Why do we need to make a decision about common descent anyway?

_{Denyse O'Leary

August 5, 2014

Human evolution, Intelligent Design}

Share: Facebook; Twitter; LinkedIn; Flipboard; Print; Email

To “Why, exactly, should we believe that humans are descended from simpler forms of life?”, Mark Frank responds,

This is really very simple. Either:

1. We descended from a simpler form of life.

2. We descended from an equally complicated form of life which has left no trace.

3. We didn’t descend from any form of life but somehow sprang into existence (as adults I guess as human babies can’t survive by themselves).

Be honest – which seems the most plausible?

Actually, it is even simpler than Mark Frank makes out. Nothing is at issue if I just decline to offer an opinion.

His 1. would seem plausible except for the people shouting that we are 98 percent chimpanzee. And they’re the strongest supporters of common descent. They want it rammed down everyone’s throat from kindergarten to the retirement home.

Yet not only is their claim implausible on its face (anyone can tell the difference between a human and a chimpanzee), it is unsatisfactory. It leaves unaccounted for everything of which we would like an account.

His 2. is hardly implausible. It would be a familiar situation to any adopted child who can’t trace birth parents. As an account, is it unsatisfactory principally because it amounts to saying that there is no information available? That might be true, but I don’t know that it is.

His 3. is really not much different from 2., in that no further information about origins is likely to be available.

So the actual choice, assuming Frank’s list is exhaustive, is between an account offered by people whose judgement can be seriously questioned and accounts that point to the futility of seeking further information.

It’s a good thing Thomas Huxley coined the term agnostic (“it is wrong for a man to say he is certain of the objective truth of any proposition unless he can produce evidence which logically justifies that certainty”). That just about characterizes what I consider the wisest position just now on common descent.

See also: What can we responsibly believe about human evolution?

Follow UD News at Twitter!

Comments

WD400, the probability of getting two dice to sum to 7, depends on the probabilistic behaviour of both. And, in a joint mutation situation as implied, the result can boil down to the probability of two effectively independent events of similar probability "simultaneously" -- meaning without any significant population culling and shifting between that would materially change the pop patterns. In particular without eliminating A or moving A to massive over-representation. And in the end, any model brought up needs to account for the epidemiological evidence of extreme pop sizes and growth rates [10^12 parasites in ONE infected individual's blood, mut rates 10^-8, perhaps ten origins of Chloroquine resistance over some decades, a contrasting drug where a one point mut would pop up resistance in jut three patients]. And playing at dismissal games only shows what is wrong. Just to begin, do you accept that P(A AND B) is distinct from P(B | A)? That is one root of error. Second, do you accept that two effectively independent events A and B will occur jointly with P(A AND B) = P(A) * P(B)? [If you do, then kindly tell us why you speak in terms of "squaring" when it is actually such a multiplication, under relevant circumstances that makes roughly independent events a reasonable "good enough for govt work" model? If you think P(A) significantly affects P(B) kindly explain how, consistent with the reported epidemiological facts or better warranted facts on Chloroquine resistance. KFkairosfocus_{August 10, 2014
August
08
Aug
10
10
2014
10:49 AM
10
10
49
AM
PDT}

You seem to be attacking your own misunderstanding of what I have said. I'll repeat one more time: 1. The method AB mentioned is a perfectly reasonable way of explaining why the specific result if 1/6th. That's all I wanted to say. 2. You can't square the probability of getting one mutation in one generation to find the probability of getting two mutations eventually. It's remarkable to me that anyone would spend any time arguing those propositions. I'm certainly not going to spend any more time defending the obvious.wd400_{August 10, 2014
August
08
Aug
10
10
2014
10:10 AM
10
10
10
AM
PDT}

ouch on italicskairosfocus_{August 10, 2014
August
08
Aug
10
10
2014
04:45 AM
4
04
45
AM
PDT}

