But not all of them. It’s interesting that even the most hardened creationists who have exposure to some science still cannot quite bring themselves to rule out the possibility of a beneficial mutation. Here’s Sal:
Much (not all) the heterozygosity and alleles were created and thus differences were strategically positioned to not cause functional compromise and most of the mutations thereafter are rare variants and slightly damaging.
So if most are slightly damaging then a few are beneficial. And if a few are beneficial then even fewer will be highly beneficial.
It’s not just Sal, but many IDCreationists seem to allow the possibility that a mutation may occur that is beneficial. Indirectly, of course, usually similarly phrased to the above. I don’t even think most of them know they are doing it.
So, Sal et al. What is it that is stopping the tiny number of beneficial mutations that you unwittingly admit happens spreading in a population? As presumably what you give with one hand you take away with the other. There must be some other mechanism preventing that, otherwise you are basically agreeing with the evilutionists. That is the topic of this thread.
Go team!
Might want to edit a fold into this @admin
They often want to conclude that if most mutations are deleterious, that the net result must be a decline in fitness. This ignores natural selection. If people find out how much more often advantageous mutations get fixed, they will see that just asking about the rates of deleterious versus advantageous mutations can be highly misleading. See for example my post on this at PT here.
Creationists often times don’t understand the difference between mutations that HAPPEN and mutations that GET FIXED. Deleterious and lethal mutations happen, but nevertheless during adaptive evolution, but those that carry them die more often, so the result is that most mutations that are fixed are neutral or beneficial.
Figure from Barrick & Lenski. Genome dynamics during experimental evolution. Nat Rev Genet. 2013 Dec;14(12):827-39. doi: 10.1038/nrg3564
Evilutionists often times don’t understand the difference between mutations that HAPPEN and mutations that GET FIXED and mutations that JUST HAPPEN to GET FIXED.
Slight comfort indeed.
A hardened yEC creationist demands evidence mutations ever mattered in biology.
Except to hurt.
Turning fish into rhinos by a trail of mutations beggers evidence.
Surely this never happened.
the glory and creative ability evolutionists give mutations easily can be instead a glory of the genetic system.
Its just complicated, even for tailless primates, and has yet to be figured out.
its more complicated then physics(things bumping into each other) and they gaga about figuring out that stuff.
Too quick they were to say biological origins and relationships were explained by old man Darwin superficially looking at corals.
Bare possibility and convenient narrative saves the day for evolution once again!
“Considering genetic drift, i.e. random fluctuations of gene frequencies in populations, Griffith and colleagues state in agreement with these authors (1999, p. 564):
Even a new mutation that is slightly favorable will usually be lost in the first few generations after it appears in the population, a victim of genetic drift. If a new mutation has a selective advantage of S in the heterozygote in which it appears, then the chance is only 2S that the mutation will ever succeed in taking over the population. So a mutation that is 1 percent better in fitness than the standard allele in the population will be lost 98 percent of the time by genetic drift.”
And this my friend is exactly why I call out Allan and Joe every time they want to play their shell game and count fitness as genes instead of individuals. Gens don’t reproduce, organisms do, thus you will never know which gene was the one responsible for the reproduction advantage. Was it the blond hair, or the longer legs, or the gene which prevents cancer, or the better lung capacity, or the gene for tongue rolling, or the gene for a longer tail, or one for strong claws, or one for nest building, or the gene for venom, was it because they were strong, or because they were fast, or because they were dumb, or because they were nervous, or the gene for color-blindness, or the gene for a bigger liver…You will never know or be able to count.
The concept of fitness is bullshit, and so claiming that some mutations were disadvantageous but thrived, is just as specious as claiming that some mutation was advantageous but declined. Allan like to make the comparison to sports, claiming that just because it is self-evident that the fastest runner is the winner, that doesn’t make it any less true. And yet, SOMETIMES, in the materialists shell game the fastest runner is the loser. You just don’t know when and why.
Design does ok, an unknown something at an unknown time somehow caused something is a pretty narrative.
Sometimes you do,
“Beneficial” mutations in the Darwinian world can mean all sorts of things. In humans sickle cell anemia, Tay sachs are considered “beneficial” by evolutionary biologists, but in the medical community these are considered illness. In the world of other creatures, blindness in cavefish, winglessness in beetles, loss of organs in parasites are “beneficial”.
