That sounds like it’s made up on the spot just to make it look like you have an answer. I have never seen anything in Christian theology that would lead anyone to the expectation of a nested hierarchy of separately created species. All I have seen are ad hoc protestations like the one you have given.
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What’s silly is that for every natural explanation, that explanation will either have another natural explanation, to which an explanation can be given, or it can be said to have naturally just happened without cause, or it can be caused by a supernatural explanation that doesn’t need to be caused.
After a few years on Reddit, slowly but surely, I found someone to agree with this statement:
Things apparently pop into existence all the time. Now the question is whether it was caused by something else that popped into existence, to which the same question applies, or it was caused by something that doesn’t pop into existence or it just popped into existence without cause.
The thing about the latter two, is that they would appear the same. Something that can affect change without changing would be unobservable, so that what it caused appears to come from nothing.
So I would assume that if someone wanted to explain to you how clouds form they would also need to explain how the universe originated?
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Personally, I find this quote from Michael Heiser pretty well aligned with the attitude I most identify with:
“Let me say first that, despite an interest in genetics, I find it hard to care about evolution, theologically. I’m not offended by the thought at all. I really don’t care what mechanism God used to do what He did.”
@T_aquaticus
Where did evolutionary theory predict that early embryonic development could not change between lineages?
You’re right, evolutionary theory does not predict that embryonic development could not change. But it’s a matter of degree. Not determined in some a priori fashion, but what can realistically / credibly be achieved by the evolutionary mechanisms as we currently know them. (As indicated in my opening post, I see the possibility that further research could find that there is some way of directing a search through sequence space; but it does look like it would need something substantially new such as this.) For more on this, see my response below to @rsewell .
@T_aquaticus
That seems to be more of a subjective intuition that some scientists had. I don’t see how it emerges from the theory itself.
I don’t think it’s a subjective intuition on the part of some scientists. Rather, they (and it seems to be most who work in this area) recognise how much of a challenge it is, especially as we increasingly recognise that biological tissues are not plastic (again, refer my 1st post) but moulded by specific molecular mechanisms which ultimately rely on DNA sequences that work.
@T_aquaticus
Leyton:
I’m not saying that there aren’t major (and minor groups) of vertebrates (and other organisms). I’m only saying that their embryonic development is so different, that it argues strongly against their common ancestry.
That seems to be an entirely subjective opinion. How much is too different, and why?
It’s not subjective, it depends on the facts. The very different early embryonic development of different classes of vertebrates points to at least these being separate. But the embryonic evidence clearly points to subgroups within these (and I’m not saying that embryonic evidence is the only basis for demarcating). For example, in amniotes, including most placental mammals the extraembryonic membranes (enclosing the amnion etc.) form after gastrulation from folds of tissue which grow from the sides of the embryo and meet / fuse above and below the embryo. In primates, the extraembryonic membranes arise before gastrulation by cavities arising within some of the early tissues (of the blastocyst). What, evolutionarily, could have driven such a huge change in so early a stage of embryonic development? And as it relates to a group within the mammals, if the primate way evolved from that of other placentals, it would need to have occurred quite recently (in geological terms).
@T_aquaticus
There’s absolutely no reason why we should expect see a nested hierarchy if species were created separately.
So your reason is just your intuition.
@rsewell
A lot can happen in 375 million years or so. Not a problem.
If you look at it objectively, you might be surprised at how little can be achieved.
I’ll illustrate it with the acquisition of resistance to some insecticides and antibiotics.
DDT acts by binding a key protein involved in nerve function. Resistance usually arises by a mutation to that protein so that DDT doesn’t bind, but the protein still functions. A typical mutation rate is in the order of 1 in a billion per nucleotide per generation. Although this is low, for insects with a population in the order of a billion, it’s not at all surprising that an appropriate mutation can arise quite quickly, eg within a generation, although it will take several generations to spread through a significant proportion of the population, even in the presence of DDT.
