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Sanford’s pro-ID thesis supported by PNAS paper, read it and weep, literally

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Cornell Geneticist John Sanford argued that Darwinism is wrong because the rate of genetic deterioration is so high that natural selection could not arrest it. If natural selection cannot arrest genetic deterioration, how then could it be the mechanism for evolutionary improvement?

Sanford predicted through his research that human genome is deteriorating. This was a daring scientific prediction, and now Michael Lynch of the elite National Academy published on the topic for his inaugural paper. The NAS has now made the paper available to the public free of charge.

Read it, and weep, literally:
Rate, Molecular Spectrum, and Consequences of Human Mutation

Unfortunately, it has become increasingly clear that most of the mutation load is associated with mutations with very small effects distributed at unpredictable locations over the entire genome, rendering the prospects for long-term management of the human gene pool by genetic counseling highly unlikely for all but perhaps a few hundred key loci underlying debilitating monogenic genetic disorders (such as those focused on in the present study).

Thus, the preceding observations paint a rather stark picture. At least in highly industrialized societies, the impact of deleterious mutations is accumulating on a time scale that is approximately the same as that for scenarios associated with global warming—perhaps not of great concern over a span of one or two generations, but with very considerable consequences on time scales of tens of generations. Without a reduction in the germline transmission of deleterious mutations, the mean phenotypes of the residents of industrialized nations are likely to be rather different in just two or three centuries, with significant incapacitation at the morphological, physiological, and neurobiological levels.

HT: T. lise

Comments
well Hue Russ got with some evolutionarily biologist and made simulation. The bacteria do under go genetic entropy but mammals that humans came form did. Mammals have large genomes while bacteria do not and bacteria live in large populations.spark300c
October 6, 2010
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Thanks Scordova for this. "Did anyone here (posting author included) read any part of the paper other than the snippet that was posted? Because the article is clearly saying that the reason the human genome is deteriorating is because advances in wealth and technology have substantially relaxed selection pressure against mildly deleterious mutations" After I read Sanford's book, I was so amazed/shocked by his thesis that, I was a bit suspicious. Guess what? The very day I finished reading the book I found this paper (another shock). I emailed Sanford asking if this "western medicine/industrialization" will come under the concept he discussed in the book known as "noise". To which he replied, Yes and went on to add " But there is already so much noise from other sources (survival of the luckiest), that eliminating this extra source of noise will not solve the selection problem."T. lise
October 4, 2010
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I think I have been the lucky beneficiary of a number of mutations.Collin
October 4, 2010
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The question was asked: "Why would a designer build a system that, without intervention, would run itself down in this way?" The principle of identity requires that for any "A" to have meaningful existence, it must be contextualized by that which is "not-A". Otherwise, there's nothing to observe, no observer, and nothing to talk about. In order for the final cause, or purpose of existence to have identifiable meaning, there must be a contextualization of what is not the meaning of existence; what is not the point of human existence; what is not "good". Final cause requires an intent; intent requires contextualization. What is intent? It is that primordial "first thing" that organizes materials and forces towards a purpose, and can apparently do so with near-infinite functional focus. Logic dictates that for meaningful divine intent to exist, it must be contextualized by that which is non-intent. What is non-intent? Entropy. For good to exist, so must evil; for intent towards that good to exist, entropic deterioration (non-purpose) must also exist.William J. Murray
October 4, 2010
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Peepul, You demand quite a lot of a designer. Overcome the laws of entropy; why wouldn't a designer do that?Collin
October 4, 2010
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Why would a designer build a system that, without intervention, would run itself down in this way?
Software upgrades are dependent upon the learning and innovation that end-users bring.Proponentist
October 4, 2010
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To counter-balance the sad news of that we are deteriorating: Fearfully and Wonderfully Made - video http://www.metacafe.com/watch/5289335/bornagain77
October 4, 2010
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scordova, you've probably seen this earlier paper by Lynch but if not: The Mutational Meltdown in Asexual Populations Excerpt: Loss of fitness due to the accumulation of deleterious mutations appears to be inevitable in small, obligately asexual populations, as these are incapable of reconstituting highly fit genotypes by recombination or back mutation. http://www.oxfordjournals.org/our_journals/jhered/freepdf/84-339.pdfbornagain77
October 3, 2010
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So I would say that any cause of death that acts with some systemmatic regularity on a population and affects the reproductive success of members of that population differently depending on their genetic makeup (and its effect on phenotype) is natural selection.