WD400: Please note my reference to the Rev Bayes, which was a clue pointing to context of reasoning. The famous Bayes Theorem pivots on precisely how probability of A AND B as events composing a joint event is different from the probability of B given A is already existing. However, there is a conflation of the two in A-B's remarks, which you have backed. Remarks that seem to be the basis for his contemptuous -- and fallacious -- dismissal of Behe's reasoning, with the loaded term, voodoo. (And BTW, A_B, that has a racial context of implicit contempt to esp. Haitian Blacks that you should be aware of and avoid.) Bayes' theorem pivots on the relationship: P(A|B) * P(B) = P(A AND B) . . . 1 Which then leads to the similar expression P(B | A) * P(A) = P( B AND A) . . . 2 From which, by commutation, we may deduce the Bayes theorem expression, in the form, which instantly translates into more familiar ones: P(A|B) * P(B) = P(B | A) * P(A) A necessary entailment of this, is that P (A|B) and P(A AND B) are quite definitively distinct. A-B's attempts to conflate the two are patently fallacious. Two dice tossed whether one go or in rapid succession have 6/36 chances of summing to seven. Though numerically the same as odds for one face of a single die, 1/6, the meaning is different. That's why Mung's seven sided (spindle) dice help. There are 49 possibilities now, and the first die can lock out a sum to 7 by coming up at 7, forcing the second die toss to go beyond 7. This underscores that we are dealing with a joint situation. Meaning is important, not just numerical value. In the context of drug resistance, two muts are req'd, and in light of the situation, we deal with a population of 10^12 parasites in a victim with a mut rate that suggests 10^4 copies of possible single muts. So, just three patients are enough (cf the Behe letter) for resistance to pop up to a drug that can be worked around by a 1-point mut. Of course, if a mut that confers resistance also lowers general fitness enough, it will not work, as it will be unable to compete otherwise. There is a further context of implied high incidence of use of the relevant drug, so that there is an effective selection pressure. A double mut can be had all at once in one cell, or in close succession in a patient or population of patients. The first option is obviously very rare. The second and third imply a context in which the first mut does not radically redefine the parasite population, i.e. it remains rare, and is not eliminated (e.g. by being fatal to the parasite). So, in that context, close sucession is effectively simultaneous and it is reasonable to analyse on p(A AND B) in all three cases. A_B's objection pivots on conflating that with P(B |A), which implies in effect mut A once it appears is quickly so dominant that the situation is diverse. This scenario is inconsistent with the reported observations on Chloroquine resistance. I add, the problem with involved exchanges in a polarised situation, is that it is likely for a chain of successive side tracks to emerge. The second order exchange on tossing two dice is a first example, and the attempt above to want to say that going into details on the implied pattern changes the situation is another. I suggest you read and respond to Behe, as clipped above, and that you address as well the distinction between the "intersection" probability P(A AND B) and the conditional one P(A GIVEN B is already in hand). Those will be first steps to addressing the actual matter in hand. KFkairosfocus_{August 10, 2014
August
08
Aug
10
10
2014
04:44 AM
4
04
44
AM
PDT}

Mung:
What does it even mean to say that two events are cumulative?
Acartia_bogart:
Sorry, but some people were obviously having a problem with the word sequential.
You thought that by introducing more ambiguity you could produce clarity?Mung_{August 9, 2014
August
08
Aug
9
09
2014
07:16 PM
7
07
16
PM
PDT}

wd400:
I said AB post showed one way that you can understand why the probability was 1/6th in the particular case. That’s all.
You did say this, but that doesn't mean it's true. A die with six faces where each face contains a symbol representing the integers 1 through 6, and when the die is tossed each face is equally likely to appear (or not), no matter how many times it is tossed, no matter what probability is assigned to each face, cannot produce a SEVEN. The idea that there is a 1/6 chance of producing a SEVEN is simply ludicrous.Mung_{August 9, 2014
August
08
Aug
9
09
2014
07:08 PM
7
07
08
PM
PDT}

Mung: "What does it even mean to say that two events are cumulative? Sorry, but some people were obviously having a problem with the word sequential.Acartia_bogart_{August 9, 2014
August
08
Aug
9
09
2014
06:37 PM
6
06
37
PM
PDT}

KF, as ever I'm left with no idea what point you think you are making. I said AB post showed one way that you can understand why the probability was 1/6th in the particular case. That's all. The rest of your comment again shows why quierius was wrong to say simultaneous and sequential are equivalent in this case:
either a double mut in a single cell, or a first mut sufficiently viable to be around for the 2nd mut to hit it, and not sufficiently superior to dominate the pop or sufficiently bad to be eliminated
wd400_{August 9, 2014
August
08
Aug
9
09
2014
06:18 PM
6
06
18
PM
PDT}

