I'm creating a new thread here to continue debate on a post made by EarthScience guy on another thread (Science and Religion > Artificial life: can it be created?, post 17). This post challenged probability calculations in an old Talkorigins article that I had linked in that thread:
http://www.talkorigins.org/faqs/abioprob/abioprob.html
Are the arguments (on creationist views) and probabilities presented reasonable in the Talkorigins article? If not, why not?
Abiogenesis and Probabilities
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Abiogenesis and Probabilities
Post #1In human affairs the sources of success are ever to be found in the fountains of quick resolve and swift stroke; and it seems to be a law, inflexible and inexorable, that he who will not risk cannot win.
John Paul Jones, 1779
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Re: Abiogenesis and Probabilities
Post #441OK.
That's not the argument you were making initially and that I responded to, but even if we pretend it is, this is your first fundamental misunderstanding.
Since having one copy of the allele is beneficial, but two is lethal, there will be an equilibrium reached where the reproductive benefit of having one copy of the allele offsets the reproductive cost of children born with two. This equilibrium will depend on both the prevalence and virulence of the local version of malaria. Once this equlibrium is reached, the rate will only increase or decrease in response to a change in one of those.
Whether or not a gene is recessive has no effect on selection pressures or whether it becomes fixed in a population. The alleles for blonde hair and blue eyes are recessive, but are popular enough in terms of sexual selection that they're prevalent in northern latitudes where they aren't deleterious. I'm not going to guess at what part you misunderstand, so if you'd like help with that, explain why you think being recessive should affect frequency.
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Re: Abiogenesis and Probabilities
Post #442Yep. And it's easy to understand.
1. Malaria, where it's endemic, often kills before one can reproduce, or it can disable to the point that one can't care for offspring or have viable offspring.
2. Sickle Cell anemia, in homozygotes, generally kills before one can reproduce.
3. If you have one gene for sickle cell, though, you experience very little discomfort (often, you aren't even aware of it) but you have very good protection against malaria.
And yes, as you suggested, that means in malaria-endemic areas, there are a lot more heterozygotes than you would otherwise expect. Here's why...
Two homozygotes for normal Hg have for kids. All of them are vulnerable to early death or infirmity from malaria.
One homozygote and one heterozygote have kids. Probability is that 75% of them will be vulnerable, but 25% will be immune to malaria.
Two heterozygotes have kids. Probability is that 25% will be vulnerable to early death or infirmity from malaria, 25% will die or be disabled from sickle cell disease, and 50% will be immune to malaria.
Which of those three tends to leave the greatest number of viable offspring? Right. The two heterozygotes.
Does that make it easier? Oh, BTW, there's a more recent mutation of Hg that provides very good protection against malaria, but even homozygotes normally don't get crippling illness or death. It's increasing in malaria areas for reasons that should now be obvious to you. Would you like to learn about that?
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Re: Abiogenesis and Probabilities
Post #443There'l be nothing like equilibrium or rather, that's what you need to explain.Difflugia wrote: ↑Thu Nov 11, 2021 10:22 am
That's not the argument you were making initially and that I responded to, but even if we pretend it is, this is your first fundamental misunderstanding.
Since having one copy of the allele is beneficial, but two is lethal, there will be an equilibrium reached where the reproductive benefit of having one copy of the allele offsets the reproductive cost of children born with two. This equilibrium will depend on both the prevalence and virulence of the local version of malaria. Once this equlibrium is reached, the rate will only increase or decrease in response to a change in one of those.
There'l always be homozygous individuals within the population, the gene frequency for sickle cell will remain roughly the same and if increases, it will be because of population increase and not en ironmental pressures. The gene frequency for those that are prone to malaria increases despite the environment ( prevelence and virulence) of the malaria.
A rough statistical hypothesis about hereditary science:
Imagine 2 familiies each with 4 children representing a population. Both parents from 1 family are heterozygous (sickle cell) and the other are both homozygous on the dominant gene.
Statistically, there's a 25% chance of having a homozygous dominant gene from family 1 and 100% chance feom family 2. The chances (of homozygous dominant) to heterygozous individuals within this population are 5:2. Even with highest prevelence and virulence, there'l be no equilibrium.
Is human preference natural or artificial selection?Whether or not a gene is recessive has no effect on selection pressures or whether it becomes fixed in a population. The alleles for blonde hair and blue eyes are recessive, but are popular enough in terms of sexual selection that they're prevalent in northern latitudes where they aren't deleterious. I'm not going to guess at what part you misunderstand, so if you'd like help with that, explain why you think being recessive should affect frequency.
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Re: Abiogenesis and Probabilities
Post #444Yeah but there's nothing within your theory has been observed in any parts of this world.The Barbarian wrote: ↑Thu Nov 11, 2021 10:27 am
Yep. And it's easy to understand.
1. Malaria, where it's endemic, often kills before one can reproduce, or it can disable to the point that one can't care for offspring or have viable offspring.
