Has natural selection really been tested and verified?

I read recently where an editor of Discovery Magazine stated that Darwin provided a testable mechanism for evolutionary change, and as such it has stood up to the rigors of such testing.I am not so sure that this is true. Can people point to tests that have verified that natural selection causes evolutionary change? What tests have they conducted? Do these tests accurately mimic the real world?I would like to stipulate that talking about bacteria (in any form) does not qualify as any type of test, because ultimately we must be taking sexual reproduction, where choices are being made into account-so bacteria is out.Ok, so what are these tests which prove (or even provide solid evidence for) natural selection is the driver of evolutionary change?Edited by Bolder-dash, : No reason given.

Ok, I have made the changes as requested, but as this forum appears to be moderated exclusively by people on the pro-Darwinian evolution side of the debate, I hope that my previous wording for fairness of discussion is kept in mind.

Thank you for your thorough reply and tips RAZD.I have to say, I don't think we are even close to answering the question however. The supposition made by the magazine editor (not by me)was that Darwin's idea of natural selection has been tested to be the driving force of evolutionary change (including of course changes in body structures, and living systems, etc).So far it seems the "tests" you and others have mentioned as evidence, provide nothing in the way of showing that it was " Darwin's natural selection" that caused this evolutionary changes._In fact what they all demonstrate is that a change was "needed" in a population and the change occurred. That is quite a different thing from showing that random mutations slowly drifted through the populations along with every other kind of random mutation, causing the change.One of the studies cited by another poster deals with a population in Papua New Guinea developing an amazingly quick resistance to a fatal brain disease called kuru:

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"Lead author Professor John Collinge, Director of the MRC Prion Unit said:
It’s absolutely fascinating to see Darwinian principles at work here. This community of people has developed their own biologically unique response to a truly terrible epidemic. The fact that this genetic evolution has happened in a matter of decades is remarkable."

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It is kind of funny that one would cite a population of people developing a resistance to disease in a few decades as evidence that Darwin's theorized process of slow gradual change, based on random mutations caused these resistances. This was a random mutation that just so happened to crop up exactly in a population that was experiencing the disease, in exactly the right time(down to the decade) that the population was being exposed to the pressure? That is some serious good fortune. I wonder who that 'one" individual is who happened to be around at just the right time to father the entire population of children and pass on the resistance is? I guess the entire population can be traced by to one very prolific and possibly still alive reproducer. That is one very inbred society. The entire population was fathered by one man (or woman), who might even still be alive!Furthermore, to really provide more evidence that it truly is random mutations, and natural selection of populations dying out that didn't receive this beneficial mutation, I would think you would need to show something like a test in which other individuals within this population happened to have resistance to all kinds of other fatal diseases, which they have never even been exposed to, which they also received through a random mutation-like some might be resistant to bubonic plague, or Kluver-Bucy Syndrome, or the Ebola virus or Lou Gehrig's disease even though they have never seen or heard of these.The other studies mentioned, such as Galapagos finches and Peppered moths, these are all old stories about evolution, but in what way do they test or show the randomness of the mutations and that caused these shifts in populations?And also, since in cases like the Galapagos finches, the populations oscillate back to their original forms of shorter beaks, under different environmental conditions, we have to show the same processes happening twice-first a random mutation causes longer beaks to sprout and then those get chosen within the population, and then later wouldn't you know it, another "random" mutation comes along and the exact same slow weeding out process of mates choosing the best beak sizes happens again; and fortuitously the need for a certain beak size remains the single most important consideration for mate selection over the vast spaces of time that natural selection requires. Quite amazing.Or even more amazing still, we have a entire list of traits we are selecting for over many many years of generations, overlapping each other- lung capacity, tail size, genital size, coloration, chirping sound, eyesight, nest building techniques, proper digestive gland sizes, and on and on..and each and every one of these needs is remaining constant long enough after all these random mutations occurred to eventually trickle their way through the selection process. So each time a beak size is being chosen for, all of these other criteria, and about 100,000 = others are also being selected for. It must be a tough choice for a pretty female finch to decide.

Ok, fair enough, I am willing to modify my statement to include what is the modern day accepted form of Darwinian evolution..that is that random mutations are the ingredients for change, and natural selection the filter. If you are in the camp of suggesting that this is not a viable theory, or you believe the modern theory of evolution differs from this, feel free to say so. I hope you can agree to either accept this theory (with caveats of genetic drift, and others if you so choose) or reject it to keep the discussion on topic.

