Evolutionists improbable becoming probable argument

And what have you produced?Easy to ignore what you don't understand, isn't it? You should learn about probability space. Then read again what I wrote.

quote:

---

And what have you produced?

---

A challenge that you seem incapable of meeting - despite your confident assertion.

quote:

---

Easy to ignore what you don't understand, isn't it?

---

I don’t find it to be so, but you seem to.

quote:

---

You should learn about probability space. Then read again what I wrote

---

I’m sure that I know at least as much as you. Enough to see that you haven’t produced any argument that could even lead to relevant calculations.Are you going to try? Or are you just going to stick with empty bluster?

I see no reason why length would have anything to do with it. It is entirely possible for the active site of a protein to be restricted to a small portion of the protein while the rest of the sequence can change quite a bit without losing function. In fact, from my experience with proteins I wouldn't be surprised if short proteins were more restrictive than large proteins.I also have no way of calculating how probable functional sequences are. ID/creationists seem to think they know, but are incapable of producing any relevant calculations.

You have yet to demonstrate this claim.

Yes, of course. It's self-evidently true that the greater the number of permutations the least likely any particular one is, including ones that make sense in English, but from following the discussion it seems that everyone understands this already. The difference of opinion lies in how to properly apply this information.I think your main point is that it's more likely for a change to be in a deleterious direction than beneficial. In essence you're arguing that the sheer unlikelihood of a beneficial mutation means that evolution isn't possible.But as I pointed out to mike the wiz in Message 4, there are around 10¹⁶ SARS-Cov-2 viruses in the world at any given point in time, and they replicate approximately every 10 hours. With 2.4 × 10¹⁶ replications per day and 10^-6 mutations per replication, that's 2.4 × 10¹⁰ mutations daily. If the odds of a beneficial mutation are 10^-9 (one in a billion) then that's in the neighborhood of 24 beneficial mutations every day. Day after day. With viruses with beneficial mutations being selected for.--Percy

So if 10% of all sequences of lenghth 200 would be useful, you would also expect that 10% of all sequences of length 200000 are useful?Because that is what it means if the number of useful gene sequenes grows as fast as the space of all possible sequences.

Empty claims from the arrogant evolutionist who produced not a single useful argument.

Well, it does not appear to be self-evident to Taq. But he thinks he understands probability better. Little does he know.Suppose we see usefull sentences of a few dozens of characters. And we also see a book of a few hundreds of thousands of characters.We would want to determine how this book formed. Does it consist of shorter stories that exist seperately or have existed in the past and for whatever reason stopped existing? Can we find possible paths along which this book developed from random changes of shorter stories?What model are you proposing for this?

quote:

---

Empty claims from the arrogant evolutionist who produced not a single useful argument.

---

Of course, all I am doing is seeing if you can back up your claims with something more than arrogant bluster.You talk about probability spaces, but you haven’t defined one, let alone a relevant probability space. So we still haven’t seen any relevant math from you at all.

I done so multiple times. Your ignorance and amateuristic level is your problem.

quote:

---

I done so multiple times

---

No, you have not. You haven’t clearly defined even one of the three parameters of a probability space.

quote:

---

Your ignorance and amateuristic level is your problem.

---

The problem is your “ignorance and amateuristic level” - and that is not my problem at all. If you actually manage to define a probability space you will find that I am quite able to discuss it. And it’s relevance to the question of evolution.

I specified the length of gene sequences to be a few hundred upto 2 million. What part of that do you not understand? In other examples, I specified lengths as well.Do you know which bases a gene consists of? Do you need people to spell everything out for you?So no, you are not capable of discussing these things you so poorly understand.

quote:

---

I specified the length of gene sequences to be a few hundred upto 2 million. What part of that do you not understand? In other examples, I specified lengths as well.