Wd400, of course you did put up a strawman, or rather back a strawman play. The issue is NOT getting to 7 given die a already tossed, but tossing two dice whether simultaneously or in succession. And with the underlying malaria case, it's either a double mut in a single cell, or a first mut sufficiently viable to be around for the 2nd mut to hit it, and not sufficiently superior to dominate the pop or sufficiently bad to be eliminated. But, if you struggle to see that tossing two dice is not the same as tossing a second die on condition of the value of a first, the problem is at basic level. P(A AND B) is not the same as P(B | A), as say the good Rev Bayes knew quite well. KFkairosfocus_{August 9, 2014
August
08
Aug
9
09
2014
06:07 PM
6
06
07
PM
PDT}

F/N: It's probably worth the while to clip Behe's full letter: ___________ >> Dear Professors Miller and Myers, Talk is cheap. Let's see your numbers. In your recent post on and earlier reviews of my book The Edge of Evolution you toss out a lot of words, but no calculations. You downplay FRS Nicholas White's straightforward estimate that -- considering the number of cells per malaria patient (a trillion), times the number of ill people over the years (billions), divided by the number of independent events (fewer than ten) -- the development of chloroquine-resistance in malaria is an event of probability about 1 in 1020 malaria-cell replications. Okay, if you don't like that, what's your estimate? Let's see your numbers. The malaria literature shows strong population genetics evidence for fewer than ten independent origins of resistance. The riddle is, why so few? Show us all your calculation for that. Here's a number to keep in mind -- 1012. That's roughly the number of malarial cells in one sick person. Here's another -- 10-8. That's a generous rounding-up of the mutation rate for malaria. (Multicellular eukaryotes are an order of magnitude less.) That means on average ten thousand copies of each and every point mutation of the malarial genome will be present in every person being treated with chloroquine. Here's another -- 3. That's the number of patients it takes for spontaneous resistance to atovaquone to appear. That makes a lot of sense since resistance to atovaquone needs only one point mutation. If atovaquone were used as widely as chloroquine, we'd expect about a billion or more origins of resistance to it by now, not a measly handful. So how do you quantitatively account for that difference -- give or take an order of magnitude? Your chief complaint against my ideas seems to be this: That the malaria parasite needs two mutations was never a point of contention, nor was it particularly worrisome. What was wrong with Behe's work is that he naïvely claimed that the two mutations had to occur simultaneously in the same individual organism, so that the probability that could happen was the product of multiplying the two individual probabilities. That's ridiculous. What's puzzling to me is your thinking the exact route to resistance matters much when the bottom line is that it's an event of probability 1 in 1020. From the sequence and laboratory evidence it's utterly parsimonious and consistent with all the data -- especially including the extreme rarity of the origin of chloroquine resistance -- to think that a first, required mutation to PfCRT is strongly deleterious while the second may partially rescue the normal, required function of the protein, plus confer low chloroquine transport activity. Those two required mutations -- including an individually deleterious one which would not be expected to segregate in the population at a significant frequency -- by themselves go a long way (on a log scale, of course) to accounting for the figure of 1 in 1020, perhaps 1 in 1015 to 1016 of it (roughly from the square of the point mutation rate up to an order of magnitude more than it). So how do your calculations account for it? It's also entirely reasonable shorthand to characterize such a situation as needing "simultaneous" or "concurrent" mutations, as has been done by others in the malaria literature, even if the second mutation actually occurs separately in the recent progeny of some sickly, rare cell that had already suffered the first, harmful mutation. Guys, please don't hide behind some dictionary or Einsteinian definition of "simultaneous." It matters not a whit to the practical bottom line. If you think it does, don't just wave your hands, show us your calculations. From the recent work of Summers et al. 2014 it's possible that a third mutation in PfCRT may also be needed (perhaps already segregating in the population as a nearly neutral or marginally deleterious mutation) to allow the parasite to survive at therapeutic levels of chloroquine. That may contribute another factor of 1 in 103 to 104 or so to the probability, to reach an aggregate factor of approximately 1 in 1020. After that minimally functioning foundation is established, further mutations could rapidly be added individually and cumulatively -- the way Darwinists like -- to help balance the complex demands on PfCRT for its native activity plus chloroquine transporting, as Summers et al. discuss. If you folks think that direct, parsimonious, rather obvious route to 1 in 1020 isn't reasonable, go ahead, calculate a different one, then tell us how much it matters, quantitatively. Posit whatever favorable or neutral mutations you want. Just make sure they're consistent with the evidence in the literature (especially the rarity of resistance, the total number of cells available, and the demonstration by Summers et al. that a minimum of two specific mutations in PfCRT is needed for chloroquine transport). Tell us about the effects of other genes, or population structures, if you think they matter much, or let us know if you disagree for some reason with a reported literature result. Or, Ken, tell us how that ARMD phenotype you like to mention affects the math. Just make sure it all works out to around 1 in 1020, or let us know why not. Everyone is looking forward to seeing your calculations. Please keep the rhetoric to a minimum. With all best wishes (especially to Professor Myers for a speedy recovery), Mike Behe >> ___________ A reasonable enough challenge. KF PS: Mung's seven sided dice (think, spindle dice) bring the point about the double out neatly, as there is a condition that if one die is 7 the total cannot be 7. That case may help clarify the point that nope it's not just P(sum = 7|a = x) = 1/6, as with 6-sided dice. The two tosses are independent but there is a lock-out condition.kairosfocus_{August 9, 2014
August
08
Aug
9
09
2014
06:00 PM
6
06
00
PM
PDT}