Thank you for taking time to respond. However the response is representative of the illogic and distorted thinking pervasive in Darwinism. It is more accurate to say, "random events may or may not induce selection pressure for certain traits (i.e. thickness of finch beaks)". You asked:
scordova, In my previous comment I forgot to ask you how you would distinguish natural selection from random death.
That is not my problem, that is a Darwinists problem! In general if the selection coefficient is weak, it is NOT distinguishable. So if evolutionists won't make the distinction, neither will I. In the experiment in question, the outcome did not accord with what one would expect for a trait being selectively favored. The problem was they couldn't make the distinction either!!!! Kimura noted that sufficiently weak differential reproductive bias for a trait is makes the trait essentially neutral, therefore the survival of such a triat is effectively modeled as a random walk, not according to Darwin's horribly naive views. One might be able to get a very weak correlation after a buzillion trials and establish that a trait might be selectively favored. But how useful would such an experimtnt be? Such an experiment would only show that NS is 99.99% irrelevant! And if it is 99.99% irrelevent to maintenance of traits, it is 99.99% irrelevant to the evolution of complexity! Here is an example to consider: say individual A is genetically superior to individual B all other factors being equal, but individual A happens to also be delicious and available to a predator in the area. Individual A serves as dinner for the preditor, and individual B lives and reproduces. Who is selectively favored? You might say, "A would usually be favored if it weren't for the lion that swallowed him". That may be true, but it only demonstrates selection often takes a back seat to random events, contrary to Dawkins claim that "selection is the exact opposite of random". Dawkins claim isn't true, and the experiments prove it! Furthermore, See: Dennett's strange idea. The problem for defining something as selectively favorable is problematic. In one context sicle cell anemia is a favorable trait, in another it is a harmful trait. This unstable subjective perception is hardly re-assuring to those seeking to make Darwinism a real scientific theory verus a naive speculation based on story telling versus experimental facts.scordova
October 2, 2010
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scordova, In my previous comment I forgot to ask you how you would distinguish natural selection from random death.AMW
October 2, 2010
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Why would a designer build a system that, without intervention, would run itself down in this way? I was going to ask the same question myself.AMW
October 2, 2010
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Before you spam this thread any more, describe what you think are causes of random death. Well, let me start with a definition of selection. From the BioPortal Glossary: Selection: 1. Differential survival and reproduction of phenotypes. So I would say that any cause of death that acts with some systemmatic regularity on a population and affects the reproductive success of members of that population differently depending on their genetic makeup (and its effect on phenotype) is natural selection. Random deaths would be things like lightning strikes, wildfires, automobile accidents, etc. Things that don't tend to favor one genotype/phenotype over another. Even the examples I just gave might have some selective element to them, though. If defensive driving has a genetic component, then automobile accidents will select in favor of that component, for instance. But I'd guess that they're pretty random. I take two individuals. I randomly starve one. Can you tell me off hand which one is more selectively fit based on which one died? No. That strikes me as a rather silly example, because you're just putting the selection pressure on a single person, instead of a population. And you're cranking the level of pressure up to the point where he couldn't survive. I think this is a more sensible take on it. I take two populations. One population is never sure where it's next meal is coming from. Death by starvation is a real threat. The variety of foods is very limited, and dairy makes up an integral part of the regular diet. The other population has food in abundance. Some people don't eat three square meals a day, but practically nobody starves to death. Moreover, food comes in all sorts of variety. If dairy's not your thing you can easily substitute meats, or fruits, or legumes, etc. Now suppose a mutation increasing the risk of lactose intolerance crops up in both populations. Which one do you think it is likely to spread the furthest in? If someone is born into a place with no food and sanitation, that’s bad luck. That has less to do whether he is selectively fit or not. It certainly is bad luck, but that doesn't mean he's not being exposed to selection pressure. If you're born into an environment with few sources of fish protein and reduced sunlight (e.g., Europe), that's bad luck in terms of getting your necessary vitamin D. But it also puts selection pressure on skin pigmentation to be lighter. Do you still stand by such a silly statement? I do.AMW
October 2, 2010
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If genetic entropy does cause decay in the genetic fitness of organisms (human and other), what mechanism has been in place to ensure that life as a whole has continued to exist for > 3 billion years, and that individual species have continued to exist for many millions of years? Is the designer intervening to shore up the quality of genomes? Why would a designer build a system that, without intervention, would run itself down in this way?Peepul
October 2, 2010
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The Lynch paper does not support what the blog claims. Until ID treats evidence with understanding and honesty, it will have no respect from the scientific community.Peepul
October 2, 2010
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2. Lack of food and bad sanitation are most certainly not causes of random death.