So yeah, “beneficial” mutations exist because Darwinists twist the notion of what is good and bad. I’m not alone in this, Allen Orr crticized Daniel Dennett. Orr referenced the creature called Gammarus Minus. I guess it is called minus becaused it beneficially “acquired” blindess.
I posted on the absurdity of the notion of “beneficial” in the Dariwnian world and related Orr’s choice words for Daniel Dennett:
and then I pointed out the absurdity of claiming the persistence of heritable disease as evidence in favor of Darwinism!
Thus, I soured on the idea that mathematics of how Selection coefficients evolve a population really describes what Darwinian selection was supposed to do, since “beneficial” has been re-defined and equivocated so as to become meaningless, or even worse in some case — to mean the opposite of what you think it should mean, since in the world of Darwin, losing organs and limbs and function are considered “beneficial” since it may increase differential reproductive success in the short term.
However, as Delbert Wiens and Stanley Salthe pointed out, this short term benefit can come at a long term cost. Both argue, somewhat qualitatively, through population genetics, that this can almost be inevitable. Wiens goes even farther to say this increase in “fitness” in the short term, after an environmental perturbation, leads to extinction. So “beneficial” is a debatable term.
Unless the beneficial mutation has a strong enough sustained selection pressure, it is likely to be eliminated by drift, especially if only arises once in the population and never appears again. This is the problem of Gambler’s ruin.
If the selection pressure coefficient is small enough, it can be approximately modeled as neutral. Also, random gametic sampling can wipe out a new mutation in the first round. So if Daddy has the mutation, junior only has half a chance of getting it. In that case, the beneficial is Dead on Arrival! Factor in spontaneous abortions in the womb, and oh well… the chances are even less because of the grim reaper.
So, if you doubt me, ask the my critics how long then expect a new beneficial mutation that just arrived in some baby somewhere, ask the experts here how long it will take and how probable it is that one day all human beings on the planet will have this new trait. There are 7-8 billion people on the planet. Ask them how long the process will be when all their descendants, maybe also in the billions will have this new beneficial trait. Next, ask them if they are aware of some selectively advantaged trait that they believe is in the minority of the population, say less than 1% that will overtake the global population.
Seriously ask! I will let them argue their case and you decide if what they say is believable.
Well, at least evolution isn’t trying to promote the factuality of a flying priest.
Who would be better at keeping the aliens away?
Glen Davidson
Anyone notice the world “usually” there? So therefore, unusually, it won’t be lost in the first few generations.
You are proving my point nicely J-Mac
In fact it’s the opposite. I’m asking what magic stops all beneficial mutations spreading. You don’t have an answer for that it appears.
Your statement would have some value in the event that evolution was stumped at the problem of beneficial mutations. But as usual you have missed the point. The point was even creationists admit beneficial mutations happen but they have failed to say why they cannot propagate.
But then again, what with boarding up the windows to prevent the next alien abduction I imagine you are somewhat busy.
In the history of life how many generations have there been? Given that, what is your claim? That it is impossible for beneficial mutations to spread? You’ve just demonstrated otherwise.
So if beneficial mutations can spread, why are you a creationist?
So then you are in agreement with the OP that SOMETIMES the fastest runner is the winner. And that’s all that is required.
You lose as you cannot now say what it is that prevents those SOMETIMES winners winning again.
And yet we have your fellow creationists approvingly quoting darwinist literature in support of the idea that beneficial mutations happen.
No it’s just math, logic and evidence.
And not lost 2 percent of the time.
Do events with a probability of 2% happen? Yes.
Only “likely”? So sometimes it will spread even without a strong enough sustained selection pressure.
And those that have a sustained selection pressure are even more likely to spread?
You are unwittingly destroying your own argument and supporting the OP.
You do know that what you’ve written regarding the age of the earth, biology etc is still available to read? You’ve made your case and nobody here, even your fellow creationists, finds it believable. So that’s an odd metric for you to choose.
Count fitness as genes? What the fuck are you even talking about?
I don’t see what the word “thus” is doing in that sentence, because what comes after does not logically follow from what comes before. At all.
