Summations Only

Wright's only substantive examples are bacterial, and the extent to which they are directed is highly contentious. There is no clear way for similar mechanisms to operate in an organism with a division between the soma and germ line.For a detailed discussion of Wright, although not in this thread, see the other thread you have just posted the same material in; starting at Message 65 and going on for a good proportion of the thread.TTFN,WKEdited by Wounded King, : No reason given.

Then you misunderstand, the system that Wright describes only 'directs' mutation in the weakest sense. Wright notes an elevated rate of mutation at specific loci associated with a particular response to the environment. She then posits that these elevated rates are more likely to produce beneficial mutations relevant to the specific challenge, although there is no actual evidence of this. There is also an elevated rate of deleterious mutations but the hypothesis relies on NS to weed those out. It is perfectly logical for the very clear reason I pointed out. In bacteria there is no division of the somatic and germ cells. There is only one cell so it can profit from the modification of it's own genome in a way that is impossible for metazoa.There is no plausible mechanism by which the phenomenon Wright describes could operate on anything other than perhaps genes involved in germ cell development itself. A complex neural system in no way serves the same purpose and it is biologically incoherent to claim that it does. In what way does your neural system act as a mechanism to derepress specific genes as an environmental response? And even if we were to accept this dubious premise how is this information supposed to be transmitted from the somatic cells to the germ cells? You would need to be activating/derepressing specific genes in the germ cells in response to the particular environmental challenge.TTFN,WK

Can you tell us how your idea is falsifiable then? What sort of evidence would you expect to see for such a mechanism. Presumably there would need to be some mechanistic system for transferring genetic information from the nervous system to the germ cells. For something to be falsifiable there needs to be a coherent framework to build testable hypotheses from, at the moment I fail to see that in your proposal.Frankly as it stands your theory might as well be that invisible pixies transmit information from the environment to the germ cells to direct mutation and there would be just as little evidence against it and it would be just as consistent with "ALL findings ln genetic biology".That is putting aside the fact that you are proposing a mechanism for a phenomenon which there is similarly no evidence of, environmentally directed mutations in metazoan germ cells. This is as opposed to the wealth of evidence for stochastic processes of mutation insensitive to fitness based on observed frequencies both in vivo, in vitro and in trans-generational studies.TTFN,WK

Wow, seriously? I wish you had asked this question a hundred or so messages ago so we had some idea just how ignorant you are of the subject you are making pivotal to your argunment.There are lots of well characterised mechanisms which affect epigenetic states. Feeding methyl supplements to pregnant mice increases DNA methylation levels in their offspring and can have significant phenotypic effects(Cooney et al., 2002). This isn't mediated by some spooky neural phenomenon, it is simple biochemistry.TTFN,WK

Yes, they mean that the authors took pains to control their experiment for every variable that might affect health and lifespan, two of the phenotypic characteristics they were interested in in those studies.This doesn't require the genome to 'know' anything about the environment. Things about an organism's lifestyle are normally experienced directly by the organism, i.e. day night cycles and sleeping patterns, diet and exercise regime. The neural system is not required to mediate this information in many cases although it does in some.You are adding another unneccessary layer of complexity. Organisms interact with their environment, that is how information from the environment is imparted to the genome, through differential success of genetic variants in a specific environment.There are published models for how information about the environment can be incroporated through natural selection (Frank, 2009).TTFN,WK

Sorry Zi Ko, I've already pointed out to you why this is wrong, either you really can't understand plain english or you are just lying at this point.The papers they referred to were not looking at the epigenome, they were looking at health and longevity. The quotes you gave were from the introduction talking about the work of others, not the epigeentic factors studied in that paper.TTFN,WK

Well duh! But that isn't what you said that I was objecting to. I've said over and over again that the environment interacts with the genome. What I was objecting to was your assumption that this is via the neural system when I have already shown you papers which detailed the routine biochemical pathways which can mediate the environmental interaction through diet and which do not require the nervous systems involvement.And 'Life style' covers so many variables that to say that 'life style' affects the genome/epigenome is to essentially say nothing. Smoking could be part of a life style, regular and prolonged sunbathing, drinking ethyl methanesulfonate or ethidium bromide could be part of a 'life style'. all of these things would affect the genome, some would even affect the germ cells producing heritable mutations. What this certainly doesn't show is that these environmental factors in any way direct the changes to the genome/epigenome that they produce.Once again you are too vague about what you want to discuss.TTFN,WK

