Natural Limitation to Evolutionary Processes (2/14/05)

Actually that's not strictly speaking accurate. Evolution is not just concerned with whether or not the gene is passed on but how often one gene is passed on relative to its allele(s). If one gene is not passed on at all, then its frequency in the population is reduced to 0. If those that posess the gene only produce an average of 1.9 reproductive offspring and those that posess its allele produce 2.0 reproductive offspring, then the frequency of the gene in the population will decrease and the frequency of its allele will increase.The less good gene may remain in the population for a long time, but it becomes less frequent than its alleles.Human evolution is complicated in that we are able to increase the potential reproductive capability of people with less than ideal genes.So, whilst our population is increasing the amount of genetic diseases also increases. Without intervention they might grow in size but still reduce in frequency. Once the population settles down to a set size (or begins to reduce) and competition for survival over resources we will then see those that are genetically less able to reproduce being the first subsets to be reduced and go extinct. In a population that is still growing, things are a little more complicated.

I was using the term allele to refer to 'rival' genes to the gene we are examining the frequency change of. It's not necessarily strictly kosher terminology but its handy to get the point across. I picked it up from Dawkins who used the same differentiation to allow for simplified explanation of the complicated concepts involved in talking about allele frequency changes.Hopefully it hasn't clouded what I meant significantly, but instead helped keep it as clear as space allows.

Of course, one can get into sticky situations when applying anthropomorphic concepts to a natural process.If we consider ToE as a mathematical model for predicting changing allele frequencies in populations it begins to make more sense. Genes replicate. The genes that replicate the most become more frequent than genes that replicate less. A gene's success at replication depends upon its environment, a gene's environment includes other genes in the gene pool.If a gene statistically reduces its own chances at reproducing itself compared with other genes (its alleles), it will become less frequent. Therefore, I fail to see what the implications of the incidence of disease in a population have with regards to the viability ToE.In a population that is not growing in size, there will be less and less genetic diseases as those without them simply out reproduce those with them. This will continue till the genetic disorder is selected out or it reaches an equilibrium. Even in cases where they don't out reproduce, they still can outlive those with the disease - meaning that they can not provide as much care for their children and grand children....which statistically reduces their fecundity anyway.In light of this, I am struggling to understand how disease has these implications. I think everyone is struggling to understand it. So, if you could explain it in as straightforward terms as you are able to communicate to us so that we can explore it.Novel genetic disorders aren't going to be a major problem since they will still be statistically against the odds to propagate throughout the population. They can still do it, but it's unlikely. When they do propagate, they will do so at a much slower rate than healthy genes propagate so the healthier genes continue to have dominance. Genetic diseases are not threatening to overwealm populations unless those populations are very small or such.So here is the conclusion. There maybe a surprisingly large number of genetic diseases out there, and some of them may be novel genetic mutations. However, they are tiny compared with the number of healthy genomes that are routinely generated - and the healthy genomes are being entirely ignored in this discussion. The frequency of healthy genes in a population is generally increasing compared with the frequency of unhealthy genes.As such, there maybe plenty of new diseases coming about and they have effect on the fecundity of the organism that has them. One could come up with a mathematical model to show at what rate of new and inherited genetic diseases in a population would cause a population a problem.It seems at the moment you have not done such a model, but instead have simply claimed it presents a problem. I think this is very premature. Indeed - the maths has been done. There is more information about Mutational load, indeed there is plenty of work in this area, you just need to know where to look.Your criticism is not something that evolutionists have ignored. The genetic/mutational load has been the subject of scrutiny of a much higher degree than you might realize. The ball remains in the court of a mathematically minded creationist to use the models to show that mutational load is a problem for evolution.edit: some creationists have used Haldane's work to try and do this very thing incidentally, but I'd be more impressed if they didn't use papers from 1957. This paper goes into further detail, but it's highly technical.Edited by Modulous, : No reason given.