Yet, in the real world, we do know, because we can in fact test that and count it. You simple measure the average reproductive success of all the carriers you can find, with all the non-carriers you can find.
People with an IQ above 90 should be able to understand why, what I just said, allows you to determine the effect of the allele in question. It takes the ability and willingness to think. Phoodoo might be able, but he’s not willing, so he won’t get it.
There is nothing specious about that. In fact you go on to give an analogy that makes perfect sense of how this can be. Accidents can happen.
This doesn’t even make sense. We usually know both. Simply by observation and interaction. If Usain bolt is last in a race, we observe that he is last in the race (and therefore you know when he was last in the race), and then somebody goes and asks him what happned? Then he might say “I sprained my ankle at the beginning”.
There isn’t a level at which your argument against the concept of fitness, fails. In totality. Of all the things uttered on this whole website, your “argument” against the concept of fitness is the most incoherent and thoroughly failing of them all.
phoodoo is objecting when we attribute fitness to genotypes at particular loci. phoodoo thinks that fitness only makes sense when it is the fitness of an individual. And that even then, fitness does not make sense. Or something. Meanwhile the whole field of population genetics ignores phoodoo’s great discovery.
How can they not realize that everything they are doing has been decisively refuted? Or whatever.
The point you raise is not entirely without merit, but still you must realise it can’t be a problem.
Our soccer team won!! Which player was responsible for that? No one in particular, but it is still reasonable to suppose that our team has several top-notch players.
In the evolutionary case, there are many soccer teams. A particular position (A) may be played by player A1, player A2, etc. And each player shows up in that position on many, but not all teams. And different combinations of players are present on different teams. So there is room for statistical study of the player’s effect on the fitness of the team. But phoodoo does not get that.
How can a beneficial (or even non-deleterious) mutation arise in the fine tuned interlaced molecular networks that you often advocate? You have conceded that the designer can introduce non-synonymous alleles into a species without disrupting the network. If such mutations are possible in principle, then what prevents them from spontaneously arising?
Corneel,
I will reply to this later when I have more time.
There’s no way of knowing which color people tend to like the most for their cars, even if some colors sell better than others we have no idea if John Doe got his red car because he liked the upholstery
#phoodoologic
phoodoo,
Yeah, we all quake in our boots when Phoodoo Of The Internet goes off on one.
Yes, sometimes, because the process is stochastic, that’s what happens. As in sport, as in life. The problem with stochastic processes is that you can’t have perfect foreknowledge of the result. That’s why they’re stochastic. If you did, they wouldn’t be stochastic. So this particular inventive criticism against evolution is that it has no fucking business being stochastic, if it were true.
Hoist once more upon the inability of Creationists to grasp probability, I’m afraid. Even Sal, gambler of note. If one can argue on the occasional case of something beneficial being lost on one run, then that’s what always happens. Despite the LLN.
Counting cards in blackjack never works, because sometimes it gives the wrong answer.
stochastic = random = evil materialism
That’s all the math creationists need
Multiple Overlapping Genetic Codes Profoundly
Reduce the Probability of Beneficial Mutation
”
Abstract
There is growing evidence that much of the DNA in higher genomes is poly-functional, with the
same nucleotide contributing to more than one type of code. Such poly-functional DNA should
logically be multiply-constrained in terms of the probability of sequence improvement via random
mutation. We describe a model of this relationship, which relates the degree of poly-functionality
and the degree of constraint on mutational improvement. We show that: a) the probability of
beneficial mutation is inversely related to the degree that a sequence is already optimized for a given
code; b) the probability of beneficial mutation drastically diminishes as the number of overlapping
codes increases. The growing evidence for a high degree of optimization in biological systems, and
the growing evidence for multiple levels of poly-functionality within DNA, both suggest that mutations
that are unambiguously beneficial must be especially rare. The theoretical scarcity of beneficial
mutations is compounded by the fact that most of the beneficial mutations that do arise should confer
extremely small increments of improvement in terms of total biological function. This makes such
mutations invisible to natural selection. Beneficial mutations that are below a population’s selection
threshold are effectively neutral in terms of selection, and so should be entirely unproductive from
an evolutionary perspective.
