to influence the machinery of the eukaryotic cell. https://portlandpress.com/essaysbiochem ... m=fulltext

• Pseudogenes have long been labeled as “junk” DNA, failed copies of genes that arise during the evolution of genomes. However, recent results are challenging this moniker; indeed, some pseudogenes appear to harbor the potential to regulate their protein-coding cousins. Far from being silent relics, many pseudogenes are transcribed into RNA, some exhibiting a tissue-specific pattern of activation. Pseudogene transcripts can be processed into short interfering RNAs that regulate coding genes through the RNAi pathway. In another remarkable discovery, it has been shown that pseudogenes are capable of regulating tumor suppressors and oncogenes by acting as microRNA decoys. The finding that pseudogenes are often deregulated during cancer progression warrants further investigation into the true extent of pseudogene function. In this review, we describe the ways in which pseudogenes exert their effect on coding genes and explore the role of pseudogenes in the increasingly complex web of noncoding RNA that contributes to normal cellular regulation. https://rnajournal.cshlp.org/content/17/5/792.full

You cannot say that most of the pseudogenes have no function because it has not been explored. The function is different than from coding DNA but pseudogenes are being shown to be far from useless.

[EarthScienceguy]

[Replying to Jose Fly in post #171]

Wow....this is unbelievable. In the same post, you actually say "rapid speciation does not happen" and "I do support the Biblical flood model so yes there would have to be a rapid adaptation and speciation".

Well, yes this is the first time I have argued through this with anyone. The next time I do will be much better.

But you still have major problems with your argument.

• 1st you still have to give me an example of rapid speciation. Using the evolutionary definition of speciation. And I am pretty sure you will not because of the evolutionary definition of species.

• 2nd There is a problem with the evolutionary definition of speciation. Which is defined as: "a group of living organisms consisting of similar individuals capable of exchanging genes or interbreeding." The problem is that this is not true.

In my previous post I showed how this evolutionary definition of species is not true. With the example of the Camel and Lama.

Camel
Kingdom: Animalia
Phylum: Chordata
Class: Mammalia
Order: Artiodactyla
Family: Camelidae
Tribe: Camelini
Genus: Camelus
Type species
Camelus dromedarius

Lama
Kingdom: Animalia
Phylum: Chordata
Class: Mammalia
Order: Artiodactyla
Family: Camelidae
Genus: Lama
Species: L. glama

A camel and a lama can mate they can interbreed. The closest relation they are family. So how is it that these two species can mate?
Wolves, coyotes and dogs: three distinct species that can interbreed. In fact, all species of the genus Canis can mate and produce fertile offspring (Wayne et al., 1997, re: A. P. Gray, Mammalian Hybrids).

So yes I do believe in rapid speciation but not in the evolutionary sense. The observational evidence actually confirms the creationist view of kinds. Which says that most animals can interbreed up to the classification of the family.

So you will not find any example of speciation using the evolutionary definition of species. But there are many examples of species (breeds) using the creationist definition.