kairosfocus, What? I'm not "swtiching contexts", just pointing out AB's comment is a prefectly reasonable way of seeing why the probability is 1/6. In the second I'm not assuming anything. I'm saying the probability of some cell ending up with two specificed mutations isn't the per-generation mutation rate squared. I didn't think that would be controversial...wd400_{August 9, 2014
August
08
Aug
9
09
2014
05:50 PM
5
05
50
PM
PDT}

Ok Mung -- I meant only that AB was explaining one way you could determine the probability ("explained by only", not "only explained by"). As you say, the order doesn't matter.wd400_{August 9, 2014
August
08
Aug
9
09
2014
05:46 PM
5
05
46
PM
PDT}

WD400: You are again switching contexts, exactly as I warned against. The relevant context is quite plainly before the two die rolls. And, in the case of Chloroquine resistance, you have no right to assume an in-hand first mutation. You have to account for the double. KFkairosfocus_{August 9, 2014
August
08
Aug
9
09
2014
05:44 PM
5
05
44
PM
PDT}

wd400:
AB is right to say the probability of getting a ’7? can be explained by only the outcome of the second roll.
Don't be silly. By the same logic, AB could also say that the probability of getting a '7' can be explained by only the outcome of the first roll. And you would be obliged to declare AB is equally right to say so. Are you really willing to go there? I acknowledge that people here may find many of my posts short and cryptic. So I'll expand (slightly): The difference lies in the following distinction: The probability of getting a ’7? can be explained by only the outcome of the second roll AND the probability of getting a ’7? can be explained by only the outcome of the first roll. The probability of getting a ’7? can be explained by only the outcome of the second roll OR the probability of getting a ’7? can be explained by only the outcome of the first roll. But now, dear reader, you're on your own.Mung_{August 9, 2014
August
08
Aug
9
09
2014
05:37 PM
5
05
37
PM
PDT}

Nevertheless, probability is the mathematical foundation upon which statistics depends, and understanding basic probability principles helps you understand what an analysis really means—and, sometimes even more important, what it does not mean.
oops.
Trying to understand probability? Be sure to use fair dice. The fuzzy ones won't work so well!
You don't say. Arcatia_bograt:
So, please explain to me again why it doesn’t make a difference whether two occurrences are simultaneous or cumulative.
What does it even mean to say that two events are cumulative?
Cumulative probability measures the odds of two, three, or more events happening. There's just one catch involved: each event needs to be independent of the others—you can't have two events that occur at the same time, or have the outcome of a first event influence the probability of the next
What's the Difference Between Probability and Cumulative Probability? P(understanding | Arcatia_bogart)Mung_{August 9, 2014
August
08
Aug
9
09
2014
05:24 PM
5
05
24
PM
PDT}