Beneficial mutations, some examples:

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a third frequent mutation in this gene, the Ser447-Stop, is reported by some investigators to underlie higher HDL cholesterol levels and would represent a beneficial genetic variant in lipoprotein metabolism

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Additionally, correctly spliced mRNA lacking the Arg661 --> Stop mutation of the maternal allele could be detected. These results demonstrate that a mutation in splice donor site of intron C can result in several variant mRNA transcripts and even permit partial correct splicing of FXIII mRNA. Further, even the minute amount of correctly processed mRNA is sufficient for producing protein capable of gamma-gamma dimerization of fibrin. This is a rare example of an inherited functional human disorder in which a mutation affecting splicing still permits some correct splicing to occur and this has a beneficial effect to the phenotype of the patients.

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Here's the rub - the standards that are used to determine a mutation that is harmful are the same as the standards to determine if it is beneficial. I have a feeling you will deny any beneficial mutation provided to you because you would state that we need to prove that it was not something already in the population to begin with.If that is the case, it sounds like you are developing an unfalsifiable hypothesis, which of course is not science. It is fine as a position to take but it is not a fine position when it comes to criticizing the science itself. The same can be said of the negative mutations. Can you prove that they weren't in the original design spec for humans and that we have weeded them out and become stronger/more fit?These mutations are only slightly beneficial, but single beneficial mutations are inevitably going to be this way because of the concept of the genespace. Taking small steps through genespace is more likely to hit on a non-lethal mutation. Non-lethal mutations are 100% more likely to be beneficial than lethal mutations - as such big changes are more likely to be lethal and obvious and beneficial changes are more likely to be comparitvely small.

You now have more than two strange contenders. You also have been given a reason as to why single beneficial mutations are much less noticable than single negative mutations if you wish to make a comment on that. If the genes weren't inherited from the parents, would you agree it must be novel? Apparantly it can if the mutation has a negative impact. You said so yourself. Why do you not accept examples which have a beneficial effect? This isn't mutation, and geneticists would not get the terms confused. If, somehow one geneticist did get the terms confused, his peers would not permit his paper to be published. I'm not sure what complex genetic processes you refer to. But genetics is a complex subject...even meiosis and sexual recombination is a complex procedure when you look at what is happening.Mutations aren't assumed to be the original cause of any trait, mutations are one of the mechanisms proposed by the theory. As with all the mechanisms of the theory they can be observed, tested and replicated. Since we are not in a lab at the moment, obviously we can't observe, test and replicate mutations so it may appear like we are 'assuming' they happened but we are just relying on the hard work of those that did the observing, testing and replications.From what we have observed/tested/replicated we can make a judgement... if basically all genes were the result of mutations et al then we'd be able to make some predictions about things we should see, the extent of differences in certain genes between related and less reltated species. We make those predictions, we find they are right. Either this is coincidence or the theory provides a good explanation. Genetic business as usual includes mutations. Mutations occur at a certain frequency, this has been observed and it has been tested. It may be difficult for you to think of these things as anything but a bad thing, but that is your problem. Plenty of other people can see why not having wisdom teeth or cardio-arterial disease is a good thing. So how on earth can you say they 'seem to be...' if you have no criteria to say that? Actually they seem to be novel mutations according to the rigorous testing standards applied by science. There is a criteria, its been shown to work, it has been tested thousands of times, replicated and its predictions have borne out. You have decided to ignore it because you are not happy with the results of these tests. You still somehow manage to say that something seems to be x without any criterian for determining how one can determine if something seems to be x. Mutations can be detected, they can be tested against known models of genetics. Assumptions in science are always put forward as predictions. 'If our assumption is true, then we should expect to see x'. If we don't see x our assumption is false. Otherwise the strength of our confidence in our assumption grows.Mutations are really easy to define. They are errors in the copying process of DNA. The ones that really matter for evolution happen in the germ line, or to be simple - the sex cells.