One of the main ways in which resistance to natural penicillin arises, is by means of an enzyme which deactivates it (beta-lactamase which was already present in bacterial populations; in the presence of penicillin, natural selection favours those that have it). To overcome this resistance, synthetic penicillins were made that were not degraded by the lactamase. But in time resistance arose to these, and by mutations to the lactamase which enabled it to degrade the synthetic compounds. Proof that evolution works! However, where the modified enzyme requires only 1 mutation, with the even larger populations (compared with insects), it is again not surprising that this can arise quickly. In some cases, 2 specific mutations are required; and, although the probability for this is only about 1 in 10^18, the much larger bacterial populations means that overall there’s a good chance of it occurring. And their short generation times means it can spread quite quickly (in the presence of the antibiotic). Some resistance involves 3 specific mutations, for which the probability is only about 1 in 10^27 which probably exceeds even bacterial population sizes. So how does it arise? Because 2 of the 3, by themselves, confer some resistance; so the intermediate stage can arise, spread through some of the population, and act as a stepping-stone to further resistance.
What’s the take-home message? Even with very large populations, it is only realistic to make progress is steps of 2 or maybe 3 coordinated mutations. If an advantageous step requires 4 or more coordinated mutations, it’s not going to happen. (This is one of the criticisms of phylogenetic trees of eg protein sequences which frequently show large jumps without any consideration to their improbability, or to the activity of intermediates.)
Second is the reality of population genetics. So many evolutionary accounts assume that if an advantageous mutation arises then it will automatically be adopted by the population, and quickly. But to give just one example, if a mutation confers a 1% increase in fitness then there is a 98% chance it will be lost; so it would need to recur independently 34 times before it had even a 50% chance of being fixed in the population. And it would take at least 100s, probably 1000s of generations to do so.
So, for vertebrates, with their much lower populations and longer generation times, how much do you think might be achieved in 375 million years?
Again, these are all mushy, subjective comparisons. There isn’t anything objective or measurable here. What is too challenging? What are the specific mechanisms, and why are they an issue for evolution? There’s nothing specific that allows one to even start to address the topic.
What’s “very different”? What units are differences measured in? You say it isn’t subjective, and then immediately use subjective language. This is the issue.
Could be any number of possible mechanisms, everything from neutral drift to selection for a specific phenotype.
No, it’s a complete lack of anyone putting forth a reason for why separately created species should necessarily fall into a nested hierarchy. On the flip side, we can predict that we should see this very pattern starting from the first principles of evolutionary mechanisms. The combination of vertical inheritance, mutations, selection, neutral drift, and speciation should absolutely produce this pattern. We can even objectively measure how well the data fits to a tree-like structure. This isn’t intuition. This is objective science.
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There are several issues with these types of claims.
First, how many combinations of 2-4 mutations will produce a beneficial phenotype in any given genome? That’s the number that these calculations never have. Instead, they commit the Sharpshooter fallacy. They focus on just the 2-4 mutations that did occur and pretend as if those are the only mutations that could have produced a beneficial phenotype. They draw a bullseye around the bullet hole. There is also the possibility that each of those mutations is beneficial on its own.
Out of 50 such mutations you would expect 1 to reach fixation after the first time it appeared.
Let’s take a look at the human population. Let’s use a constant population of 1 million, a mutation rate of 50 mutations per person (which has been empirically measured), a 25 year generation time, and 5 million years of time. That would be (1E6 * 50 * 5E6)/25 or 10 trillion mutations over that time. If these were evenly distributed across the human genome that would be enough mutations to hit every base more than 3,000 times. There are only ~40 million mutations that separate humans and chimps. I’m not seeing an issue with getting 40 million differences if 10 trillion occurred in the human lineage at one point or another.
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The problem with a great deal of such statistical arguments, is that a teleological objective is assumed as an evolutionary goal. For every species that has come about, how many have never existed because it just did not happen for them? Mutation and environmental change is constant. Fidelity and stability are absent from nature. The same odds that are against you and I demand that somebody win the lottery.
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Why is this a problem for the providential evolutionist? I find it to be more of a problem when it is assumed otherwise.
It may not be. It is just that if God draws from a barrel of possibilities, from our vantage there would be no way to distinguish that from a non teleological world.
There is room for wonder at the beauty of creation within methodological naturalism. I still feel wonder at snow. And supernatural explanations can often be terrifying–demon possession, witchcraft, and the like. It has led to terrible human rights abuses.
