Rebuttal To Creationists - "Since We Can't Directly Observe Evolution..."

You didn't answer the question. Why would you multiply the probabilities?

Troll.

Do you?Let's say we have three adaptive mutations: lactase persistance, lower melanin production in higher latitudes, and malarial resistance.If these adaptive mutations were in three different unlinked genes, would they be dependent or independent? Could all three mutations start moving towards fixation at the same time, or would they have to move towards fixation one at a time? Why?

Hilarious. How can you criticise Kleinman when you don't even understand the basics of probability maths?

The problem is how Kleinman tries to apply probabilities to genetics. He seems to think that if one beneficial mutation is at a frequency of 0.5 then all other beneficial mutations throughout the genome can not add up to more than a frequency of 0.5. I hope you can see how ridiculous that is.

Kleinman:

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When did I reject Mendelian genetics?

Taq:

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You reject Mendelian genetics when you require the percentage distribution of alleles in different genes to add up to 1. You keep doing this. I bet you do it later in this post.

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What a pleasant surprise. Welcome back Taq. I thought I was going to be stuck debating the C- team or Tany who thinks that DNA evolution for viruses, bacteria, and yeast differs from complex, multicellular, sexually replicating organisms. As you already know ploidy doesn't change the math much and you still haven't quite figured out how random recombination can affect reproductive fitness.And of course, I'm going to require that the sum of the individual frequencies of the different variants in a population must add up to 1. That's because, like probabilities where the sum of all possible outcomes must equal 1, the same applies to frequency distributions. That's why the sum of the frequencies in a population of all members with beneficial allele A at one genetic locus plus the frequency of all the members that have beneficial allele B at a different genetic locus plus the frequency of all members in that population that have neither beneficial allele must equal 1. Perhaps you imagine some other subset in that population such as a member with both A and B alleles already?

Kleinman:

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Why can't you add these frequencies? You have 3 subsets in the population. One subset has allele A at one genetic locus. Another subset has allele B at a different genetic locus and a third subset has neither allele. Unless there is an intersection of any of these three subsets, they are mutually exclusive. Each of these 3 subsets has a subpopulation size associated with their corresponding subset and if you add up these subpopulation sizes, you get the total population size.

Taq:

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And there it is. You still don't understand basic Mendelian genetics, at least at the time you wrote this post.

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Taq, Mendelian Genetics doesn't change that math. If you want to include the possibility of heterozygosity, that just reduces the probability of an AB variant offspring occurring. We can do that math if you like but I suggest you start by assumming homozygosity where the math is a little simpler and the probabilities are a little greater for your AB recombination event occurring.

Taq:

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Let's see how this works out. Let's use 3 hypothetical disease alleles (e.g. cystic fibrosis, achondroplasia). Let's say 1 out of 1,000 people carries the diseases allele, or 0.1% of the population. This would mean that 99.9% of people don't carry the disease allele but the healthy allele. Let's call these Aa, Bb, and Cc alleles for genes A, B, C. According to you, I should be able to add up the number of people with the A, B, and C allele and get an accurate population count. Is that true?
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NO!!!
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If I do as you suggest I will get about 3x the actual population number. Do you know why?

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Taq, you are confusing the use of the addition rule for mutually exclusive events and the addition rule for arbitrary events (events where there are intersections in the subsets you are trying to add). The subsets of a population that don't have your hypothetical disease alleles intersect. To do that frequency calculation correctly, you must subtract the intersection components, otherwise you will get about 3x the actual population number since most of the population do not have the disease alleles. You should know better than this. This is something you should have learned in your introductory probability theory class.

Kleinman:

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Fixation by selection involves the most fit allele going to a frequency of 1. Other adaptive alleles that give a smaller increase in fitness are not increasing in frequency.

Taq:

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You still don't understand how sexual reproduction works.

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So, when Haldane did his computation for fixation of a beneficial allele, he was really doing the math for the fixation of multiple different beneficial alleles at different genetic loci simultaneously. Why don't you explain to us how that works?

Kleinman:

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How about every real, measurable, and repeatable empirical example of DNA evolution? Start with the Kishony and Lenski experiments, then go on with the success of combination herbicides, pesticides, and rodenticides inhibiting the evolution of selection pressure resistant variants. How about mathematical models that predict and simulate the behaviors of these evolutionary processes?

Taq:

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How about learning how genetics works? Why don't you start there?
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You seem to think that there is just one gene per genome. Perhaps you could start by learning how meiosis works, or perhaps what a chromosome is. Maybe you could learn that there are multiple genes in a genome, each with it's own set of alleles.