-Q (shaking head)
That rattling noise isn't two six-sided die is it? It seems to me that the probability of the sum of two die faces totaling seven is 1/6. There are 6 ways in which two die faces could sum to SEVEN and 30 ways in which the two faces could sum to NOT SEVEN. So why does the house only pay 4 to 1 for any seven? Now this [probability] is the case regardless of whether both die land face up simultaneously or one comes to rest face up before the other. Now given that one die has come up a six, this does not impact the overall probability. The probability of a sum of SEVEN isn't changed just because the roll of the second die has not yet been revealed. Isn't this what they mean by independent events? But this should not be confused with conditional probability. (Aren't all probabilities conditional?) When calculating the probability of a sum of SEVEN, it's conditioned upon two die being thrown and the die being fair. So what, precisely, is the objection to Behe? Is it that the two events to confer chloroquine resistance are not independent? Is there equivocation over what it means for two events to be independent from a probability standpoint? What does whether the events are simultaneous or not have to do with anything? Pr(Newbies) want to know.Mung_{August 9, 2014
August
08
Aug
9
09
2014
05:10 PM
5
05
10
PM
PDT}

Upright BiPed:
Oh, the irony.
Being he connoisseur of irony that I am, it's one of the things that keeps me coming back to UD. :)Mung_{August 9, 2014
August
08
Aug
9
09
2014
04:38 PM
4
04
38
PM
PDT}

Querius, Read again. The problem is that you are conflating consecutive with sequential. It's not the time between trials that matter, but the number of trials. To use your dice example: what's the probability of getting two 5s in two throws That's (1/6)^2 =1/36 yes?) Now, what's the probability of getting two (or more) 5s in 10 throws? It should be obvious that it's greater than 1/36th, and indeed if you the calculation you'll see it's something a little more than 1/5. Since there is requirement that mutations giving the phenotype occur back-to-back (just that they eventually accrue in one daughter cell of the first mutant) you were wrong in #56, and subsequently, to claim there is no difference probability for the simultaneaous and sequential cases as they apply to the accumulation of mutations.wd400_{August 9, 2014
August
08
Aug
9
09
2014
04:15 PM
4
04
15
PM
PDT}

Kairosfocus@81, Exactly. This is about as basic probability as you can get, but there are complicating factors depending on the amount of time it takes for the second mutation to appear as you pointed out. However, given the extremely large numbers of malaria organisms and the amount of time, one can calculate the time it would take to finally get a resistant individual. These calculations are already being done with antibiotics.
Mathematical modeling suggests that heterogeneous antibiotic use may limit the emergence of resistance.
For context, see http://aac.asm.org/content/48/8/2861.full For WD400 and AB, all I can say is talk to someone in your math department and try to explain to them your theory about the binomial theorum regarding "simultaneous" versus sequential events. Your ignorance on the subject is profound. Ask yourselves this, how much time can pass between two events for them to still be considered "simultaneous." If your answer is zero, then there are no simultaneous events in nature (unless you want to argue Planck time). And AB, as a "statistician," you should know about anecdotal evidence in statistics. -Q (shaking head)Querius_{August 9, 2014
August
08
Aug
9
09
2014
03:50 PM
3
03
50
PM
PDT}

Another example. Martians syndrome is a connective tissue disorder that affects one in 5000 people. It's symptoms can include myopia, scoliosis, mitral valve problems, aortic aneurism, spontaneous pneumothorax, among other manifestation. Now, with no background information, what is my probability of having this syndrome? One in 5000? That would be a reasonable prediction. And that is as far as Behe went. He completely ignored the fact that the mutations could accumulate over time. Now, what if I said that my father had Marfans? What are my probabilities now? One in two? That is a far cry from one in 5000. Now, what if I told you that I am myopic, have scoliosis and have had a pneumothorax. Without even having a confirmatory test I can reasonably predict that my probability of having Marfans is close to one. So, by taking history into account the probability has changed from one in 5000 to close to one. So, please explain to me again why it doesn't make a difference whether two occurrences are simultaneous or cumulative.Acartia_bogart_{August 9, 2014
August
08
Aug
9
09
2014
03:01 PM
3
03
01
PM
PDT}