AMW, If you're modelling it according to evolutionary population genetics it is. To see why. I take two individuals. I randomly starve one. Can you tell me off hand which one is more selectively fit based on which one died? No. Thus death by starvation is more appropriately modeled as a random death, not death by natural selection! Same would be true if I killed an individual by lack of sanitation. If someone is born into a place with no food and sanitation, that's bad luck. That has less to do whether he is selectively fit or not. If you're arguing that people who die from starvation are of necessity either more or less fit just by the fact they were starved, that's silly times 10!
2. Lack of food and bad sanitation are most certainly not causes of random death.
Do you still stand by such a silly statement? Before you spam this thread any more, describe what you think are causes of random death.scordova
October 2, 2010
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1. From the paper you linked, it looks like Muller was off by a factor of 4.5 to 22.5. A thousand times? That would be 200 de novo deleterious mutations per human child. 2. Lack of food and bad sanitation are most certainly not causes of random death. They're a mundane fact of existence for nearly every organism on the planet. Mutations could easily be deleterious via their impact on an individual's resistance to fecal-born diseases, or its ability to absorb nutrients from one type of food or allergic reaction to another. 3. The paper Joseph cites (or rather, the abstract of it that I had access too) indicates that selection sped up early life development (the targeted trait) by around 20%. It doesn't say that natural selection can't get rid of deleterious mutations. It says it has a rather hard time causing unambiguously beneficial mutations to be fixed in a population. There's a world of difference. 4. I'd be interested if you could give me a link to the paper by Nachman and Crowell. But all of the above is a bit of a side show. My central point is that the paper that you originally linked does not support Sanford on any claim that is contrary to the theory of evolution. It does not demonstrate that humans living living closer to a state of nature systematically accumulate deleterious mutations, and it most certainly says nothing about the genomes of non-human life. And what's more, unless I've not been reading carefully enough, none of your ancillary points have demonstrated Sanford to be correct on these points. So at present I stand by my last comment. You are pointing to the rising sun and blowing a raspberry at Copernicus.AMW
October 1, 2010
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Am I missing something?
