Why Darwinism is wrong

Why Darwins theory of speciation or biodiversity by random mutation and natural selection (RMNS) is wrong?1. Different species has different chromosomal karyotypesDifferent species in sexual animals almost all have karyotic changes, which means chromosomal differences detected under microscope. They are deletion, amplification, duplication, insertion, and inversion, even chromosomal number changes. Neo-Darwinism is based on change of allele frequencies, which cannot provide explanation how allele change lead to addition, deletion of pieces of chromosome, or change of chromosomal numbers.2. Against all scientific evidences so far availableFor example, lateral transfer in bacteria, polyploids in plants, generation of asexuals from sexual animals (virgin births), generation of SARS or HIV and many virus, incorporation of mitochondria by symbiosis, etc. they all fall into instantaneous biodiversity, not gradual one by RMNS mechanism.
Can anybody give me an example of speciation by RMNS? (do not just tell difference allele frequencies in different groups of same species).3. Lack of explanatory powerBeside lack of transitional fossils, there are more examples, such as chicken-egg paradox, atavisms, innovative organ, bottleneck effect, mosaic evolution, Cambrian explosion, rate of evolutionary change, few speciation in big mammals, RMNS mechanism poorly explains these phenomena.4. Un-falsificationBecause RMNS model has no predictory power, there is no way falsifying it, and you cannot prove it wrong by scientific methods. In other words, it stands in any outcomes. By Popperian criteria, Neo-Darwinism is a pseudo-science.5. Too complicatedAccording Neo-Darwinists, there are several mechanisms of speciation (biodiversity): genetic drifting, natural selection, geographical isolation, sexual selection and instantaneous speciation. Among geographical isolation, there is vicariant speciation, peripatric speciation, also parapatric speciation. Each mechanism has own myths and assumptions. Worse than that, nobody can tell which organisms come into beings by which mechanism; they are just intensive exercise of your imagination.This message has been edited by Jianyi Zhang, 04-26-2005 12:17 PMThis message has been edited by Jianyi Zhang, 04-26-2005 12:18 PM

Thread moved here from the Proposed New Topics forum.

I don't want to poison the well, but IMHO it's worth pointing out that Dr. Zhang has a history. A new theory of speciation

I have a history there as well.
me on Ggroups
It looked like Zhang ran into the same ""David Jensen two years later. It only reaffirms why I dont post there any more. Writing in black and white is clearer. Z says that adaptation never creates a new species but no matter what NS keeps the thing fit. I'll have to read a little more. That is a perspective I have not seen before in print.This message has been edited by Brad McFall, 04-26-2005 02:49 PM

Before I reply, it should be noted that I am actually a physics student and that my understanding of biology and population genetics is limited to what I had learned back in the days when I was a biology major. It is not entirely true that speciation can only result from an immediate change in allele frequency. At least in plants, polyploidy is a very common phenomenon that leads to new plant species. Tarantulas. I'm not sure how to interpret what you stated above. Could you be more specific? Actually, Darwin said it himself in Origin of Species that if a true altruistic species ever be found, it would falsify his theory. Aside from the "too complicated" claim, which I'm not sure that it has anything to do with what we are talking about, I don't think the underlined statement is true.Off the top of my head, I can name several examples of species that came from geographical isolation. But just for kicks, you can fly to any of the islands in South America to find examples of such species.

If you read my website, http://chickensfirst.net and you will get better ideas.Darwin's RMNS is wrong from many scientific perspectives. The correct answer of mechanism for speciation in any sexaul organism is twins mutation and inbreeding.

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Jianyi Zhang

http://eggsfirst.net !!no just kidding.

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אָרַח

well, the lack of what creationists are willing to call transitional fossils. that's not a lack of fossils, it's a lack of will. granted, we don't have enough dots that any idiot playing "connect the dots" could see that the work's already been done for him. but there's enough that we can make a picture. uh. you know what came first? something that was only almost a chicken. recessive traits. genetics makes life easier. explain. hard parts. we have lots of pre-cambrian fossils, really. it's just that HARD PARTS fossilize a lot better than soft ones. since we're only changing a little bit at a time, and big animals have a lot more little bits than small ones, it'd stand to reason... prediction: species will give to birth to animals of roughly the same genetic makeup, and all change will be gradualy compounding, even when accelerated.falsification: if one species gave birth to another.
falsification: if no compounding changes took place.as one may notice, we have two things that would falsify random-mutation-natural-selection. either of those things would disprove it. we can observe that the second is untrue: we breed cats and dogs and can see the changes pretty plainly. the first, to my knowledge has never occured.