KF, AB is right to say the probability of getting a '7' can be explained by only the outcome of the second roll. No matter what the first roll might be there is always precisely one way to get to 7 from that value, so the probability is 1/6th. The rest of your post just seems to agree that 'sequential' need not mean 'consecutive' so Querius was wrong to use the example?wd400_{August 9, 2014
August
08
Aug
9
09
2014
01:44 PM
1
01
44
PM
PDT}

PPS: I probably should leave it at 1st mut not excessively deleterious. KFkairosfocus_{August 9, 2014
August
08
Aug
9
09
2014
01:40 PM
1
01
40
PM
PDT}

PS: Let's note Behe's letter, courtesy BA77 in 70: >> An Open Letter to Kenneth Miller and PZ Myers – Michael Behe July 21, 2014 Dear Professors Miller and Myers, Talk is cheap. Let’s see your numbers. In your recent post on and earlier reviews of my book The Edge of Evolution you toss out a lot of words, but no calculations. You downplay FRS Nicholas White’s straightforward estimate that — considering the number of cells per malaria patient (a trillion), times the number of ill people over the years (billions), divided by the number of independent events (fewer than ten) — the development of chloroquine-resistance in malaria is an event of probability about 1 in 10^20 malaria-cell replications. Okay, if you don’t like that, what’s your estimate? Let’s see your numbers.,,, ,,, If you folks think that direct, parsimonious, rather obvious route to 1 in 10^20 isn’t reasonable, go ahead, calculate a different one, then tell us how much it matters, quantitatively. Posit whatever favorable or neutral mutations you want. Just make sure they’re consistent with the evidence in the literature (especially the rarity of resistance, the total number of cells available, and the demonstration by Summers et al. that a minimum of two specific mutations in PfCRT is needed for chloroquine transport). Tell us about the effects of other genes, or population structures, if you think they matter much, or let us know if you disagree for some reason with a reported literature result. Or, Ken, tell us how that ARMD phenotype you like to mention affects the math. Just make sure it all works out to around 1 in 10^20, or let us know why not. Everyone is looking forward to seeing your calculations. Please keep the rhetoric to a minimum. With all best wishes (especially to Professor Myers for a speedy recovery), Mike Behe >>kairosfocus_{August 9, 2014
August
08
Aug
9
09
2014
01:22 PM
1
01
22
PM
PDT}

A_b:
When you roll two dice sequentially, the probability of them summing 7 is based on the second die alone. And the probability is always 1/6.
Pardon a note, the event is COMPOSITE: START --> {roll a, roll b} --> Read sum = a + b --> END The relevant probability is that at the point, start, not that at the point roll a done now for b. The odds of any given value of b will be 1 in 6 indeed, but the event is to have a and b to sum. It so happens that there are six of 36 ways to sum a 7 with the usual dice, but the result is composite. Now, Mung actually envisions seven-sided dice . . . most easily done with spindle-shaped dice. If the pips run 1 to 7, there are 49 possibilities and still only six ways to sum to 7, as the case where one die already is 7 forces a sum in excess of 7. Tossing a single seven sided die gives odds of 1 in 7. And notice, principle of indifference underlying the matter. Now, Q at 78:
We know that for malaria to develop chloroquine resistance, two specific mutations are required. The mutations can occur simultaneously or sequentially, it doesn’t matter, but both mutations must be in the malaria organism at the same time (i.e. simultaneously present). What Behe did was multiply the probability of mutation #1 times the probability of mutation #2. It turns out that this is an extremely small probability. But knowing the following information - The reproduction rate of malaria - The number of malaria organisms in each infected person who is being treated with chloroquine. - The number of people being treated with chloroquine. - The length of time of treatment He estimated how many years it would take before resistant malaria would appear. Turns out his estimate was reasonably accurate. Oh horrors.
Obviously, the issue is for malaria parasites to meed Chloroquine and resist the drug. Presumably the muts can be simultaneous or sequential. If the latter, having the first should not be too deleterious or it will be eliminated, and it cannot be too advantageous as the new variety would have rapidly dominated. That is, the mut must be quasi-neutral, for positions A and B, so they are effectively only significant if we have A and B and the drug providing selection pressure. KFkairosfocus_{August 9, 2014
August
08
Aug
9
09
2014
01:15 PM
1
01
15
PM
PDT}