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Biologists still haven't figured out the genetics of descent with modification in asexually reproducing populations. What makes you think you can correctly explain descent with modification in sexual replicators? You should start by learning how to use the addition rule to compute frequencies of different variants in a population.We are waiting for you to give a coherent (mathematical) explanation of how meiosis with one parent with a beneficial allele A at one genetic locus and the other parent with a beneficial B at a different genetic locus gives an offspring with both beneficial alleles A and B when you have a population of different variants A, B, and C (the C variants have neither beneficial allele).

Taq:

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Me: You claim that the frequency of any two mutations anywhere in the genome can not add up to more than 1. Obviously, that is false.

Kleinman:

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You: Don't be silly, I haven't made a claim like that. And of course, frequencies are always less than or equal to 1. Frequencies range from 0 to 1. Why do believe that there can be frequencies greater than 1?

Taq:

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So you claim you don't make that claim, and then make that very claim in the next sentence. You effing moron.

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I'm not making that claim, you are by using the addition rule incorrectly. The addition rule works differently for mutually exclusive events than for arbitrary events (when there are intersections of the subsets). It seems they didn't teach you that in your survey of math class.

Taq:

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Quiz for Kleinman:
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Why are gene 1 and 2 linked in the first example but not in the other two examples?
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What effects does linkage have on relative allele distributions between linked genes compared to unlinked genes?

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You can have hitchhiking mutational alleles that will increase in frequency as the variant with the most beneficial allele moves to fixation. Are you claiming that the A and B alleles end up being linked or not linked? Do you think that increases the probability of one parent with an A allele and the other parent with a B allele having an offspring with both A and B alleles? I'm already assuming the best possible case where the A and B mating will always give an AB offspring. If you want to introduce Mendelian Genetics into the math or whether the genes are linked or not does not increase that probability, it decreases it.

Dredge:

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If you flip a coin three times, for example, each flip is an indepedent event. How would you calculate the probability of getting 3 heads from 3 flips?

Taq:

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We are getting more distant from the actual genetic system that got this all going.
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Kleinman is claiming that if we add up all of the allele frequencies for all genes in a genome that we will get 1. That's ridiculous. That shows a massive misunderstanding of the basic mathematics of genetics.
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Let's just say that there are two alleles for each of the ~30,000 genes in the human genome, and the frequency of each allele is 0.5, or 1.0 for each gene. If we add them up like Kleinman claims we can then we get 30,000, not 1.

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Now you are just being stupid Taq. That is your calculation, not mine. You obviously need a lesson on the addition rule of probabilities, something which you didn't get in your survey of math course.
Probability - Wikipedia

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Mutually exclusive events
Main article: Mutual exclusivity
If either event A or event B can occur but never both simultaneously, then they are called mutually exclusive events.

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If two events are mutually exclusive, then the probability of both occurring is denoted as P(A ∩ B) and

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P(A and B) = P(A ∩ B)

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If two events are mutually exclusive, then the probability of either occurring is denoted as P(A ∪ B) and

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P(A or B) = P(A ∪ B) = P(A) + P(B) - P(A ∩ B) = P(A) + P(B) - 0 = P(A) + P(B)

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For example, the chance of rolling a 1 or 2 on a six-sided die is P(1 or 2) = P(1) + P(2) = 1/6 + 1/6 = 1/3

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Not mutually exclusive events

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If the events are not mutually exclusive then

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P(A or B) = P(A ∪ B) = P(A) + P(B) - P(A ∩ B)

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For example, when drawing a card from a deck of cards, the chance of getting a heart or a face card (J,Q,K) (or both) is
13/52 + 12/52 - 3/52 = 11/26, since among the 52 cards of a deck, 13 are hearts, 12 are face cards, and 3 are both: here the possibilities included in the "3 that are both" are included in each of the "13 hearts" and the "12 face cards", but should only be counted once.

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Taq, do not attribute your mathematical blunders to me. You are doing mathematics like your C- team does math. You are the one adding frequencies that are not mutually exclusive. Stop being a dummy, otherwise, you are going to be booted back to the C- team.

Kleinman:

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Don't hold your breath for Tany's explanation of how DNA evolution for viruses, bacteria, and yeasts differs from DNA evolution for complex, multicellular, sexually reproducing organisms.

Taq:

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We could start here:

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And how do crossing over and recombination create new alleles?
We are still waiting for your mathematical explanation of how two different adaptive alleles A and B at different genetic loci in different members of a population end up in an offspring. Perhaps you are running a breeding program?

