Uncommon Descent Serving The Intelligent Design Community

P.falciparum – No Black Swan Observed


The tired old “ID is not scientific” has reared its ugly head again in another thread. This is simply not true.

Karl Popper famously stated that a hypothesis is scientific if it can be falsified. He used swans as an example. He stated a hypothesis:

All swans are white.

Popper said that it can never be proven that all swans are white because there is always the possibility that a black swan exists somewhere but has not yet been observed. He stated that the hypothesis is still scientific because it can be falsified – the observation of a single black swan will falsify it.

The biological ID hypothesis can be stated as:

All complex biological systems are generated by intelligent agents.

We already know, or may reasonably presume, that complex biological systems can be generated by intelligent agents. There’s a whole discipline called “Genetic Engineering” devoted to it. What we don’t know is whether any non-intelligent means can generate complex biological systems. A single observation of a complex biological system generated by a non-intelligent cause will falsify the biological ID hypothesis.

P.falciparum replicating billions of trillions of times in the past few decades represents the largest search to date for a “black swan”. This is orders of magnitude more replications than took place in the evolution of reptiles to mammals wherein there are many exceedingly complex biological systems that separate them. If P.falciparum had been seen generating any complex biological systems such as those that distinguish mammals from reptiles then it would have falsified the ID hypothesis. None were observed. This doesn’t prove ID but it certainly lends strong support to it. All perfectly scientific.

P.S. I understand that an actual black swan has been observed and Popper’s hypothetical example was indeed falsified. That is exactly how science is supposed to work. Now it’s up to the time & chance worshippers to falsify the ID hypothesis. Good luck.