Yes. The number muller provided was too small, the real number is at least 15 times larger if not a 1000 times larger based on recent mainstream papers. I already pointed out the supposition that modern medicine is the primary cause for deterioration is suspect. As I pointed out: 1. all the random death in the non-industrial world reduces the excess offspring to make selection effective! For NS to work optimally you want birth defects killing the kids, not lack of sanitation and food! 2. Slight mutations (like say slightly degraded eyesight, a silent mutation that could allow more servere mutations in the future, a slightly more allergic reaction, an introduction of a new slightly harmful recessive, etc.) These sort of mutants won't be killed off by a non-industrialized environment. The question of deterioration prior to modern medicine is still a serious unsolved problem. If each child has around 3 mutations, NO amount of selection will probably arrest the decay. That was in a paper by Nachman and Crowell. Further you totally ignored the experimental evidence against the efficacy of natural selection provided by Joseph. It was a step in the right direction that the mainstream is recognizing large scale deterioration in the industrialized world. Once we recognize it in the non-industrialized world that will seal the deal on Sanford's work. That will distinguish him from all the rest. So far he's right, his claims have not been falsified (which is more that we can say for Darwin). If we see unabated deterioration in the non-industrialized world, it would seem reasonable to assert, Darwinian evolution had nothing to do with the arrival of man because it cannot seem to even keep his species alive. So far so good for Dr. Sanford, not so good for those who, like Huxley (Darwin's Bulldog) adn Darwin himself who argued the human race would keep progressing indefinitely. By the way, one example of a disease not being eradicated by NS in the non-industrialized world: SICLE CELL ANEMIA. Selection ain't doing too much to get rid of it in Africa, in fact selection is helping it persist in the population. So much for Lynch's assertion that natural selection will purge heritable disease in the non-industrialized world. You can add to that cystic fibrosis in certain African populations.scordova
October 1, 2010
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scordova, The PNAS paper you link to cites a 1950 paper by Muller where the possibility of humans accumulating deleterious mutations is enhanced because we've got technological ways to live with those mutations, allowing us to pass them on to our offspring. In other words, there is little selection pressure against some deleterious mutations in modern humans (or, rather, humans living a modern lifestyle). This observation was made 60 years ago and is apparently not controversial among mainstream (read: evolutionist) scientists. (Or perhaps it is controversial, but there's no overwhelming consensus against it.) This shouldn't be surprising, because it's consistent with the Neo-Darwinian synthesis. Random mutation without selection is no boon to a species. On to Sanford. He claims that the human genome is deteriorating, and he suspects that the genomes of other species are deteriorating as well (albeit not necessarily so quickly). His claims with regard to humans are compatible with the Theory of Evolution. His claims with regard to other animals, who aren't so shielded from natural selection against deleterious mutations, are not compatible with it (so far as I can see). Now here's what I don't get. You post a link to a paper giving evidence for the portion of Sanford's claims that are perfectly compatible with the Theory of Evolution. But you are making it out as though this also validates the portion of his claims that are not compatible with the Theory, and which are not examined in the paper itself. That's rather like pointing to the sun rising in the East and setting in the West as evidence for the Ptolemaic model rather than the Copernican one. The problem is, both models predict the phenomenon. To test them against each other, you have to gather data where their predictions diverge. Am I missing something?AMW
October 1, 2010
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Before I reply to your comment, I want to make sure I’ve got Sanford’s argument correct. Does he claim that all genomes are deteriorating, and this is because natural selection cannot weed out deleterious genomes fast enough to prevent deterioration?
He claims human genomes are deteriorating, specifically, he has not officially published on other genomes, but I can relate some of his thoughts. In a discussion with him (so this is not published material) he expects bacterial genomes to be substantially more successful in combatting geentic entropy because of the reproductive excess and size of the genome. The rest of biological organism lie somewhere in between bacteria and man, approximately. BTW, decreating fitness is a distorted measure of genetic entropy. See: Dennett's Strange Idea I pointed out fitness, since it is so poorly defined and equivocated with all the renormalizations of what it means to be fit ( i.e. sickle cell anemia is fit in one context, unfit in another), the better metric for the lack of purifying seleciton is sequence divergence which can be measured by the generational increase of novel single-nucleotide-polymorphisms. If sanford is correct this number will increase even in non-industrialized populations. Regarding other genomes, there is concern for mutational meltdown there. Even in sexually reproducing species, there are some aspects that can be modeled as asexual because of geneder specific chromosomes and even linkage blocks that will frustate the effectiveness of recombination for dealing with the bad mutations. Finally, extinction is technically genetic decay! You shouldn't bias the sample sizes by looking only at extant creatures and exclude accidental extinction of genomes. Accidents are part of the environment whcih Darwin claims to fascilitate evolution, so excluding them is a bit disingenuous, imho.scordova
October 1, 2010
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scordova, Before I reply to your comment, I want to make sure I've got Sanford's argument correct. Does he claim that all genomes are deteriorating, and this is because natural selection cannot weed out deleterious genomes fast enough to prevent deterioration?AMW
October 1, 2010
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Graham, "...it is a nice chance to produce yet more bible quotes." For a person like yourself, wrapped up in his intellectual enlightenment, it must be sorely depressing to realize all you can do is produce derogatory snark on the sidelines.Upright BiPed
October 1, 2010
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Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.