If you wish to win an argument based on sheer volume of typing, I will simply defer now. I won't however defer based on your tired and worn out theme of "well you just don't know biology, so you are wrong" argument (I even suggested when I first proposed this topic that this type of defense be excluded, because its simply not saying a dam thing.., but the admin required me to remove that part of my suggestion-although I knew it wouldn't take long for someone to drag it out).I think you answers are basically fit for a 7 year old. I know exactly what the theory suggests, every bit as much as you do.First, I could provide the exact article for this quote, but it is beside the point. The question is not what the editor meant, the question is have random mutations and natural selection been rigorously tested. Why obscure this point.

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changes in "body structure and living systems" are actually the accumulation of many smaller changes, taking place over multiple generations, so no, you are not going to see this kind of change in one study.

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I think this provides your answer with much more brevity. No this can't be tested.Furthermore, I take exception with your claim that by asking for evidence of natural selection creating evolutionary change, it is moving the goal posts to require that this takes random mutations into account. If you don't feel that random mutations must be evidenced in the study of natural selction-then what the heck are we saying exactly? That some animals with bad gentics die, and some with good gentics live longer? Ok, I accept that. So what does that tell us about anything? You mean to suggest that you wanted to just take the literal meaning of natural, and the literal meaning of selection and show that things are natural, and thing are selected? Yes, I agree, we are not made of unnatural things like teflon, and yes, people select their partners for the most part. Not very breathtaking science in this day and age.I appreciate your participation, but honestly I wasn't coming here to get a 6th grade lecture from you-I come here seeking depth and insight.If you wish to argue the finer points of evolution, you can't just gloss over all the logical assumptions one must make to have the theory make any sense at all. If people in one region of the world suddenly develop a resistance to a rare disease, a resistance people in other parts of the world never seem to spontaneously develop, we must think long and hard about how and why that happened. Was it really just that one guy happened to get this fortunate mutation. Do people in other parts of the world occassional get a similar random mutation? Do people in other parts of the world occassionally get born with resistance to bubonic plague, to Lou Gehrig's disease, to the anthrax virus, to arsenic? How often does this happen randomly?These are just some of the questions that have to be asked and tested before we can say that this "theory" has been vigorously verified.

Hello cosmic chimp,The author of the study himself declared that this resistance happened in a matter of a few decades.Now you might expect that this protective polymorphism would be disproportionately represented in a population which has been exposed to this disease-but the fact remains, we still have to account for how it got there in the first place in a logical fashion. ONE individual must have gotten this mutation first, yes?How often do you suppose this exact mutation happens in the entire population of the world? Every 10,000 individuals gets this? If we tested 10,000 Americans, would we find at least one with this mutation? 100,000? How about a random mutation for resistance to dioxin? How many individuals presently living in the world have a resistance to dioxin? One in a million? One in a billion? Does anyone have this? Rabies? How many people are born every year with a random mutation for resistance to rabies?Don't we need to know this, to know just how fortunate were the odds that one of the members of this small tribe just so happened to be born with a random resistance to kuru disease? When did it happen, 100 years ago? 1000 years ago?

Ok, well, I will answer some of these as time permits.The point you seem to be making is that you will only likely find these types of beneficial mutations in populations where there is pressure for that mutation to spread throughout its population. But that is not addressing what I am saying at all.I was discussing the starting point for these kinds of mutations to arise. For such a resistance to begin within a population, first there must be ONE singular carrier of that beneficial mutation. Or if you wish to say so, one can suppose that maybe several individuals within the population got the same mutation. Either way, we need to be able to look at the odds of that happening, and one way to do that would be to see in a random sampling of individuals NOT exposed to any of these diseases, are they still occasionally getting this kind of mutations at birth. Do one in 10,000 people get born with a mutation that would just so happen to provide a resistance to kuru disease? Or to rabies? Or is it much less than that? After all, we are saying these mutations are random, so why only look at individuals in populations with pressure to select for this. If you were able to test the entire world's population, would 1 in a billion have this genetic mistake-not as a trait that was inherited, but simply because these kinds of things are common genetic mistakes?When we can show that these kinds of mutations-resistance to diseases, beneficial additions to existing body structures and so forth, are happening all the time randomly, then we can at least be closer to showing a basis for how this theory logically can work.You know, one part of the theory suggests that in order to build complex parts, small mutations occasionally arise which have piggybacked onto existing body plans and caused a reproductive advantage. So do we see this as well, say in human populations? Do people get born with mutated depressions right in the sockets of the eyes, in such a way that they actually experience vision better than all other people do, simply because they have this unusual mutation? Furthermore, are there people that are born with similar mutated depressions, but they don't happen to be in their eye sockets, but instead they happen to be in the middle of their shin, but if they were in the middle of their eye sockets it would be useful? And these kinds of mutations keep cropping up in all different parts of people's bodies, and sometimes they just so happen to hit in a perfect location-just like a hole formed in the side of an individuals face, in such a way, that it made hearing possible or better. Maybe some people are born with an extra hole in their head, and if they survive long enough to have babies, they can make an entire subset of individuals with this extra hole, and one day that can turn into a third ear..ones which can pick up unknown frequencies of vibrating strings in the cosmic ether.Any evidence for these kinds of things occurring with regularity?