Kleinman:

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This does occur but you have to have very large populations in that family. That's why universal common descent is not possible for primate precursor/human-chimp evolution. There isn't a large enough population size for adaptive evolution to operate to account for the fitness differences between humans and chimps. Taq understood this and tried to address this problem with recombination. But random recombination is also governed by the multiplication rule. Taq tried to address this with a physically impossible claim and he knew it. That's why he abandoned the discussion.

Taq:

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Bullshit, K-man. Life happens, and I got busy elsewhere.
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Let's revisit this classic you used in post 311

Kleinman:

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Define the following variables:
n – is the total population size.
nA – is the number of members in the population with beneficial allele A.
nB – is the number of members in the population with beneficial allele B.
nC – is the number of members in the population that have neither beneficial allele A nor beneficial allele B.
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In addition, we have the following condition: nA + nB + nC = n.
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And the frequency of each of the variants are:
f_A = nA/n
f_B = nB/n
f_C = nC/n

Taq:

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Do you still stand by this? Do you add the allele frequencies for alleles in different genes?

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Absolutely, I stand by this, slow learner. You obviously didn't review your introductory probability theory in your time away from here. This math couldn't be simpler. You have one subset of the population that has beneficial allele A at one genetic locus, a second subset of the population the population that has beneficial allele B at a different genetic locus, and the remainder of the population has neither allele A nor allele B. And these subsets are mutually exclusive. Understand rubberband?

Taq:

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What about the healthy alleles for 3 different genes associated with a genetic disease, each with a frequency of 0.999?
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0.999A + 0.999B + 0.999C != 1
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OOOOOPPPPPSSS!!!! Your math doesn't work.

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This is your math, not my math. I know well enough that these frequencies are not mutually exclusive, you don't. When it comes to mathematics, biologists are pathetic. Learn how to use the addition rule you dummy.

Kleinman:

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Do you know when random adaptive mutations are dependent or independent?

Taq:

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Do you?
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Let's say we have three adaptive mutations: lactase persistance, lower melanin production in higher latitudes, and malarial resistance.
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If these adaptive mutations were in three different unlinked genes, would they be dependent or independent? Could all three mutations start moving towards fixation at the same time, or would they have to move towards fixation one at a time? Why?

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Sure I know when random adaptive mutations are dependent or independent. Think back on the definition of conditional probabilities. For example, you want to calculate the probability that a lactase persistance mutation occurs on a member that already has the lower melanin production in higher altitudes mutation. You are computing that probability on a reduced sample space, ie., those members that already have the lower melanin production mutation in higher altitudes. If you want to see how to do this mathematically, read this paper:
The mathematics of random mutation and natural selection for multiple simultaneous selection pressures and the evolution of antimicrobial drug resistance
The math for your case starts at paragraph 1.4 on page 5396. That's how you do the math for DNA evolution of 3 adaptive alleles occurring in some member of a population. In this case, all these mutations are dependent events if they are to occur in members that already have the other adaptive alleles.While you were away, I posted a video that explains how to do conditional probabilities for novices, laymen, and biologists. Watch this video, it will help you understand this topic.

Dredge:

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How can you criticise Kleinman when you don't even understand the basics of probability maths?

Taq:

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The problem is how Kleinman tries to apply probabilities to genetics. He seems to think that if one beneficial mutation is at a frequency of 0.5 then all other beneficial mutations throughout the genome can not add up to more than a frequency of 0.5. I hope you can see how ridiculous that is.

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What are you talking about? You still haven't figured out how to compute the frequencies of different variants in a population. You are starting to make the C- team look smart.