---

And? Even if that is going to be your sample space - and I think it a bad choice - there are still the event space and the probability function to define,To explain why gene sequence is a bad choice for sample space, consider this: Why would specific gene sequences matter? Surely the issue is what they do - and that is dependent on the context provided by other genes and the environment, and can be realised in multiple different sequences. Dembski’s concept of specification may be flawed but it is far better than looking at raw events as others have pointed out,

quote:

---

Do you know which bases a gene consists of? Do you need people to spell everything out for you?

---

I need you to explain your argument - since you seem incredibly reluctant to actually do it - and if it involves a probability space you need to define that - which you still haven’t come close to doing.

quote:

---

So no, you are not capable of discussing these things you so poorly understand.

---

Apparently I understand them better than you, and that is another problem for you. You can’t baffle me with bullshit if I know enough to see that you are bullshitting.

I think you're placing greater trust in errors in words and sentences as an accurate analogy to mutations in a gene than anyone else here. The analogy might serve as a helpful introduction to the concept of mutations but shouldn't be carried too far. Taq has experience as a molecular biologist, and he echoed my thought (or maybe I echoed his, I forget who said it first) that longer genes might be more tolerant of random mutations than short ones.Here's an example. Take the sentence, "I found a watch," and assume it's an analogy to a gene with the nucleotide sequence "CAG...TAC" Now introduce a random mutation so that the sentence becomes, "I found a wmtch," and that analogically the nucleotide sequence becomes "CAG...AAC". In your opinion is the sentence destroyed, or would most people make the right supposition anyway. I certainly don't know. And for the nucleotide sequence where TAC becomes AAC, in terms of what the protein does in the organism does it matter that the last amino acid is now asparagine instead of tyrosine? I don't know that either.But you are in effect claiming you know while at the same time are apparently unable to communicate that knowledge to anyone else. Hence the skepticism everyone's expressing. At least in this sub-discussion with me, your belief that errors in words and sentences are an accurate analogy to the occurrence and selection of mutations is a barrier to developing a common understanding. The analogy could be improved if you added the creation of copies of the sentence and a selection mechanism.What we do know is that nearly every reproductive event includes mutations. Reproduction is imperfect. Someone mentioned that each human averages about 50 mutations. I thought the figure was around 100, but 50 is fine, too. The key point is that despite the mutations the human race continues. It is, in fact, evolving faster than ever, because the more babies born every year the more mutations introduced into the world population. It's also worth pointing out that zygotes and fetuses with sufficiently deleterious mutations are often spontaneously aborted, so early that many women never suspect they were pregnant.Writing about this made me curious about what percent of the world population has genetic disorders. This is according to Genetic disorder - Wikipedia:

Wikipedia:

---

Around 65% of people have some kind of health problem as a result of congenital genetic mutations.

---

That's much higher than I would have suspected, and if this is accurate then the majority of these health problems must be minor. The article also says that about 600 genetic orders are treatable. For example, LVH (left ventricular hypertrophy - thickened heart muscle around the left ventricle that prevents the heart from efficiently pumping high volumes) has a strong genetic component but little practical effect (in most cases) unless you want to become an elite athlete, and it's treatable with medication. Are conditions like that included in the 65%? I suspect that they are including minor conditions like this. The prevalence of life-impacting genetic disorders must be much less, and looking up just one, muscular dystrophy, for example, I see that it occurs at a .03% rate.Realize that if it were true that deleterious mutations win out over neutral and beneficial ones that all life would have come to an end long ago. You have to keep in mind that evolution includes mutation *and* selection. Disadvantageous mutations are selected against and tend to be removed from populations or at least become uncommon, while beneficial mutations spread rapidly through populations, and if they're sufficiently beneficial then their alleles becomes fixed (means every individual has them).--Percy

It is unknown how many sequences are useful. What is known is that relatively short peptides can be useful. This would mean that a longer protein has more sequence to find function. If anything, I would suspect that longer proteins have a better chance of being functional than short ones.I think you are under the false assumption that the entire length of a protein has to contribute to function. This just isn't the case.