This is a discussion about natural selection including the mutations that are necessary to drive the selection. You need a mutation in order to have varying genetic models to choose from. Is that hard for you to gather?

I don't believe that you are an evolutionary biologist, so I am not sure how you can know what they may or may not understand. If as it appears you can not understand the logical questions with the selection process, and the need for continued new starting points to select for, I shall move on to others.

Has the question become Can I prove it is not evolution? rather than has the scientific community shown that it is- through rigorous testing and conformation?

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This paragraph shows a common misconception about evolution: The timing of the mutation is concurrent with the timing of its value. It is not. The mutation may have happened a thousand generations prior.

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Say a simple mutation makes an apparently unimportant change in an apparently unimportant protein. This protein is passed down in happenstance fashion for twenty thousand years and now 2% of the tribe has it.

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It is not a misconception about how the theory works. The original mutation may very well have happened 100's or even 1000's of years before, or it may have happened ten years ago-you are simply guessing at this. I suppose one way to test your theory would be to test other groups of populations that have never been exposed to the disease, and see if they also have 25 of the population with this kind of mutation. Is 2% a normal variation we see randomly in populations?Many of the arguments to support the ToE seem to stem from people saying..."well, suppose this happened...blah blah." Ok, if we are going to use the idea of suppose this happened, then fair enough. But by the same token, since you can't prove what did happen through testing, I guess all supposition are fair game for scrutiny.So you can guess if you like, that this kind of resistance was a slow gradual process that took thousands of years to achieve, but since we also have evidences of other evolutionary change NOT happening in quite the very slow gradual way over many thousands of years that natural selection is said to occur, but often in a more rapid fashion, your guess is no better than a guess that says it didn't happen thousands of years ago.That is why I said it is funny that the poster would use this as one example of a test of natural selection's abilities. The author of the study himself said he was surprised that this could happen so quickly, over a few decades. If you want to show proof of your theory as a slow natural selection process it is kind of ironic to site a study which shows exactly the opposite of slow, don't you think? Edited by Bolder-dash, : for clarity, and to segment the quotes better-I don't know how to do that!

You are going to need to improve your comprehension skills, before you can so arrogantly accuse others of not understanding.Point: I NEVER said that the Theory suggests changes based on need, I said that the evidence from those studies only demonstrate change when it was needed! I was saying the exact opposite of what you inferred. Here is the exact quote:"So far it seems the "tests" you and others have mentioned as evidence, provide nothing in the way of showing that it was " Darwin's natural selection" that caused this evolutionary changes._In fact what they all demonstrate is that a change was "needed" in a population and the change occurred."Now from that VERY simple sentence you have concluded that I was saying the ToE suggest change occurs when needed. How wrong can you be.So if you can't even get this very simple bit of logic, how can you possibly understand the rest.I say "the tests you provided don't indicate random mutations and then slow eventual change but rather demonstate changes occurring quickly when needed", and you say the "ToE of evolution doesn't suggest that change occurs based on need, see you don't understand the theory" No kidding it doesn't suggest that. What the hell do you think I was saying!And you want to use this brilliant deduction to say I don't know what I am talking about. Terrific.Forgive me if I don't cloud this discussion with replying to such inanity in the future.

Well so far we have peppered moths, finches with oscillating populations of varying beak sizes, and a resistance to disease occurring in a population is a few short decades. Not a very impressive list to show that the ToE has got it all pegged correctly so far if you ask me.Heck, I am not even a creationist, but I can certainly see why plenty of people would want other theories discussed in schools...or at least hope that we start looking for some other theories. Edited by Bolder-dash, : spelling...poor eyesight