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אָרַח

http://chickensfirst.net/model.htm

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The proposed mechanism of speciation has four major steps; the whole process is called gross mutations in cluster and mutants inbreeding (GMCMI). Viviparous animals (living young not eggs are produced) is used to explain the model, slight modifications might be needed to accommodate unlimited biological variations.
1. Formation of two fertilized eggs of the opposite sex
Animal development begins when a sperm fertilizes an egg to form a zygote. Fraternal twins zygotes are formed when two eggs combines with an X and Y chromosome bearing sperm.
2. Gross mutations on the zygotes
In fertilized eggs, DNA synthesis is very active and these eggs are extremely sensitive to mutagens. Mutations might arise from mutagenic insults or errors in DNA replication. The mutations are random processes, determined by the nature of mutants and the microenvironments of the zygotes. These mutations can have deleterious or nondeleterious effects, and could occur at one locus or multiple loci. In addition, chromosomes can be affected through addition, deletion, and translocations. The outcome of these changes will generate a mutant organism with new genetic structures.
3. Self-replication of fertilized eggs
The mutant zygotes can self-replicate to form mixed multiple identical zygotes with gross mutations (MMIZWGM), which could develop into mixed identical supertwins with gross mutation (MISTWGM).
4. Mating among the siblings from the same gestation
The majority of the mutants would die during the embryo stage, leaving a very small number to survive as MISTWGM. Of these, even a smaller number would become adults. The characteristics of the novelties are determined by how the mutations occur. The mutations would be not only demonstrated in the somatic cells of offspring with the novel characteristics, but also inherited, and passed into their gamete cells.

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Could/would you please Sir indicate how this vision is any shorter, different, or better than

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Experimentally, therefore, the theory is confirmed that the pea hybrids form egg and pollen cells which, in their constitution, represent in equal numbers all constant forms which result from the combination of the characters united in fertilization.
The difference of the forms among the progeny of the hybrids, as well as the respective ratios of the numbers in which they are observed, find a sufficient explanation in the principle above deduced. The simplest case is afforded by the developmental series of each pair of differentiating characters. This series is represented by the expression A+2Aa+a, in which A and a signify the forms with constant differentiating characters, and Aa the hybrid form of both. It includes in 3 different classes 4 individuals. In the formation of these, pollen and egg cells of the form A and a take part on the average equally in the fertilization; hence each form [occurs] twice, since four individuals are formed. There participate consequently in the fertilization
the pollen cells A+A+a+a,
the egg cells A+A+a+a.
It remains, therefore, purely a matter of chance which of the two sorts of pollen will become united with each separate egg cell. According, however, to the law of probability, it will always happen, on the average of many cases, that each pollen form A and a will unite equally often with each egg cell form A and a, consequently one of the two pollen cells A in the fertilization will meet with the egg cell A and the other with the egg cell a, and so likewise one pollen cell a will unite with an egg cell A, and the other with the egg cell a.
Pollen cells A A a a
| \ / |
| X |
| / \ |
Egg cells A A a a
The result of the fertilization may be made clear by putting the signs for the conjoined egg and pollen cells in the form of fractions, those for the pollen cells above and those for the egg cells below the line. We then have
A A a a
----- + ----- + ----- + -----
A a A a
In the first and fourth term the egg and pollen cells are of like kind, consequently the product of their union must be constant, namely A and a; in the second and third, on the other hand, there again results a union of the two differentiating characters of the stocks, consequently the forms resulting from these fertilizations are identical with those of the hybrid from which they sprang. There occurs accordingly a repeated hybridization. This explains the striking fact that the hybrids are able to produce, besides the two parental forms, offspring which are like themselves;
A a
----- and -----
a A
both give the same union Aa, since, as already remarked above, it makes no difference in the result of fertilization to which of the two characters the pollen or egg cells belong. We may write then
A A a a
--- + --- + --- + --- = A + 2Aa + a
A a A a
This represents the average result of the self-fertilization of the hybrids when two differentiating characters are united in them.

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Mendel's Paper (English-Collaborative)If I am not mistaken your notion would divide the dashed line above EITHER vertically OR horizontally and yet I see no mathematical incorporation of the two different kinds of 1-D symmetry Weyl distinguised in SYMMETRY(book). The two eves idea no matter about the initial diversity of genetic variance across the line a progeniture motion crosses seems to give SHAPE to the dashed line. I had not seen your proposal before because *this* is not supported by anymath or any metric application I am aware of. I cant see how all species that would be comparable to paleontologically names ones MUST have identical structure. There surely is some variation in individual traits and yet the recursion your work remands seems to fly the middle without any slight variation on either side except size between the eves. Something other than magnitude is needed to composite morphospace it seems to me. How would you get 1:3 traits in the generations rather than the simple bifurcation your work seems to ply again. I suspect that the "similarity" is at alevel of physics below"" the language model of DNA-RNA-PROTEIN but that is unsubstantiated and is my own reading.You had it asked

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Why do you propose twins zygotes mutation in the model?