We conclude that beneficial mutations that are unambiguous (not deleterious
at any level), and useful (subject to natural selection), should be extremely rare.
1. Introduction
It is almost universally acknowledged that beneficial mutations are rare compared
to deleterious mutations [1–10]. However, there is controversy regarding just how
rare beneficial mutations actually are. It appears that beneficial mutations may be
too rare to actually allow the accurate measurement of how rare they are …
….Our analysis suggests that increasing either the number of overlapping codes or
the degree of optimization has negative effects on the probability of producing a
beneficial mutation. A high degree of optimization makes beneficial mutations
unlikely — even when considering just one code. As more codes are considered,
the probability of beneficial mutation diminishes rapidly, as is shown in Figures 3,
4 and 5. The ratio of beneficial to deleterious mutations decreases so rapidly that
for L3 nucleotides in highly optimized sequences, the number of deleterious mutations
expected before the first beneficial arose would be greater than the genome
size of a typical bacterium. For L5 nucleotides, the number of deleterious mutations
expected before the first beneficial arose would be greater than the genome
size of a typical mammal. While relaxing the optimization assumption reduces the
severity of the problem (as can be seen in Figure 4), increasing the number of
overlapping codes diminishes the likelihood of attaining a net beneficial mutation
even for weakly optimized systems. If we allow, within a functional sequence, for
overall optimization values as low as 50%, deleterious mutations remain roughly
a thousand times more likely than beneficial mutations in the presence of twelve
overlapping codes. As the organism becomes more optimized, the probability of
receiving an overall beneficial mutation falls rapidly….
3. Discussion
Beneficial mutations in nature appear to be so rare that after decades of research
we still cannot empirically determine just how rare they are [11]. This suggests
they are very rare indeed. There are many reasons to believe that beneficial mutations
must be very rare….
4. Conclusions
Our analysis confirms mathematically what would seem intuitively obvious —
multiple overlapping codes within the genome must radically change our expectations
regarding the rate of beneficial mutations.
As the number of overlapping
codes increases, the rate of potential beneficial mutation decreases exponentially,
quickly approaching zero. Therefore the new evidence for ubiquitous overlapping
codes in higher genomes strongly indicates that beneficial mutations should be
extremely rare. This evidence combined with increasing evidence that biological
systems are highly optimized, and evidence that only relatively high-impact beneficial
mutations can be effectively amplified by natural selection, lead us to conclude
that mutations which are both selectable and unambiguously beneficial must
be vanishingly rare. This conclusion raises serious questions. How might such
vanishingly rare beneficial mutations ever be sufficient for genome building? How
might genetic degeneration ever be averted, given the continuous accumulation of
low impact deleterious mutations?
http://www.cs.cmu.edu/~gmontane/pdfs/montanez-binps-2013.pdf
It can, but it is a low probability event far from expectation. To visualize the problem, a random mechanism like a tornado can’t be reasonably expected to create a configuration like the one depicted below which I built. One doesn’t have to build something exactly like the one I built. In fact there are an infinite variety of possible configurations of cards and dominos, but some configurations just aren’t reasonably expected of a random (uncertainty inducing) process:
J-mac cites another excellent paper co-authored by John Sanford. 🙂
stcordova,
Say no more.
I was referring especially to the Kimura’s theories that most molecular evolution is neutral. The smaller the population the less effective selection becomes because of Ohta’s formula:
s lessthan 1/Ne,
so if Ne is small, selection pressure low, and further, it cannot be distributed to too many traits. Say a founding couple of a population have 2 kids in the extreme case. Selection for traits isn’t very particulate is it? You can’t simultaneously select effectively for 1000 traits in such a situation, so that shows population size is important.
On the other hand with large population sizes you get into other difficulties. You could try to answer the question I posed now that we have a global population of 7-8 billion people. How many new selectively favored traits that you see in the population today but only reside in a minority of individuals?
Name a few, seriously, that you think will overtake the population in 1 million years. Can you name 10 traits, 5 traits, 1 trait (well maybe adult milk digestion, but we’ll see). This is relevant to OMagain’s question. If you can only name 1 or 2 measily such traits you expect to fix into the human global population over then next million years, I think you highlight the problem quite well. You guys swear by natural selection, but you can’t find good examples of it for human populations today. If you can’t find good examples of it today, then what business do you have asserting it as truth for all time?