bornagain77: Please give proof for an unambiguous beneficial mutation. Please replace mentally "beneficial mutation" with "ambiguous beneficial mutation" in my arguments above. Hu
Hu, You cited this article for your basis of beneficial mutations of 1 in 10,000: Fitness effects of advantageous mutations in evolving Escherichia coli populations http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=14717 And in this study they do indeed state your 1 in 10,000 number, but also mention the fact that it is often negated by what they term "clonal interference" which in reality refers to the 100% polyfunctionality of the genome. In other words your study is flawed in that it says: This is the rate of beneficial mutations (1 in 10,000): Yet at the same time they clearly state that the effect of the beneficial mutations is negated by other "beneficial mutations". Thus we are back to Garrish and Lenski's 1 in 1,000,000 estimate for beneficial mutations being beneficial. Yet even in Garrish and Lenski's study, I will maintain that the parent species will always be found to have more information. In other words Hu, beneficial mutation studies always come with a flaw of some sort. When you dig deep enough you always find their flaw. Since the study you cited was on e-coli, here is a paper that gives some detail to what I am talking about: http://www.answersingenesis.org/docs2007/0131observation.asp bornagain77
Hu, you stated: However, the situation changes if there’s a set of slightly beneficial mutations that together give a substantial advantage. Please give proof for an unambiguous beneficial mutation. I have failed to see any evidence for beneficial mutations. The primary thing that is crushing to the evolutionary theory is this fact. Of the random mutations that do occur, and have manifested traits in organisms that can be measured, at least 999,999 out of 1,000,000 (99.9999%) of these mutations to the DNA have been found to produce traits in organisms that are harmful and/or fa^tal to the life-form having the mutation! (Sanford; Genetic Entropy page 38) “I have seen estimates of the incidence of beneficial mutations which range from one in one thousand up to one in one million. The best estimates seem to be one in one million (Gerrish and Lenski, 1998) Since neutral mutations can be inferred to almost never occur in a genome, then the ratio of deleterious to beneficial mutations seems to be one million to one.” (Sanford; Genetic Entropy, page 38: Note: this statement has been revised to reflect the evolutionary belief of some totally neutral mutations of Gerrish and Lenski) http://myxo.css.msu.edu/lenski/pdf/1998,%20Genetica,%20Gerrish%20&%20Lenski.pdf Even if there were totally neutral mutations, which is highly unlikely given the overwhelming interrelated complexity of the genome, Gerrish and Lenski most likely used a incomplete measure of fitness/information in order to arrive at their one in a million number for beneficial mutations. I maintain that their, one in a million, estimate for beneficial mutations is flawed and that ALL mutations to a genome will be found to be harmful/fatal when using a correct measure of fitness/information. The following articles points out this flaw, in measuring the total fitness/information of a organism, by evolutionary scientists and thus skewing the already crushing, but biased, mutational studies: http://www.answersingenesis.org/docs2007/0131observation.asp http://www.answersingenesis.org/home/area/re2/chapter5.asp ” Bergman (2004) has studied the topic of beneficial mutations. Among other things, he did a simple literature search via Biological Abstracts and Medline. He found 453,732 “mutation” hits, but among these only 186 mentioned the word “beneficial” (about 4 in 10,000). When those 186 references were reviewed, almost all the presumed “beneficial mutations” were only beneficial in a very narrow sense- but each mutation consistently involved loss of function changes-hence loss of information.” In fact, from consistent findings such as these, it is increasingly apparent that Genetic Entropy is the overriding foundational rule for all of biological life with no exceptions at all, and that belief in beneficial mutations is nothing more than wishful speculation that has no foundation in science whatsoever: The foundational rule for biology can be stated like this: All adaptations away from a parent species for a sub-species, which increase fitness to a particular environment, will always come at a loss of information from the parent species. (Note: At present viruses are excluded from this rule.) Professional evolutionary biologists are hard-pressed to cite even one clear-cut example of evolution through a beneficial mutation to DNA that would violate the principle of genetic entropy. Although evolutionists try to claim the lactase persistence mutation as a lonely example of a beneficial mutation in humans, lactase persistence is actually a loss of a instruction in the genome to turn the lactase enzyme off, so the mutation clearly does not violate genetic entropy. Yet at the same time, the evidence for the detrimental nature of mutations in humans is clearly overwhelming, for doctors have already cited over 3500 mutational disorders (Dr. Gary Parker). “It is entirely in line with the al nature of naturally occurring mutations that extensive tests have agreed in showing the vast majority of them to be detrimental to the organisms in its job of surviving and reproducing, just as changes ally introduced into any artificial mechanism are predominantly harmful to its useful operation” H.J. Muller (Received a Nobel Prize for his work on mutations to DNA) “But there is no evidence that DNA mutations can provide the sorts of variation needed for evolution… There is no evidence for beneficial mutations at the level of macroevolution, but there is also no evidence at the level of what is commonly regarded as microevolution.” Jonathan Wells (PhD. Molecular Biology) So Hu, please do give an unambiguous example of a beneficial mutation that has not in reality involved loss of either function or information, before you state beneficial mutations might occur! bornagain77