Oh, the irony.Upright BiPed_{August 9, 2014
August
08
Aug
9
09
2014
11:21 AM
11
11
21
AM
PDT}

I thought I’d never say this, wd400, but thank you Well, I wouldn't get too carried away Querius, because everything else you said is.... confused at best. You're not really taking about the binomial thereom, which is how you you expand equations of the form (x + a)^n. That thereom is the basis of the binomial distribution, but you are wrong to say sequential and silmntaneaous don't matter in this case. In your example you calculate the probability from two back-to-back rolls. What relevance do you think this has the accumulation of mutations? What are the equivalent of the back-to-back rolls? The only comparison I can think of are back-to-back cell divisions, but that doesn't work because there is nothing special about the order of cell divisions. Getting the second mutation 100 divisions after the first is still getting both mutation, moreover, there may be many more copies of the first mutation in the population by that time. So you are wrong to say the binomial [probability density] doesn't rely on time, even a single lineage the probability get's higher as more cell divisions occur. Finally, you are very confused about what Behe actually claimed. In the above you seem to be saying he guessed how long it would take for P. falciparum to aquire drug resistance, but that was known well before he wrote his book. Indeed -- the 10^20 guestimate he pulled from a paper is based on this rate.wd400_{August 9, 2014
August
08
Aug
9
09
2014
11:13 AM
11
11
13
AM
PDT}

Let me understand this. What you're saying is that when you wrote
But since you insist. 1/6 and 1/7, respectively.
you really didn't make a mistake, but that the 7 was a typo and that you really truly meant to write the following:
But since you insist. 1/6 and 1/6, respectively.
Respectively? Methinks you're a weasel. But now that we've settled that with the binomial theorem, it doesn't matter whether events are simultaneous or sequential, let's look at Behe's math. We know that for malaria to develop chloroquine resistance, two specific mutations are required. The mutations can occur simultaneously or sequentially, it doesn't matter, but both mutations must be in the malaria organism at the same time (i.e. simultaneously present). What Behe did was multiply the probability of mutation #1 times the probability of mutation #2. It turns out that this is an extremely small probability. But knowing the following information - The reproduction rate of malaria - The number of malaria organisms in each infected person who is being treated with chloroquine. - The number of people being treated with chloroquine. - The length of time of treatment He estimated how many years it would take before resistant malaria would appear. Turns out his estimate was reasonably accurate. Oh horrors. But you haven't explained your statistical reasons behind your reference to "Behe’s voodoo magic pseudostatistics." It would seem to me that these statements are simply groundless ad hominem attacks on your part. Right? Or will you explain mathematically or statistically what was wrong with Dr. Behe's math. -QQuerius_{August 8, 2014
August
08
Aug
8
08
2014
10:17 PM
10
10
17
PM
PDT}

Mung, no. When you roll two dice sequentially, the probability of them summing 7 is based on the second die alone. And the probability is always 1/6.Acartia_bogart_{August 8, 2014
August
08
Aug
8
08
2014
07:37 PM
7
07
37
PM
PDT}

When you roll a single die, any outcome can still result in a seven
Given it's a seven-sided die and each face is equally probable, I suppose that's correct. So given two seven sided die, where each face is equally likely ... Does it matter whether you toss them simultaneously?Mung_{August 8, 2014
August
08
Aug
8
08
2014
07:28 PM
7
07
28
PM
PDT}

Sorry WD200. Big thumb, small buttons. It should have been 1/6. After all, there are only six faces on a die. My point was simply that the mutations don't need to occur simultaneously, which is the basis of Behe's weak argument. They can be the result of accumulated mutations, fixed in the population by drift. Behe either doesn't understand this proven concept or choses to misrepresent it. I vote for intentional misrepresentation of the facts.Acartia_bogart_{August 8, 2014
August
08
Aug
8
08
2014
07:18 PM
7
07
18
PM
PDT}

Prev 1 2 3 4 5 Next

You must be logged in to post a comment.

Leave a Reply