Is Darwin's Theory of Evolution True? Part 4.1

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You can keep repeating yourself. Not being able to reproduce is a loss of function.
Not being able to reproduce with the parent species is a loss of function. Being able to reproduce with the daughter species is a gain in function. One loss; one gain.

rossum
 
Let’s take this example to imply illustrate some of th issues with an evolutionary approach to explaining the diversity of life.

I won’t be talking about the actual existence of organisms in their own right, nor how there instinctive nature more than anything defines what they are. Such is th case in the life form we know best, ourselves.

I’m asserting that to call the moth example evolution is a misnomer. There are mechanisms in the physiology of the organism and the cells of which it is comprised, that react to stresses in the environmnet. In this regard you may wish to look into the NASA twin study. The moths’ DNA may undergo a series of changes simply because of the increased threat of being seen, which they may or may not perceive. Alternatively, it has been shown that much of speciation is the result of gene deletion. The coding for colour is glitched by random physical factors, completely or in such a manner that lighter shades are produced at a lower frequency. Natural selection is the clean up mechanism that does away with what does not work. It simply involves interaction of the whole organism with its environment. With regards to a previous post, human beings are changing, they are evolving in the broad sense of the word. In spite of improved nutrition and public health measures which are known to improve IQ, the average for human beings was shown to be actually decreasing at a pretty dramatic rate of 1 point per decade since measurements were first taken 140 years ago. And we do live in an environment with natural selection always at work. Sorry that there’s a lot here presented in a cursory fashion, but there’s so much more. You may wish to review the previous more that 8000 posts on the subject that preceded this thread.
 
No, you only have a vague (or nonexistent) interest in challenging your creationist views. Don’t get it twisted
 
Dude but can’t you see that something like that could lead to new species? What if the other moths had died and only these survived?
It’s just a built-in ability, just like it is for the chameleon lizard, are chameleon starting to grow feathers now?
 
ALL abilities are built in abilities in natural selection. That’s the point.

There’s a bunch of trees in the savannah with fruits: giraffes don’t grow long necks to get he fruit, ONLY those giraffes with ALREADY long enough necks that they get through RANDOM mutations will eat the fruit and not die of hunger like the others. Only those giraffes will survive and pass on their genes to their kids who will inherit this condition, and so on.

If you still don’t get it, there’s nothing more I can do for you
 
You need to explain what was all these environmental pressures that was triggering random mutations to build all the millions of different kinds of plants and animal species.There would have to be millions of transitional stages all needing environmental pressures to mutate every stage.
No, no, you misunderstand. It doesn’t take some special environmental pressure to trigger random mutations. DNA is mutating all the time. Every time our cells divide, for instance, we are vulnerable to mutations. Even though these mutations happen without being repaired at the time at an extremely low rate, it happens often enough to add up.

The important mutations for this topic are “germ line” mutuations…that is, mutations in genes destined to be passed on. For instance, there are locations identified at which a certain mutation will give rise to hemophilia A and in another region the result is hemophilia B. That is a mutation that does not bode well for the survival of the bloodline. A family might also pass on a genotype that is merely vulnerable to being “turned on” or “turned off” and by that causing disease. It is even possible to have a gene that causes disease if you have two copies of it but gives resistance if you have even one copy. An example of this is the sickle cell gene, which gives inherited resistance to malaria. Another example is cystic fibrosis, which gives resistance to the enteric effects of cholera. These genes are more prevalent in areas where those diseases are endemic; a family that has them would lose unlucky members felled by the genetic disorder, but would preserve other members because of the resistance a single copy gives to other members of the family. There are many other examples.

 
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So what was all the environmental catalyst for all this mutation to occur ?
Mutations happen all of the time. It is just that usually mutations are not a good thing.

For instance, look at all the different breeds of dogs. These came about because some dog somewhere or other had some random mutation. Because the dog was domesticated, what would probably be a fatal mutation if it were a wild animal–being extremely small isn’t going to help a wolf’s chances of survival–instead made it more likely that the dog would be bred to preserve some new odd feature or other that humans like.

When the environment goes through a big change, what is a survival advantage and what is a disadvantage can also change. If domesticated dogs went through an environmental change where they had to return to pack life and fend for themselves, the gene lines that lead to Yorkies would probably die out very quickly. The long hair is a disadvantage, the small size is a disadvantage, and so on. The other canine gene lines would outcompete that one. In a few generations, any wild dogs that survived the withdrawal of human support would settle down to one or a few different kinds of dog. It might be that wild dogs couldn’t compete with other predators and they’d just die out.
 
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There’s a bunch of trees in the savannah with fruits: giraffes don’t grow long necks to get he fruit, ONLY those giraffes with ALREADY long enough necks that they get through RANDOM mutations will eat the fruit and not die of hunger like the others
How did the small juveniles and the short females survive ?
 