DaveScot: Total number of replications where mutations are heritable is all that counts when probability of any certain mutation occuring is what you’re trying to ascertain. Yes, that's obvious. (Any realistic difference in mutation rates is clearly dwarfed by the difference in population sizes.) The same applies to any set of simultaneous mutations. However, the situation changes if there's a set of slightly beneficial mutations that together give a substantial advantage. In the huge population of P. falciparum, many mutations certainly keep occurring over and over again, but if there's a number of them that individually have only a slight beneficial effect in the presence of chloroquine and none otherwise, they haven't had the time to spread much, so there's little overlap. A tiny fraction of the total number of replications can suffice to produce a suitable combination if selection has enough time to make the mutations prevalent. I gave a specific theoretical example. Hu
Good point, although I'd add that you cannot please everyone. For example, some Darwinists are perfectly fine with using the term "Darwinist". Others object to its usage, since they believe it does not reflect the changes to evolutionary biology. But I haven't heard a good replacement term to describe the group as a whole. Same thing with "RM+NS". Personally I was using it to reference all possible Darwinian mechanisms. But I can see how that can be confusing. So I now prefer RV+NS. Patrick
Patrick, Thanks for editing the FAQ. I'm just trying to help make sure that we use the standard terms when talking science. Not using the standard terms would detract from our credibility. getawitness
I edited the FAQ (Dave wrote the original version but I've been editing and adding a lot of content). Personally I think quibbling over the usage of "replications" or "generations" is a waste of time since it's irrelevant to the main points. But I'd rather make the change than have people get caught up in analyzing minutiae. Patrick
DaveScot, Re my comment [75], the moderation FAQ has been corrected. Uh, you're welcome? getawitness
DaveScot said,
Total number of replications where mutations are heritable is all that counts when probability of any certain mutation occuring is what you’re trying to ascertain.
If you're looking for the probability of a "certain mutation" occurring, you're looking for something that's already happened, which means the probability is 1. Stanton Rockwell
DaveScot, I don't know enough to assess the debate between you and Hu. But I have to say, the term "generations" is misused all over the place here, and not just in this thread. Consider the moderation FAQ: Behe’s latest work of analyzing what billions of trillions of generations of p.falciparum accomplished in the way of generating novel complexity without benefit of intelligent agency supports the prediction that only intelligent agency is capable of producing complex specified information. When I search for "billions of trillions of generations" as a phrase, I get six hits. I think that, for each of those times, you really mean "replications." Thanks. You probably don't want to change the comments, 'cause that would erase the history, but you might want to change the "arguments not to use" page. getawitness
Hu Total number of replications where mutations are heritable is all that counts when probability of any certain mutation occuring is what you're trying to ascertain. If you cast a single die the chance of getting a six is one in six. If you cast a thousand die at once the chance of getting a six is almost 100%. You can cast a single die a thousand times and the chance of getting a six in one of those casts is the same as casting a thousand at once. DaveScot
DaveScot: Thank you for the data supporting a more precise estimate on the basic mutation rate. The estimates on beneficial mutation rates seem to vary by several orders of magnitude, and my assumption seems to fall within the empirically supported range. (See Perfeito L, Fernandes L, Mota C, Gordo I Adaptive mutations in bacteria: high rate and small effects. Science. 2007 Aug 10;317(5839):813-5.) Anyway, accepting your estimate for the sake of argument, one only needs to multiply the effect of a mutation by three and the size of the smaller population by ten to obtain similar results. My point stands: under identical assumptions, time can be vastly more important than population size. The total number of replication events is an inadequate measure. Hu
Extrapolating from this the probability of a set of 8 simultaneous beneficial nucleotide changes would be 5 in 10^80. Clearly that number is far too large to have any reasonable chance of ever happening. Even just 3 simultaneous beneficial nucleotide changes, 5 chances in 10^30 individuals, is essentially out of reach for even such a prolific species of eukaryote as falciparum. The only real chance of ever getting 8 beneficial mutations in one individual falciparum is through a sequence of 8 single-nucleotide beneficial mutations (maybe one dual-nucleotide mutation in the sequence) where each single or dual event is selectable by itself.