Well, I don't think it was incoherent. The point of the hole in the head is that we have to account for ALL forms of living systems through this process if the theory is correct, so we must account for how ears developed, and how new systems will develop in the future. For the theory to make sense, it should make sense from a practical standpoint of how could it happen. So instead of thinking about just disease resistance, think of other body parts, because these can be seen with the naked eye, whereas disease resistant mutations can't be.Before I expand on that, let me answer your second point. I disagree; it would give us lots of worthwhile information. If for example this type of protective mutation occurs at a common frequency, then it would not seem so unlikely that the natural selection process could work to drift it into an entire population that does get exposed to kuru, because it would be happening to lots of individuals, and so it wouldn't seem so strange that those who are exposed to it also have a percentage of people with this mutation.However, if we were to find that this type of protective mutation almost never happens in the general population not exposed to the disease..then we have to start considering whether or not there is a relation between a population that gets the disease and a population that gets the mutation; or at least what the likelihood of the ONE individual who got this protective mutation being a part of the chain of bloodlines of people who actually get the disease. If there is a correlation between where these mutations have occurred, and where the disease exists, we have to consider that maybe it is no longer a random cause and effect situation, but instead something is causing a protective response. That is quite a different story.So now back to the mutations which we can actually see. let's take the same scenario..an individual gets a mutation, and it continues into a population, until eventually an environmental situation occurs which just so happens to coincide in a beneficial way with the conditions of this mutation. this is ins a sense exactly what the ToE proposes. A random mutation just so happens to have a beneficial effect. Later further mutations in that same bloodline expand upon that first mutation, making it an even better functioning system, or appendage, etc.. The mutations..which may be (likely would be )many generations after the first mutation, in one way or another improve upon this first mutation. Now this is not me saying how it works, this is how Dawkins, and many others all claim it could work...like in his blind watchmakers example. A species gets a light sensitive patch, and then further mutations down the bloodline get a depression in the light sensitive patch which focuses light better, and so on-with each successive mutation being selected for.So, why is it important to know how often these various types of mutations can happen? Well, because we can then consider the possibility of this actually working in practice.Now, these kinds of mutations should be visible..after all, they are affecting functioning body parts. So mutations like light sensitive patches of skin, and depression in the skin where a light sensitive patch could focus light better..these are all visible, or at least detectable things. So if these kinds of events are common, then it doesn't seem so strange that eventually a depression in the skin could actually occur right where the light sensitive patch happens to be. After all, if a mutation for a skin depression is common, of course eventually some species which already has a light sensitive patch would likely get the depression all over their body, and eventually one of them would be right exactly on the spot where it can concentrate light better (again, not my theory, Dawkin's' and others).However, if mutations for skin depression (and these of course must be mutations which effect the DNA and so are inheritable) are not common, then getting a skin depression once in a billion times, but getting it right were it would be beneficial for focusing light better becomes more troublesome. So how can we know how frequent these types of mutations are? Well, we can look at existing populations of species. For example, if an eye first developed in an octopus, how often do octopus get mutations which cause specific depressions in their body which they pass on to their offspring.Do we see this? Do we see random mutations in octopus which give specific depression-and which are actually part of a mistaken DNA coding? Do they happen everywhere..say in every 10,000 individuals, will one get a depression, somewhere, anywhere. And how about light sensitive patches, are they common? Do you have any friends who have light sensitive patches on their arms because of a genetic mutation? Do Zebras? Do cats? If they are common, why don't we see more of them?I am guessing that these types of genetic mutations are rare. very very very very rare. So rare in fact, that its not countable. ut even if just very very rare, and not very very very rare..it still makes it even more unlikely that one of the individuals of this bloodline with this light sensitive patch, would ALSO get this rare defect of a depression which could focus light better (and please don't give me the argument about, well, once the first one got the light sensitive patch, many more offspring thousands of years later then also have it, so there were more individuals around who could get the depression-its still going to be a rare occurrence). Its still going to be rare enough that getting the depression EXACTLY where it could actually be useful is again going to be unlikely -IF we are assuming these mutations are simply random.And its going to be even rarer rarer still that thousands of years after that, another depression is going to come along again in the eye socket region, and not elsewhere, that is going to deepen it further and focus light even better-so much better that those who don't have this new mutation will all die out.And on and on and on..for every system, every body part, every thing you can think of that makes up a complex organism. And because there are so many millions of parts and systems, these mutations and selections are all happening in tandem. That's A LOT of things to be selecting for!This is JUST ONE of the MANY problems the ToE has to address before it should expect thinking people to all just accept it as a reasonable explanation in my opinion. Especially, since it seems as you all are showing, that we really can't test this. Don't just say its nonsense..spend time thinking about it. Edited by Bolder-dash, : spelling..wrote I instead of aEdited by Bolder-dash, : clarifying individuals to mean those extended offspring of the one who got the mutation.

No, your reply is stupid. In fact many of your replies (most, as I have seen) have nothing to say, other than trying to express your own brand of not very interesting glibness.Natural selection must choose from a variety of different genetic groups. How do we get these different genetic groups if not through mutations?If you wish to suggest that it is not through genetic mutations, but other forces that create this great diversity, I am certainly willing to entertain your theory. For instance, if you wish to explain how an eye developed through natural selection-please include the entire process. I would be very interested.