2. Sickle Cell anemia, in homozygotes, generally kills before one can reproduce.
3. If you have one gene for sickle cell, though, you experience very little discomfort (often, you aren't even aware of it) but you have very good protection against malaria.
And yes, as you suggested, that means in malaria-endemic areas, there are a lot more heterozygotes than you would otherwise expect. Here's why...
Two homozygotes for normal Hg have for kids. All of them are vulnerable to early death or infirmity from malaria.
One homozygote and one heterozygote have kids. Probability is that 75% of them will be vulnerable, but 25% will be immune to malaria.
Two heterozygotes have kids. Probability is that 25% will be vulnerable to early death or infirmity from malaria, 25% will die or be disabled from sickle cell disease, and 50% will be immune to malaria.
Which of those three tends to leave the greatest number of viable offspring? Right. The two heterozygotes.
Does that make it easier? Oh, BTW, there's a more recent mutation of Hg that provides very good protection against malaria, but even homozygotes normally don't get crippling illness or death. It's increasing in malaria areas for reasons that should now be obvious to you. Would you like to learn about that?
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Re: Abiogenesis and Probabilities
Post #445I don't need to explain it since I'm not the one struggling to put together a claim, but I will.
This is so much word salad and I don't know how to correct it to make it right, so I'll just explain what will happen.Noose001 wrote: ↑Thu Nov 11, 2021 12:05 pmThere'l always be homozygous individuals within the population, the gene frequency for sickle cell will remain roughly the same and if increases, it will be because of population increase and not en ironmental pressures. The gene frequency for those that are prone to malaria increases despite the environment ( prevelence and virulence) of the malaria.
A rough statistical hypothesis about hereditary science:
Imagine 2 familiies each with 4 children representing a population. Both parents from 1 family are heterozygous (sickle cell) and the other are both homozygous on the dominant gene.
Statistically, there's a 25% chance of having a homozygous dominant gene from family 1 and 100% chance feom family 2. The chances (of homozygous dominant) to heterygozous individuals within this population are 5:2. Even with highest prevelence and virulence, there'l be no equilibrium.
If we have two families with four children each, then a simple measure of reproductive success is how many children survive to adulthood to have children of their own.
In the absence of malaria, a heterozygous couple will have three children that make it to adulthood versus four for the couple lacking the sickle cell gene. Since carrying a sickle cell gene means a significantly reduced reproductive success, the non-sickle gene will eventually become fixed in the population.
If malaria kills 100% of unprotected children before adulthood (but we somehow have a few unprotected adults for the thought experiment), then the reproductive success of two heterozygous parents is 50% because both homozygous children die before adulthood. The reproductive success of a mixed couple (one heterozygous and one homozygous) is also 50% (again, both homozygous children died). The reproductive success of a pair of homozygous non-sickle parents is 0% as all four of their children succumb to malaria. In this scenario, since homozygous for either allele is fatal, both alleles will remain in roughly the same proportion in the population and effectively 100% of adults will have a single copy of each allele.
Those are the boundary conditions. Malaria can kill no fewer than 0% and no more than 100% of unprotected individuals. If malaria kills more than 0% and fewer than 100% of unprotected individuals, the fraction of adults that are carriers will likewise be somewhere between 0% and 100%.
Independent of malaria, two copies of the sickle cell allele are lethal, so it will never become fixed in the population. Even if everyone without at least one copy dies, the non-sickle allele must remain in the pool.
Finally, at least in the case of sickle cell, you're using "recessive" incorrectly. A properly recessive allele has no phenotypic effect if a dominant allele is present. Since a single copy of the sickle cell allele confers resistance to malaria, that's quite definitely a phenotypic effect.
Natural selection.Noose001 wrote: ↑Thu Nov 11, 2021 12:05 pmIs human preference natural or artificial selection?Whether or not a gene is recessive has no effect on selection pressures or whether it becomes fixed in a population. The alleles for blonde hair and blue eyes are recessive, but are popular enough in terms of sexual selection that they're prevalent in northern latitudes where they aren't deleterious. I'm not going to guess at what part you misunderstand, so if you'd like help with that, explain why you think being recessive should affect frequency.
Preference based on perceived attractiveness is natural selection. It would only be considered artificial selection if one were selecting mates to consciously produce blonde offspring even if one finds blonde hair to decrease sexual attractiveness.
Once again, your attempt at a rhetorical question fails because of an underlying misunderstanding.
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Re: Abiogenesis and Probabilities
Post #446[Replying to Noose001 in post #426]
Came in late on this, but looks like you've gotten plenty of education on the subject so far. Is any of it sticking though?Then 'proven' must mean different things for different people. Sickle cell anaemia, a killer disease which is as old as the human race has increased with increase in population. It certainly kills even before one is able to sire an offspring?
Explain.
In human affairs the sources of success are ever to be found in the fountains of quick resolve and swift stroke; and it seems to be a law, inflexible and inexorable, that he who will not risk cannot win.
John Paul Jones, 1779
The man who does not read has no advantage over the man who cannot read.