Like Hu, I remember reading about speculations that a gradual/stepwise direct pathway existed for developing CQ resistance. The main issue is that such pathways should not be conflated with indirect non-gradualistic pathways that require simultaneous changes (it's not stepwise). Behe of course is focused on analyzing those types of non-gradual indirect pathways since the majority of objects under debate cannot be broken down into gradual/stepwise direct pathways. I'll just quote myself here (with some mods): The interesting thing about the Darwinist commentators on Amazon is that they were so focused on "we must prove Behe to be wrong somehow" that they fail to realize they're shooting themselves in the foot. If CQ resistance did indeed come about by a gradual/stepwise direct pathway scenario then all that does is make this example of the "all-mighty powers of Darwinian mechanisms" even more trivial than before! After all, a direct stepwise scenario is much more likely to occur than one that requires simultaneous changes or an indirect pathway. Yet even then Darwinian mechanisms have a hard time bring about such a change even with the extremely high number of replications (in comparison to higher animals). (BTW, I would rank in order of difficulty from easiest to hardest: direct gradual, indirect gradual, direct multiple/simultaneous, and then a combination of direct gradual changes combined with indirect multiple/simultaneous) Now I have seen excerpts where scientists hypothesize more complicated gradual scenarios...
Current evidence from transfection studies (71, 187) strongly suggests that the mechanism of P. falciparum resistance to CQ is linked to mutations in the pfcrt gene, especially the substitution of threonine for lysine at position 76. However, other mutations in the pfcrt gene at positions 72 to 78, 97, 220, 271, 326, 356, and 371, as well as mutations in other genes such as pfmdr1, might be involved in the modulation of resistance (173, 223). CQ resistance seems to involve a progressive accumulation of mutations in the pfcrt gene, and the mutation at position 76 seems to be the last in the long process leading to CQ clinical failure (53, 92).
...mutation 4 allows parasites to infect people 6 days after treatment rather than 7 days. The relatively rapid elimination of CQ means that these are rather weak selective forces (6) and that the spread of these first mutations will be slow. Eventually, mutation 8 arises, which allows the parasite to survive therapeutic levels of CQ. Once above this threshold, the selective advantage conferred by this mutation becomes enormous...
Behe is of course narrowing the focus down to position 76 and 220. But just because other scientists are discussing other scenarios for generating CQ resistance that "must" mean Behe is lying in the minds of many Darwinists. Also, this may be the information Hu was thinking of. Otherwise, many of the Amazon commentators do not seem to have bothered to read what Behe had said previously:
Incidentally, this bears on Coyne’s comment on Miller’s review that “one of the two mutations that Behe claims are ‘required’ for CQR is not actually required (Chen et al. 2003, reference accidentally omitted from Miller’s piece).” If you read that paper you see that, yes, A220S is not found in some resistant strains, as it is in most. (By the way, I was always quite careful in my book to state that A220S had been found in most strains, because I was quite aware of the several exceptions.) However, one also reads that the strains missing A220S have several other, novel mutations, which may be playing a comparable role in them that the mutation at position 220 plays in most other strains. My argument does not depend on exactly which changes are needed in the protein. Rather, the important point is that multiple changes appear to be required for resistance in the wild.
DaveScot, I thought Hu [55] was using "generations" correctly. But I may have been mistaken; I'm still learning this stuff. getawitness
Stanton The mistake was someone else using "generations" instead of "replications". Each of you and your siblings can have different heritable mutations. Each of you represents one chance for random mutation to generate descent with modification. So if you have 3 siblings that's only one generation but 4 chances for random heritable change. I merely pointed out that the definition for generation and replication must be equivalent if you want to swap terms like that. DaveScot
Hu Every new individual has 1 chance in 10^6 to carry a new slightly beneficial mutation Presuming falciparum has the average eukaryote mutation rate of 1 in 10^9 nucleotides copied then with a genome of 23 million base pairs only 3% of the individuals will have any mutation at all while 97% are perfect copies. If the beneficial mutation rate of 1 in 10^6 mutations (Gerrish and Lenski, 1998) is correct then for falciparum the number of individuals with a single beneficial mutation is 3 per 10^8 individuals. This seems reliable enough for falciparum since atovaquone resistance, which requires only a single changed nucleotide, arises in approximately 5 of 10^10 individuals. Chloroquine resistance requires 2 simultaneous point mutations for any benefit at all and one or more additional point mutations on top of that for full resistance. The chance of getting a two-nucleotide beneficial mutation in one individual falciparum, based on the observed atovaquone rate, is about 5 in 10^20 individuals. This also seems reliable enough since chloroquine resistance arises about 3 times per year (10^20 replications). Extrapolating from this the probability of a set of 8 simultaneous beneficial nucleotide changes would be 5 in 10^80. Clearly that number is far too large to have any reasonable chance of ever happening. Even just 3 simultaneous beneficial nucleotide changes, 5 chances in 10^30 individuals, is essentially out of reach for even such a prolific species of eukaryote as falciparum. The only real chance of ever getting 8 beneficial mutations in one individual falciparum is through a sequence of 8 single-nucleotide beneficial mutations (maybe one dual-nucleotide mutation in the sequence) where each single or dual event is selectable by itself. Thus the "edge of evolution" is established by observation that matches what is predicted given numbers of 1 of 10^9 nucleotide copy errors and 1 in 10^6 of those being beneficial. The $64,000 question is how, in light of the observational evidence in falciparum, could reptiles evolve into mammals by random mutation when the number of replications for that transition is orders of magnitude fewer than observed in falciparum and the number of beneficial mutations required in the transition is orders of magnitude greater than what falciparum was able to accomplish. Non sequitur. DaveScot