There is a known issue that selection fails most of the time! See: Gambler's Ruin Is Darwin's Ruin Nice to see the prestigious scientific journal Nature affirming claims made here at UD!scordova
October 1, 2010
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further notes: This following study confirmed the detrimental mutation rate for humans, of 100 to 300 per generation, estimated by John Sanford in his book 'Genetic Entropy' in 2005: Human mutation rate revealed: August 2009 Every time human DNA is passed from one generation to the next it accumulates 100–200 new mutations, according to a DNA-sequencing analysis of the Y chromosome. (Of note: this number is derived after "compensatory mutations") http://www.nature.com/news/2009/090827/full/news.2009.864.html This 'slightly detrimental' mutation rate of 100 to 200 per generation is far greater than even what evolutionists agree is an acceptable mutation rate for an organism: Beyond A 'Speed Limit' On Mutations, Species Risk Extinction Excerpt: Shakhnovich's group found that for most organisms, including viruses and bacteria, an organism's rate of genome mutation must stay below 6 mutations per genome per generation to prevent the accumulation of too many potentially lethal changes in genetic material. http://www.sciencedaily.com/releases/2007/10/071001172753.htmbornagain77
October 1, 2010
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Here is Dr. Sanford's computer program 'Mendel's Accountant', in which different populations (bacteria, human, etc..) can be analyzed for their resistance to the effects of Genetic Entropy: Using Computer Simulation to Understand Mutation Accumulation Dynamics and Genetic Load: Excerpt: We apply a biologically realistic forward-time population genetics program to study human mutation accumulation under a wide-range of circumstances. Using realistic estimates for the relevant biological parameters, we investigate the rate of mutation accumulation, the distribution of the fitness effects of the accumulating mutations, and the overall effect on mean genotypic fitness. Our numerical simulations consistently show that deleterious mutations accumulate linearly across a large portion of the relevant parameter space. http://bioinformatics.cau.edu.cn/lecture/chinaproof.pdf MENDEL’S ACCOUNTANT: J. SANFORD†, J. BAUMGARDNER‡, W. BREWER§, P. GIBSON¶, AND W. REMINE http://mendelsaccount.sourceforge.net http://www.scpe.org/vols/vol08/no2/SCPE_8_2_02.pdf It is also extremely interesting to note, the principle of Genetic Entropy lends itself very well to mathematical analysis by computer simulation, Whereas, evolution has no rigorous mathematical foundation with which we can rigorously analyze it in any computer simulation: "No human investigation can be called true science without passing through mathematical tests." Leonardo Da Vinci A comparative approach for the investigation of biological information processing: An examination of the structure and function of computer hard drives and DNA – David J D’Onofrio1, Gary An – Jan. 2010 Excerpt: It is also important to note that attempting to reprogram a cell’s operations by manipulating its components (mutations) is akin to attempting to reprogram a computer by manipulating the bits on the hard drive without fully understanding the context of the operating system. (T)he idea of redirecting cellular behavior by manipulating molecular switches may be fundamentally flawed; that concept is predicated on a simplistic view of cellular computing and control. Rather, (it) may be more fruitful to attempt to manipulate cells by changing their external inputs: in general, the majority of daily functions of a computer are achieved not through reprogramming, but rather the varied inputs the computer receives through its user interface and connections to other machines. http://www.tbiomed.com/content/7/1/3 In computer science we recognize the algorithmic principle described by Darwin - the linear accumulation of small changes through random variation - as hill climbing, more specifically random mutation hill climbing. However, we also recognize that hill climbing is the simplest possible form of optimization and is known to work well only on a limited class of problems. Watson R.A. - 2006 - Compositional Evolution - MIT Press - Pg. 272 In the following podcast, Robert Marks gives a very informative talk as to the strict limits we can expect from any evolutionary computer program (evolutionary algorithm): Darwin as the Pinball Wizard: Talking Probability with Robert Marks - podcast http://www.idthefuture.com/2010/03/darwin_as_the_pinball_wizard_t.html etc.. etc.. If one were honest with themselves, they must ask themselves why in the world is this exactly the opposite of what we should expect to find if Darwinism were actually true,,i.e. Why do we not see a overwhelming majority of 'slightly beneficial' mutations spreading throughout the populations instead of seeing a overwhelming majority of 'slightly detrimental' mutations spreading? Why do beneficial mutations never spread throughout the populations (as is clearly illustrated in Joseph's referenced long term fruit fly experiment?)bornagain77
October 1, 2010
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Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.