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Mutation is a random, rare, unpredictable event, it is very, very unlikely for any identical mutation occur IF they are at totally non-associated situations

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but as i continue to read it you could theoretically get two identical mutations by TWO different physical chemical paths if 1-D symmetry was a adapted continuum and not a chance junkyard art display.This message has been edited by Brad McFall, 04-26-2005 05:05 PM

The theory of evolution does not claim that changes in allele frequency result in karyotype changes. Changes in karyotype may, however, affect allele frequency (i.e. if an allele is deleted or duplicated). You will need to explain how the existence of various karyotypes is meant to be a challenge to the theory. This is no challenge to neo darwinism. It just means that our population genetics models have to be modified when we study bacteria. The existence of HGT challenges neither the existence of mutations nor the existence of natural selection. In fact HGT is rightly viewed as just another mechanism (among many) that generates genetic variability within populations, i.e. the bedrock of neoDarwinism. I fail to understand how abnormal cell division, resulting in duplication of the genome, is meant to challenge evolutionary theory. A polyploid cell resulting from whole genome duplication isn't "instantaneous biodiversity". It's just a normal individual with twice the amount of genetic material. The molecular evolution of HIV is in fact rather well understood and you are simply wrong to say it reflects "instantaneous biodiversity". There are around five distinct forms of SIV, each associated with a different primate species, and there are chimeric forms in hybrid zones; and it's clear that human HIV evolved from SIV and didn't appear instantaneously. The molecular evolution of HIV is explained well by neoDarwinism, showing purifying selection on some regions of the viral genome and diversifying selection on others. Are you really suggesting that HIV didn't evolve from SIV? You are way off the mark on this one. The plastid genomes of eukaryotes are highly diverse, and they are subject to ongoing evolution (i.e. http://www.ncbi.nlm.nih.gov/entrez/...).
{Shortened display form of URL, to restore page width to normal. - Adminnemooseus} They could well have arisen by multiple endosymbiotic events, not just one spontaneous event. Just compare a chloroplast or a mitochondrion to a bacterium, and look at the diversity of chloroplast structure in plants, to see that this wasn't just an instantaneous transition that has been frozen over the millenia. I find it difficult to see what you are trying to get at here... What exactly is it about bottlenecks or different evolutionary rates that evolutionary theory can't account for? Your examples are rather odd. For example evolutionary theory (or more specifically population genetics) has a very sensible explanation for the rareness of speciation events in big mammals (hint: it has to do with generation time) You are just betraying your own ignorance here. it's a complicated world out there.This message has been edited by Adminnemooseus, 04-27-2005 02:03 AM

I went in other sites and just come back.The idea in the website is very simple:I propose a new model that suggests twins mutation and inbreeding, only one step assumed. For speciation of a sexual organism (viviparous), there are only four steps in whole process.1. Formation of fraternal twins zygotes (male and female).
2. Similar gross mutations on these zygotes by a certain probability (even very low).
3. Self-splitting of zygotes into two groups of identical zygotes in both genders.
4. Development of zygotes with birth of babies and inbreeding when they matureFor oviparous animals and asexual organism, these principles will be same, i.e. gross changes in genetic material, instantaneous biodiversity, and inbreeding (if sexual organism). Only step 2 is assumed, the rest 3 steps are natural phenomena.Many unsolved myths have answers under the proposed mechanism, which are discussed in the website. Also I list several falsifiable mechanisms to the model.I had some discussions in talk.origins, I answer major critiques in FAQ section of a website. I never thought any metric application necessary, and I do not know them anyway. Why do I have to get 1:3 traits? With similar gross mutations at both zygotes (female and male), inbreeding among them would generate a new species with new genomic struture. Why two different physical chemical paths? Same type virus can infect both twin zygotes easily with same gross mutation.