Oops, typo: A set of 8 slightly beneficial mutations has 1 chance in 10^6, not 1 in 10^65, of being strongly beneficial. Sorry for forgetting to proofread. Hu
Please bare with me. I know a bit about the theory of evolution, and I'm trying to find out whether the evidence for ID is stronger. I'm not convinced by your example, as you don't take into account a factor that potentially has a huge impact. I'll present an oversimplified mathematical model just to illustrate that one point. Suppose we have two populations, one of which consists of 10^21 individuals, the other of 10^6 individuals. After one time unit, all individuals are replaced by their immediate descendants. (A time unit for P. falciparum would be two days, for a proto-mammal maybe a year or two.) Every new individual has 1 chance in 10^6 to carry a new slightly beneficial mutation, which increases its procreation probability by 10^-4. You can imagine every normal individual gets 10,000 lottery tickets and every mutant 10,001 tickets. As many tickets are drawn at random as there are individuals in the population, and each lucky draw corresponds to a descendant. Usually, the effect of k mutations in the same individual is just k times the effect of one mutation, i.e., the individual gets 10,000 + k tickets. However, any combination of 8 mutations has 1 chance in 10^65 of being strongly beneficial and becoming prevalent in a very short time. What happens to the large population in 10,000 units of time? In one unit of time, the number of carriers of existing mutations is multiplied roughly by 1.0001, and 10^15 new mutations will occur. Unless some roundoff errors accumulate more than I estimated in my head, somewhat less than 2x10^19 individuals or 2% of the population will carry at least 1 mutation. Assuming the mutations are mixed well by sexual reproduction, the number of individuals with 8 mutations will be about 10^21 / (50^8 x 8!) or about 600. If new combinations of mutations are created at each time unit, the expected number of lucky combinations is certainly less than (600 x 10,000)/10^6 = 6. How about the smaller population? On the average, one beneficial mutation occurs in one unit of time. It has 1 chance in 10,000 to become prevalent, so once in 10,000 time units a new beneficial mutation will start the process of spreading to the entire population. In about 150,000 time units, it will spread to the majority. In 400,000 time units, there will be about 25 well-established mutations around, and there are a bit more than 10^6 ways to choose 8 mutations out of 25. So, even assuming that the 17 mutations that weren't part of the lucky combination are totally out of luck and will never have an effect, it won't take more than about 2,400,000 time units for the smaller population to achieve more than the larger population did in 10,000 time units. I saw it mentioned somewhere that chloroquine resistance seems to be caused by 8 mutations, but I'm afraid I lost the URL. I took your estimate of the population size of P. falciparum and my own calculation of the time involved. I pulled the rest of the numbers out of thin air, trying to be vaguely realistic and tweaking them to get within an order of magnitude from observations. If you can show that some factor I left out (there are many) essentially nullifies my argument, I'll be very eager to learn from my mistake. Hu
DaveScot,"Each replication is a new generation. Ergo there have been billions of trillions of generations in the last several decades." I'm no expert in this area, but it seems to me that using this definition of "generation" that my siblings and I should be considered of different generations? Stanton Rockwell
Pantrog, "and ‘generation’ is, as we have learnt, ambiguous." Not really. From The Oxford Dictionary of Science: A group of organisms of approximately the same age within a population. Organisms that are crossed to produce offspring in a genetics study are referred to as the parent generation and their offspring are the first filial generation. DaveScot's point is beyond my understanding, but his language isn't: he was clearly using "generation" in a non-standard sense. getawitness
[correction] There are perhaps 40 cell divisions between human male zygote and sertoli cells. (they're not somatic if the eventually contribute to the germline - and 'generation' is, as we have learnt, ambiguous.) Pantrog
"Yes but those are somatic cells and mutations in them are not heritable" You've forgotten sperm, There are perhaps 40 somatic cell generations between human male zygote and sertoli cells - there are then thousands of germline replications - all with the potential for heritable change. Pantrog