This all boils down to what one is trying to model with the math (maths to British types). The entire point of this is what model we would use to calculate a probability for abiogenesis.Ideally, we would already know how it would happen. While we don't know that yet, we do have good ideas of how it would have to, including what kind of math models we would need to use as well as which kinds of models would be totally unsuited. In Dredge's and Kleinman's case they are deploying an entirely unsuited math model -- while Kleinman has fundamental problems with math models, he might know a little about the science behind abiogenesis whereas Dredge is completely ignorant of both abiogenesis and of science (plus he is willfully stupid in his adamant refusal to even try to learn something).But what's happening now is a tangential argument (AKA "rabbit trail") to draw you away from the main point (ie, how to calculate the probability of abiogenesis) by miring you in a side argument.Both Dredge and Kleinman have decided that the model for abiogenesis would be winning the lottery many times in a row. Since no creationist has ever answered the question of how they think evolution is supposed to work (and hence they will also be deathly silent about abiogenesis), I would have to guess that, being creationists, they believe in saltation (the false idea that new species or complex organs just appear suddenly in one single massive step (eg, "a snake lays an egg and a bird hatches out") ).That means that in their model (if it could even be called such), abiogenesis would require random chemicals to suddenly all fall together to form a complete modern unicellular organism. The very fact that that uses single step selection makes the probability for success virtually impossible. Which is basically what happens when you play the lottery or any other gambling game.In my Message 35 I compare that with cumulative selection as they pertain to Dawkins' WEASEL. Creationists always try to saddle evolution with single step selection whose performance is abysmal whereas cumulative selection succeeds quickly and without fail.I was very surprised by Kleinman's Message 799 in which for perhaps the very first time in this thread he actually offered something that contributed to discussion. That was his link to the Wikipedia article, Joint probability distribution which contains a link to their related article, Complementary event. A basic problem in researching a topic is that you first need to know what it's called, kind of like needing to know how to spell a word before you can look it up in a dictionary to see how to spell it. I've been using joint probabilities for four decades and I invented using complementary events about three decades ago (and have only now learned what it's called). 
So, here's the basic problem with their misuse of a lottery analogy: it describes things that work almost completely unlike abiogenesis would have worked. Abiogenesis would involve billions or trillions (be they US/UK billions/trillions or real ones) of independent parallel paths involving chains of chemical reactions which do not need to happen one right after the other (basically part of what you've been trying to tell them).They're misrepresenting abiogenesis as requiring single events, each individual event being like "winning the lottery", but then requiring that that happen a thousand times over in strict sequence without any failed step at any point (at least that's what it looks like they're claiming, but since creationist never answer The Question, "What the hell are you talking about?", ... ). Hence they "model" it with joint probabilities, which is wrong.Instead of the analogy of "what's the probability of one person winning the lottery many times in a row", the far better analogy would be "what's the probability of at least one person among all the players winning?" That analogy is not based on joint probabilities (although it does use them in intermediate calculations), but rather on complementary events.Basing a model on joint probabilities will usually result in very low probabilities. However, using complementary events can result in success becoming inevitable because the probability of constant and persistent failure for all attempts becomes so low as to be virtually impossible.Here's how it works. So, let's apply this to the lottery, California's Super Lotto Plus to be exact:

• The probability P(A) of an individual winning a single game is 1:41,417,353 = 2.414515×10^-8
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• The probability Q(A) of an individual losing a single game is 1 - P(A) = 0.999999976
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• Assume 39,000,000 attempts per game. This is about the population of the state of California so, since most players buy more than one number, it's a reasonable number.
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• The probability Q(B) of every single one of those 39 million attempts failing is the only joint probability in this: Q(B) = Q(A)^39,000,000 = 0.39
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• The probability P(B) of at least one of those 39 million tickets winning: P(B) = 1 - Q(B) = 0.61
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• The game is played twice a week, so what is the probability of at least one ticket winning within the week:
  1. Probability Q(C) of every single ticket losing: Q(C) = Q(B)² = 0.1521
  2. Probability P(C) of at least one win in a week: P(C) = 1 - Q(C) = 0.8479
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• Now just for fun, what are the odds for a full month assuming 4 weeks in a month:
  1. Probability Q(D) of every single ticket losing: Q(D) = Q(C)⁴ = 5.352×10^-4
  2. Probability P(D) of at least one win in a month: P(D) = 1 - Q(D) = 0.9994648
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• Let's double down and figure the odds of at least one win in a year (52 weeks):
  1. Probability Q(E) of every single ticket losing all year long: Q(E) = Q(C)⁵² = 2.9561×10^-43
  2. Probability P(E) of at least one win in a month: P(E) = 1 - Q(E) ≈ 1

So we see how the number of independent attempts affects the probability of at least one attempt succeeding (in most cases, we only need one success). Even if the probability for a single event succeeding is very improbable.We also see that the "model" being pushed by Dredge and Kleinman is the completely wrong one. No part of it has anything to do with how abiogenesis would work.And of course, once the ability to replicate has been established, then evolution would take over with cumulative selection. 

How can YOU side with Kleinman when you admit to being an idiot?

dwise1:

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This all boils down to what one is trying to model with the math (maths to British types).

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Oh boy, dwise1 is going to do the mathematics of descent with modification!

dwise1:

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The entire point of this is what model we would use to calculate a probability for abiogenesis.

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Oh well, don't expect dwise1 to present experimental evidence of his model.