Mark Twain
John Paul Jones, 1779
The man who does not read has no advantage over the man who cannot read.
Mark Twain
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Re: Abiogenesis and Probabilities
Post #447[Replying to Noose001 in post #444]
Malaria does not have 100% kill rate. Is this why natural selection isn't happening?
Malaria does not have 100% kill rate. Is this why natural selection isn't happening?
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Re: Abiogenesis and Probabilities
Post #448Sorry, you're wrong. For example there is a large population of people in the United States descended from people whose ancestors lived in malaria-endemic areas of Africa. Would you think that over hundreds of years, the incidence of sickle cell genes in that population might have changed? Turns out, it has, which as you know is predicted by evolutionary theory. Would you like to see the Punnett squares for these?Noose001 wrote: ↑Thu Nov 11, 2021 12:35 pmYeah but there's nothing within your theory has been observed in any parts of this world.The Barbarian wrote: ↑Thu Nov 11, 2021 10:27 am
Yep. And it's easy to understand.
1. Malaria, where it's endemic, often kills before one can reproduce, or it can disable to the point that one can't care for offspring or have viable offspring.
2. Sickle Cell anemia, in homozygotes, generally kills before one can reproduce.
3. If you have one gene for sickle cell, though, you experience very little discomfort (often, you aren't even aware of it) but you have very good protection against malaria.
And yes, as you suggested, that means in malaria-endemic areas, there are a lot more heterozygotes than you would otherwise expect. Here's why...
Two homozygotes for normal Hg have for kids. All of them are vulnerable to early death or infirmity from malaria.
One homozygote and one heterozygote have kids. Probability is that 75% of them will be vulnerable, but 25% will be immune to malaria.
Two heterozygotes have kids. Probability is that 25% will be vulnerable to early death or infirmity from malaria, 25% will die or be disabled from sickle cell disease, and 50% will be immune to malaria.
Which of those three tends to leave the greatest number of viable offspring? Right. The two heterozygotes.
Does that make it easier? Oh, BTW, there's a more recent mutation of Hg that provides very good protection against malaria, but even homozygotes normally don't get crippling illness or death. It's increasing in malaria areas for reasons that should now be obvious to you. Would you like to learn about that?
https://bmcresnotes.biomedcentral.com/a ... 019-4682-5
https://www.cdc.gov/ncbddd/sicklecell/f ... trait.html
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Re: Abiogenesis and Probabilities
Post #449We all got that. You just don't realize what "language" means. Sign language and use of written communication is language, and mediated by the same parts of the brain as spoken language.
It's a good idea to use words as everyone else does. Aids communication.I know we have body language, sign language and the rest but what i meant is words with specific pronunciation and meaning.
This has been going on for a long time.A deaf man learnt a language? Which one and how?
https://www.healthline.com/health/can-d ... munication
The technique mentioned here, goes back to the 1800s:
https://www.thehealthboard.com/how-do-d ... -aloud.htm
You've confused making sounds with language. The sounds are just ways to code the words for others. Notice that you're (probably) having no trouble with the words you're reading right now, even though there is no sound whatever. I'm just coding them into symbols and then you're decoding them back into sounds. Or if you're a really good reader, you're bypassing sounds entirely and just using the symbols to get the meaning.
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Re: Abiogenesis and Probabilities
Post #450Difflugia wrote: ↑Thu Nov 11, 2021 9:33 am I think you have at least one fundamental misunderstanding of the sickle cell allele and its relation to genetics, so your rhetorical questions mean something completely different to you than they do to everyone else. Instead of relying on rhetorical questions, maybe you could just explain in detail what you think is happening and why it's inconsistent with natural selection.
No. It is expected that it will reach an equilibrium. Unless malaria and sickle cell disease, takes every vulnerable person, and kills or disables everyone infected or with the mutation, there will be an expected ratio of normal homozygotes, heterozygotes, and sickle cell homozygotes in the population. Would you like me to show you a simple simulation, given a specific level of malaria?
Only if malaria incidence in normals is 100 percent and all of the infected people are disabled or killed.So whatever study you are quoting should clearly show an increase in one and a decrease in another.
It varies by the local prevalence of malaria. And yes, when control programs or other factors change infection rates, the ratios change.My point is, even in malaria endemic areas, there's no increase in people with the trait,
Let's suppose that everyone without a certain recessive gene dies. That means everyone in the population will be either heterozygous or homozygous for the recessive gene. A heterozygote and an heterozygote (H,h),if they mate, have a 25% chance of their offspring dying. On the other hand, homozygotes (h,h) have a 0 percent chance of offspring dying from this, even if they mate with a heterozygote (H,h). As a result, heterozygotes are only 75% as likely to leave viable offspring.there can never be an increase in frequency because it is a recessive gene.
Which means that the proportion of homozygotes for the recessive trait will continue to increase in the population. At some point, it is very likely to reach fixation, and to be the only allele in the population. You could simulate this with decimal dice, and see for yourself.
No. See above.An increase will only be attributed to population increase and not natural selection.