It is both. The environment interacts with the genome by testing it and providing the matrix within which variants experience differential reproductive success so as to give rise to the patterns of natural selection. Certain elements of the environment also interact with DNA either directly or indirectly, such as the examples I gave of mutagens and the methyl supplements. The vast majority of such genetic/epigenetic modifiying interactions occur in the somatic cells, but a small proportion occur in the germ cells. In these cases there are well understood biochemical pathways for the modifications that arise both in somatic cells, germ cells and the cells of developing embryos. you mean like when I then went on to give several examples of environmental factors which could affect genomes? How was that not being specific? There is some pretty convincing evidence that many aspects of the nervous system are affected by epigenetics, including elements of memory. What there isn't is any reason to believe that this in any way means that the nervous system modifies the genome/epigenome of the germ cells as would be required for heritability. Well what meaning do you give to the word 'direct' or indeed to the term 'non-random'? If you simply mean that not all mutations are equiprobable then it is trivially obvious but has nothing to do with what you have been talking about. A definition of what you mean by information would also be very useful, and possibly what you mean by epigenetics.So why don't you do the clarification for a change since this is supposed to be your theory after all?TTFN,WK

Well the first paragraph refers to both 'observable phenomena' and 'empirical data' . If you look further down in the article you will see that it lists 'It is supported by many strands of evidence' as one of the key criteria of a scientific theory.TTFN,WK

What difficulties particularly? The ones that come to my mind are the 'absolutely no evidence for a role' one and the 'no plausible mechanism' one. If you believe this then I suggest you go and re-read your opening post. You said a whole lot more, most of it totally made up off the top of your head, with not a scintilla of evidence to support any of it. If this is supposed to be a clear explanation with defined terms then I'm afraid it is a failure of epic proportions. At least it has the advantage of brevity.TTFN,WK

Like what? There is a vast amount of research into the workings of the neural system and an equally vast amount into genetics and epigenetics including epigenetics within the nervous system. None of these researches suggest that a mechanism such as the one your theory would require, but which you can't describe, exists.I agree that there is an inherent difficulty in finding things that don't exist, but that is hardly in favour of your position. I quite clearly said what would be useful in moving this discussion forward ... You addressed absolutely none of these things in your word salad response. You used many of the words but not in a coherent way that would allow anyone to understand what you mean.TTFN,WK

Lets be fair now, I think by this point it should be clear to everyone that that isn't what Zi Ko means. What he means is that environmental factors affect the genome by actually causing mutations, or epimutations, and affecting the nature and prevalence of those mutations.This in and of itself is wholly uncontroversial, what is is the way he wants to parley this into mutation directed for non-random beneficial traits and even more so his belief that this has something to do with what he calls 'empathy'.TTFN,WK

There is not a shred of evidence for any of these claims, nor any conceivable mechanism by which such a process might occur. You also make the mistake of assuming that because some environmental influences, which for the sake of argument we might call 'information', can affect the genome through mutation then all forms of information can, but there is no evidence to suggest that this is the case.TTFN,WK

OK so we need to add 'Stress' to the list of words you just use willy nilly. The article is talking about specific cellular stresses, this is in no way the same thing as emotional stress.The article also seems to be from the Intelligent Design site Evolution News & Views and the language is heavily skewed to a subjective interpretation from that perspective, which explains why their argument about a specified system being unable to evolve through random evolution makes no sense. As far as I can see it has no possible relevance to your claims, if you feel it does you will have to rely on something more substantial than mere semantics to demonstrate it.TTFN,WK

OK, so apparently you don't understand the concept of analogy either or if you do then you should realise that the fact you can draw an analogy between 2 things doesn't mean that their similarities extend any further than the actual analogous features that can be identified.If you had a really compelling analogy then you might even go as far as to predict the existence of a previously unrecognised feature of one of the systems, but in the absence of evidence it would only be speculation.Sadly for your argument you are nowhere near that depth of analogy, indeed you don't actually put forward any reason why emotional stress and environmental stress on a cell are actually analogous. You merely claim this is obvious, but the basis for this seems to be nothing more than the commonality of the term 'stress', as I said semantics. Well everything you quoted was nothing more than that, it presented nothing substantive. The idea that cells react to certain particular environmental stimuli in specific ways, and to certain types of genetic damage, is wholly uncontroversial. The only thing that article does is rehash widely accepted science with an ID spin. Really, by now you should have realised that all your insistent and endless appeals to authority do is make it look like you have absolutely nothing to say.If you want to discuss the research of those authors then do that, but don't just throw them out there like some magical talisman against actually having to provide evidence and an argument.If you think that the article you cited actually has anything relevant to your claims then maybe you could highlight what it was, what you quoted so far just suggests that you can't do better to support your position than picking up ID propaganda that happens to have a particular keyword you are fixated on associated with it.TTFN,WKEdited by Wounded King, : No reason given.