Here's evolutionary theory falsified in a decades-long lab test. Researchers expected (predicted) that they'd find "selection sweeps" from advantageous mutations in the fruit fly population -- especially since they intelligently designed the experiments for the most ideal result. Instead ...
We conclude that, at least for life history characters such as development time, unconditionally advantageous alleles rarely arise, are associated with small net fitness gains or cannot fix because selection coefficients change over time.
So, what was predicted was falsified. The theory should be dead now. But, in a true Darwinian process, the theory can adapt to this new data and provide greater insights than ever. The spin will probably be that this study proves that micro-evolution is real and therefore ET is correct. Everything else will be ignored, including the fact that even the 'soft sweeps' lead gave rise to reverse evolution.Proponentist
October 1, 2010
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Joseph,
selection does not readily expunge genetic variation in sexual populations, a finding which in turn should motivate efforts to discover why this is seemingly the case.
Awesome find. Studly. Salscordova
October 1, 2010
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Here is a relevant paper on genetic entropy in other species: Muller's Ratchet and compensatory mutation in Caenorhabditis briggsae mitochondrial genome evolutionscordova
October 1, 2010
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I wonder, has Sanford only predicted the deterioration of the human genome, or of all life? They appear to be two separate issues with humans making such great advances in medicine; we are able to care for medical issues that would generally lead to death in any other species (except for pets, to an extent).
All life eventuallly, but humans are especially vulnerable. Bacteria have smaller genomes and higher reproduction rates therefore are substantially more immune. Humans have much more fragile and a much smaller reproduction rate. One viable bacteria out of a population of bad can "rescue" the bacterial population because of the high reproduction rate relative to the size of its genome. It's not the same for humans. But with respect to bacteria, here is a relevant experiment that shows if the bacterial population is small enough, it can go extinct via genetic entropy: Mutational Meltdown in Yeastscordova
October 1, 2010
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Did anyone here (posting author included) read any part of the paper other than the snippet that was posted? Because the article is clearly saying that the reason the human genome is deteriorating is because advances in wealth and technology have substantially relaxed selection pressure against mildly deleterious mutations
The paper claims that, but it doesn't justify it! If the mutation rate is high enough, even the harsh selective environment in non-industrialized countries will only slow the rate of deterioration, it will not stop it. Further, if infant mortality in non-industrialized world is due to non selective factors (like lack of food, bad sanitation etc.) you've reduced the excess breeding population to non-selective factors, therefore a lot of deaths are not do to someone being less functional, but just bad luck! So the non-industrialized world doesn't necessarily kill off that many more defective mutatants via natural selection than the industrialized world except maybe the severe conditions like diabetes, but severe conditions are not the issue, it's the SLIGHTLY deleterious mutations that are not immediately killed off. The point is the issue is now on the table, and it will be studied and tracked, and so far Sanford is not wrong, and looks to be spot on with every passing day.scordova
October 1, 2010
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An very interesting paper came out yesterday: Burke, Dunham et al, “Genome-wide analysis of a long-term evolution experiment with Drosophila,” Nature 467, 587-590 (30 September 2010); doi:10.1038/nature09352
Our work provides a new perspective on the genetic basis of adaptation. Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles. This is notable because in wild populations we expect the strength of natural selection to be less intense and the environment unlikely to remain constant for ~600 generations. Consequently, the probability of fixation in wild populations should be even lower than its likelihood in these experiments. This suggests that selection does not readily expunge genetic variation in sexual populations, a finding which in turn should motivate efforts to discover why this is seemingly the case.
My prediction is that evolutionsist will make up one or more excuses such as "fruit flies have reached their pinnacle of evolution"Joseph
October 1, 2010
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