Juveniles were fed by parents. Short females died or were fed by others. In any case, with no long necks in any of them they would die
 
I thought the moth study was a known example of being faulty/possibly fraudulent, sorta like piltdown man.

But I would imagine those arguing for creationism would know it to be so if true, so who knows
 
ALL abilities are built in abilities in natural selection. That’s the point.

There’s a bunch of trees in the savannah with fruits: giraffes don’t grow long necks to get he fruit, ONLY those giraffes with ALREADY long enough necks that they get through RANDOM mutations will eat the fruit and not die of hunger like the others. Only those giraffes will survive and pass on their genes to their kids who will inherit this condition, and so on.

If you still don’t get it, there’s nothing more I can do for you
"No, no, you misunderstand. It doesn’t take some special environmental pressure to trigger random mutations".-PetraG
 
ALL abilities are built in abilities in natural selection. That’s the point.

There’s a bunch of trees in the savannah with fruits: giraffes don’t grow long necks to get he fruit, ONLY those giraffes with ALREADY long enough necks that they get through RANDOM mutations will eat the fruit and not die of hunger like the others. Only those giraffes will survive and pass on their genes to their kids who will inherit this condition, and so on.

If you still don’t get it, there’s nothing more I can do for you
We now know natural selection is a conservative process not a creative one.

These are adaptations.
 
I thought the moth study was a known example of being faulty/possibly fraudulent, sorta like piltdown man.

But I would imagine those arguing for creationism would know it to be so if true, so who knows
The main problem with evolution as a scientific mechanism is not in the business of subspecies and genetic lines within a species. Those are documented over and over and over again.

The main problem not solved in explaining evolution is the mechanism by which a breeding population with one number of chromosomes arises from a breeding population with an incompatible number of chromosomes. As far as I know, a mechanism by which this can occur spontaneously has never been demonstrated at all, let alone demonstrated to have actually happened in nature. Single mutations work fine if the mutated individual is still fertile and has a breeding population to consort with in order to pass the mutation along. What if the individual has the wrong number of chromosomes to breed with any others of its kind? That has dead-end written all over it.

Therefore, even though there is indirect evidence of evolution as a mechanism for creation all over the place, that one problem is still an unanswered question. It is not fatal to the theory only because no one has a better theory to explain the genetic evidence that does not have that “Miracle Occurs in Step Two” kind of problem. When that happens, the theory that explains things the best survives, provided the problem with it is an unknown step and not a step that can be shown to be impossible.
 
No, no, you misunderstand. It doesn’t take some special environmental pressure to trigger random mutations. DNA is mutating all the time. Every time our cells divide, for instance, we are vulnerable to mutations. Even though these mutations happen without being repaired at the time at an extremely low rate, it happens often enough to add up.

The important mutations for this topic are “germ line” mutuations…that is, mutations in genes destined to be passed on. For instance, there are locations identified at which a certain mutation will give rise to hemophilia A and in another region the result is hemophilia B. That is a mutation that does not bode well for the survival of the bloodline. A family might also pass on a genotype that is merely vulnerable to being “turned on” or “turned off” and by that causing disease. It is even possible to have a gene that causes disease if you have two copies of it but gives resistance if you have even one copy. An example of this is the sickle cell gene, which gives inherited resistance to malaria. Another example is cystic fibrosis, which gives resistance to the enteric effects of cholera. These genes are more prevalent in areas where those diseases are endemic; a family that has them would lose unlucky members felled by the genetic disorder, but would preserve other members because of the resistance a single copy gives to other members of the family. There are many other examples.
You are correct. DNA has several repair mechanisms and only after these corrective measures fail will a mutation have a chance to stick. The odds are very low and increases the time needed for evolution.
 
Mutations happen all of the time. It is just that usually mutations are not a good thing.

For instance, look at all the different breeds of dogs. These came about because some dog somewhere or other had some random mutation. Because the dog was domesticated, what would probably be a fatal mutation if it were a wild animal–being extremely small isn’t going to help a wolf’s chances of survival–instead made it more likely that the dog would be bred to preserve some new odd feature or other that humans like.

When the environment goes through a big change, what is a survival advantage and what is a disadvantage can also change. If domesticated dogs went through an environmental change where they had to return to pack life and fend for themselves, the gene lines that lead to Yorkies would probably die out very quickly. The long hair is a disadvantage, the small size is a disadvantage, and so on. The other canine gene lines would outcompete that one. In a few generations, any wild dogs that survived the withdrawal of human support would settle down to one or a few different kinds of dog. It might be that wild dogs couldn’t compete with other predators and they’d just die out.
What is left? Dogs.
 
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