I think a parallel can be drawn to the type of humanism that supposes the cause of the universe is unaware of its action.
This feels like up is down, and down up.
No it’s reason.
Everything that has been.
Except you taking your thumbs out of your ears, your fingers from your eyes whilst la-la-la-ing.
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Would your meaning change at all if methodological was crossed out?
And nothing is more terrifying than solipsism which is perfectly natural to our fallen nature and totally at odds with the rights of others.
Picking up from the article you sent me, I find this to be a poor characterization of the approach the theistic evolutionist takes.
God did it, but let’s look at what happened so we can better understand the world he has given us. In other words:
“So, whether the origin of life was “natural” or “supernatural” it was of God, and there is nothing to be lost by attempting to investigate it through the scientific method.”
And if it can be reasonably assumed that God did not do it, like a “cause” that is unaware of its action, then I’m ok with that too… (sort of).
Frederick Copleston has a great passage on the subject of Aquinas’ synthesis that relates to this, which I may be able to quote later today.
@T_aquaticus
What units are differences measured in?
Nucleotides. Ultimately, the differences in embryonic development are due to differences in DNA, measurable as differences in nucleotide sequences. If vertebrates have evolved from a common ancestor, then evolutionary mechanisms need to be a credible explanation for how these differences arose.
@T_aquaticus
Could be any number of possible mechanisms, everything from neutral drift to selection for a specific phenotype.
Yes, but progress through neutral drift would be even more difficult than the example I gave. If there is no selective advantage, then the chance of being fixed falls to 1/2N (where N is the effective population size) so is much less than eg the 2% for a variation with a selective advantage of 1%. And it takes much longer for a neutral mutation to spread through a population.
My example was of selection for a specific phenotype (having resistance to the presence of a pesticide / antibiotic).
@T_aquaticus
They focus on just the 2-4 mutations that did occur and pretend as if those are the only mutations that could have produced a beneficial phenotype.
In typical insect and bacterial populations, most if not all possible nucleotide changes will arise in most generations. But in every case they result in a decrease in fitness, except when an insecticide / antibiotic is present; in which case, if the nucleotide change confers resistance, then it will have increased fitness relative to its neighbours while the insecticide / antibiotic is present. Organisms with resistance invariably are less fit than the normal (wild type) which is why, in my previous post, I included the continued presence of the pesticide / antibiotic while the resistant form is spreading through the population.
So, although all mutations occur and will be ‘tried out’ by natural selection, only those which confer resistance, and do not disable the relevant protein, will be successful. Which is a good reason to focus on them.
@T_aquaticus
Out of 50 such mutations you would expect 1 to reach fixation after the first time it appeared.
Not quite, in the example I gave it would still be only about 73%; but let’s suppose the mutation conferred an increase in fitness of about 4% so that there was approx. 99% chance of fixation with 50 attempts. You have to wait 50 times as long for the mutation(s) to arise that many times. If you want the attempts to run in parallel, then you have to consider how unlikely it is for the beneficial mutation(s) to arise simultaneously. Which depends on the size of the population: not a problem for bacteria, which is why resistance arises; but more of a problem for small populations such as vertebrates.
@T_aquaticus
Let’s take a look at the human population. Let’s use a constant population of 1 million, a mutation rate of 50 mutations per person (which has been empirically measured), a 25 year generation time, and 5 million years of time. That would be (1E6 * 50 * 5E6)/25 or 10 trillion mutations over that time. If these were evenly distributed across the human genome that would be enough mutations to hit every base more than 3,000 times. There are only ~40 million mutations that separate humans and chimps. I’m not seeing an issue with getting 40 million differences if 10 trillion occurred in the human lineage at one point or another.
You are completely ignoring that, when a mutation arises, unless it confers an advantage, it will just mutate to something else. Even if, combined with other mutations that may occur in the future, it could contribute to a substantial change.
@rsewel
The problem with a great deal of such statistical arguments, is that a teleological objective is assumed as an evolutionary goal.
Not at all. As indicated above, I assume that mutations will occur throughout the genome. But unless they confer a benefit, they will be lost / randomised.
@Klax
Everything that has been.
That’s just a circular argument.