Why? Look at his Vitae:
stcordova,
Credential mongering. I could show you the credentials of people who think Creationism utter bunk. Would that persuade you one iota of the validity of their arguments?
Sanford has made real advances, but – sorry to do the Reverse Argument From Authority – he is a Creationist and hence takes the one-eyed approach to science typical of his (your) ilk when it impinges on his religion.
I might ask where is the peer review of his paper?
Ann Gauger stumbled upon a beneficial mutation in one of her experiments. Creationists debunking their own crap. Priceless
stcordova,
The future pattern in our slightly unusual population (small Ne, vast census size, growing) tells us zip about historical evolution. Unless you think that all populations ever were huge with a small Ne and growing. Another gem for the this-therefore-all shelf, one above few-therefore-none.
Sandford et all: “Beneficial mutations that are below a population’s selection threshold are effectively neutral in terms of selection, and so should be entirely unproductive from an evolutionary perspective”
So for the authors of this paper, neutral evolution is “unproductive from an evolutionary perspective”. Do they back that up at all?
To OMagain’s question:
Gee, maybe I could be persuaded I’m wrong if the TSZ Darwinists could identify 10 traits that are only in a minority of individuals today that they expect will spread and overtake the global population. Adult milk digestion is about the only one I’ve heard so far.
If they can’t give answers, then they should explain why they can’t give answers. Thus they can give OMagain a better answer than I can. C’mon guys, have at it. 🙂
dazz,
He misses the LLN thing again. If the ‘selection threshold’ is (say) 0.001, each allele with selection coefficient below that will ‘act neutral’. But one would still expect an excess of fixations of beneficial mutation over the long run, even if all were below that threshold when considered in a single run through the smaller population. Two serial tries with two beneficial alleles with the same selection coefficient in a population of 1,000 are equivalent to one try of a single such allele in a population of 2,000, in terms of the probability that a beneficial allele will fix at the end (eta – I think!). The pool of beneficial alleles can cross the threshold, when one alone cannot.
Allan Miller,
Allan,
The OP was “most of the mutations”, what you point out is most of the beneficials will be lost. Thank you very much for proving my point.
But to OMagain’s question….
How about a list of 10 traits that are only in a minority of human individuals today that you expect will spread and overtake the global population. Since you’re so confident I’m wrong, surely you can provide 10 measily traits out of the possible tens of thousands.
Lets try to quantify what “tiny” number of highly beneficials mean. Here’s a teachable moment for OMagain. So far, “tiny” is closer to zero than it is to 10.
C’mon guys, where’s your list. Haven’t you guys been exercising your critical thinking skills and asking these sorts of questions about your own theory? This is The SKEPTICAL Zone (TSZ) after all, not Believe in Darwinism Blindly Zone (BDBZ).
If they occur, natural selection will increase their frequency in the population. But that is not my point now. This is:
Yes, you explained this many times. But the point is: these systems do not tolerate variation. They are like machines that need a specific configuration to keep working. That is what prevents them from evolving, right? Yet the originally created kinds needed to combine several configurations of later extant species, and of course modern sexual species have loads of functional variation, and are in the habit of exchanging it.
I see, thanks Allan.
Is “selection threshold” something he made up on the spot? Is he ignoring population size too? For all I know larger populations make selection increasingly more capable of getting mutations with low selection coefficient fixed
ETA: according to wikipedia, the threshold is one divided by the effective population size, so it’s a thing and doesn’t ignore population size
stcordova,
I was talking only of the beneficials with a selection coefficient below the neutral threshold – ie tendencies in smaller populations and for a particular fraction of the whole – and ‘most’ is an awfully vague number.
The absolute proportion fixing still depends on proportions produced, and the effectiveness of the population.
My argument also applies equally to slightly deleterious alleles. You (and Sanford) believe that they will accumulate and never be eliminated, again ignoring the effect of repeat runs approaching the LLN. Multiple runs of a smaller population are more efficient than any one. And, selection does not stop once an allele has fixed. If an allele is deleterious, it is more likely to be dislodged by new mutation than is an equivalent beneficial.