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Jianyi Zhang

To address some of your points.1:- It is true that these are certainly not expicitly covered in either Darwin's original formulation nor in the original neo-darwinian 'modern synthesis'. It is worth remembering though that even the 'modern synthesis' is now at least 20 years old.The relevance of your karyotypic changes escapes me. Changes in allele frequencies do not explain these karyoptypic changes because many of these changes are themeselves changes in allelic frequency. Duplications, deletions, inversions, amplifications and insertion may all lead to a change in allele frequency in a population, although they do not neccessarily do so.These are some of the forms of mutation upon which natural selection may act.It is also by no means a given that differences in karyotype are the be all and end all of speciation.2:- None of these are evidences against the operation of RMNS, all they show is that there are many more sources of variation than had been supposed when the 'modern synthesis' was being developed. As has been pointed out they are by no means 'instantaneous' biodiversity any more than a point mutation is.3:- Rather than a lack of explanatory power these seem rather to be areas which might more profitably be researched. I'm sure people could come up with half a dozen ad-hoc just so stories for how RMNS could lead to any of these, the important thing is to do enough research to have a good idea what actually happened.In the case of the chicken and egg the answer is obviously egg. Reptiles and various species of bird had been laying eggs long before chickens turned up.4:- I don't see how RMNS makes no predictions. there are many papers investigating the theoretical exploration of fitness landscapes providing testable models of how organisms adapt to selective pressures and a number of experimental approaches, especially in bacterial cell culture, to test such hypotheses.5:- Too complicated, well maybe. But then living things are complicated. It may appear messy but that doesn't actually suggest it is wrong.TTFN,WKP.S. Are you the first author on 'Testing the Chromosomal Speciation Hypothesis for Humans and Chimpanzees' from Genome Research? Feel free not to answer, I'm well aware of the problems associated with publicising ones real life identity in such an open forum. It just seemed that that research, not to mention the authors name, concurred very well with the first question you were asking.After looking at your website you obviously aren't the same J. Zhang, never mind.This message has been edited by Wounded King, 04-27-2005 10:22 AM

Thnaks for your response. I hope you continue...The "unsolved myth" that your assumption solves is simply the extrapolation of Ian Stewarts statement

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Tobacco mosaic virus...is a hollow rod...This helps bridge the gap between the inorganic and the organic worlds by showing that one of the most striking features of the living world -replication - is here a consequence of molecular architecture; it does not require further intervention, either by genetics or God.

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p66(Life's Other Secrect) scaled into population thinking and yet your website seems to read red as if this is done contra Stewarts position on the FUTURE of math and biology, namlely that it is closer to my own approach than that of Stewart's (page243)But I have another thread working where contra Holmes a bit I will show that the two step(inbreeding and mutation are not a unified stepper no matter how linked the ladder chains the being to it) is not what is dancing here. I dont have any more time this week. I will agree with ONE but yours is not this uno or moko. Your reply still seems more complicated than Mendel to me. Even granting no god or more genetics I cant find on the web site how I am supposed to add up the mutations gross or otherwise. Perhaps I just missed that. If so, my bad esle back to Homes.la la le la la la. Anyway I will try to show how the bacterial flagellum is not IC(suffiently) to the inversion metrically of the TB virus(structure) and point out how there are two chemical paths in the same population by use of phase reasons. But more later. God might still be and genetics, well, again, where is that ? it still didnt take shape.If I cant write down the illustration, delimit the equation and solve for space time and form I am no longer interested in science. But hey, that's just me. By the way, one such equation, IS is likely refering to was Murray's approach to leopard spots and it is because the equations they wrote down at Oxford were not general to say your notion that I DID NOT go that way for grad work. That thing exists.

Folks, though I'm replying to JonF, this is to everyone. JonF pointed out that Jianyi Zhang had a thread on this issue at talk.origins. If you decide to participate in this thread, be sure you set your frustration tolerance level to maximum. Example:From message 1 of his talk.origins thread: From message 39: Enjoy, but stay within the Forum Guidelines.

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--	Percy
	EvC Forum Director

Original post by Wounded King The key is changes of allele frequency a gradual process, also at population level; it occurs by NS, however, duplications, deletions, inversions, amplifications and insertion are instantaneous processes at individual level, which occur without NS, and subject to NS effect after they are generated. Yes, not all differences in karyotypes leads to speciation, but different species almost have different karyotic patterns, some gross mutations can not be seen by karyotypic study, as they are not big enough to be seen. All of these evidences are against RMNS as the mechanism of speciation. Can you tell me how polyploids in plants occur by RMNS?
If you still think polyploids consistent with RMNS, you should read some books by E. Mayr, top Darwinists. How about virgin birth of shark in zoo? How do you apply RMNS to it?
http://news.nationalgeographic.com/...20925_virginshark.html Do you mean eggs give a birth to a new species? There is no way to predict anything with RMNS. BWT, does a new bacteria a new species? Almost all antibiotics bacterai are generated from lateral transfer, which is an instantaneous process, regardless of existence of antibiotics, they were there, ones have no way to find out them.

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Jianyi Zhang