After all there will be thousands of asexual cell divisions between you and your offspring. By convention these aren’t generations. Yes but those are somatic cells and mutations in them are not heritable. Falciparum has no somatic cells. Any genetic change in falciparum, whether it occured during sexual or asexual reproduction, is heritable. I would have thought that clear without belaboring the point but evidently it wasn't clear to everyone. I guess I should have known since Bob O'Hara, an expert I believe in fungi, claimed that evolution doesn't occur in individual mycelial colonies and that it could only happen when spores are produced by sexual reproduction. I still don't think he gets it that each cell in the colony can mutate during asexual reproduction and any clonal cell has the potential for participating in sexual reproduction. By all rights falciparum should be an extremely rapid evolver. Each year a billion isolated clonal populations of up to a trillion parasites grow in human hosts. The fittest of these are then sampled by God only knows how many billions of mosquitos and in the mosquito's gut recombination occurs allowing any of the beneficial mutations in the clonal populations to spread into other cell lines. It's difficult to imagine a more opportune situation for random mutation and natural selection to do what it is claimed it can do. DaveScot
For clarity it would probably be better to use the term 'replication'. In the malaria literature 'generation' is often used to refer to the time between fertilized zygotes (~2 weeks+). e.g. "A generation in malaria is the average time taken for it to complete its life cycle" The Evolution of Drug-Resistant Malaria: The Role of Drug Elimination Half-Life Ian M. Hastings, William M. Watkins, Nicholas J. White Philosophical Transactions: Biological Sciences, Vol. 357, No. 1420, Reviews and a Special Collection of Papers on Human Migration (Apr. 29, 2002), pp. 505-519 After all there will be thousands of asexual cell divisions between you and your offspring. By convention these aren't generations. Alternatively you could refer to 'generations of merozoites' that would also be clearer. Pantrog
Every single time an individual parasite replicates, be it asexual or sexual, its genome is copied from mother to daughter. Each and every time the genome is copied to a daughter cell there is an opportunity for random mutation to introduce changes. These changes are heritable. Each replication is a new generation. Ergo there have been billions of trillions of generations in the last several decades. DaveScot
And of course although release of a new generation of merozoites is every couple of days - the parasite is effectively clonal and haploid, the time between meotic events (when recombination can take place between strains) is weeks. Gametocyte production starts 1 - 2 weeks after infection, then they need ingested by a mosquito - then theres the sequence of ookinete, oocyst and sporozoites formation which may add days to the amount of time before inoculation of the new clone generation. Still there's a big replication potential. Pantrog
I was calling all those countless currently existing falciparum parasites one generation. The previous generation, the immediate ancestors of the current one, lived mostly two days ago, the generation before that four days ago and so on. I presume the concept is clear, even though I may be using the wrong terminology. Anyway, at the rate of one "generation" in two days, you get about 11,000 "generations" in the time chloroquine has been used as an antimalarial, about 60 years. (I thought chloroquine was a more recent invention and didn't check; hence "several thousand". I'm sorry.) Of course, I'm not denying that each such "generation" consists of a huge number of individual parasites, but that's less important than time. Hu
Hu How do you figure only thousands of generations for falciparum? It infects a billion humans every year, asexually replicates itself into a trillion parasites in a full blown infection, and is carried by God only knows how many mosquitoes (presumably more mosquito hosts than human hosts) where it reproduces sexually. That's billions of trillions of generations. DaveScot
Panrog, Dr. Behe addressed this objection here; Kenneth R. Miller and the Problem of Evil, Part 3 http://www.amazon.com/gp/blog/A3DGRQ0IO7KYQ2/103-2763420-3159839/ref=cm_blog_dp_artist_blog/103-2763420-3159839 Here is an excerpt; Why couldn’t a grieving mother justifiably demand of an infinitely powerful God that He explain why He chose such a sloppy process to make life, instead of a more efficient process that would not produce natural evils such as parasites and tsunamis? One that wouldn’t cause such enormous pain? It seems to me that designing a poor Darwinian process that inevitably spins off natural evils leaves One as vulnerable to being sued for incompetence as directly designing them as finished products. My own view (which Miller spectacularly fails to grasp) is that, as a scientist, one is obliged to look at the evidence of nature dispassionately and nonjudgmentally. If the coherence and complexity of the malaria parasite point to its purposeful design by an intelligent agent, then that’s where the data point. As a scientist, one is not allowed to pass judgment on the morality of nature. To reject the weight of evidence because it shows the universe to be something unpalatable is to betray science. On the other hand, as a theist one can make an argument that what strikes us as evil in nature is part of a larger whole which is good. In his recent book Francisco Ayala wrote that one could regard tsunamis as the unintended side effect of a good process (plate tectonics) which is necessary to build a habitable world. Well, heck, one can make the same argument for parasites and viruses. It may well be that such seemingly vile creatures actually play positive roles in the economy of biology, of which we are in large part unaware. If that’s the case, then directly designing parasites and viruses is as defensible in terms of the overall goodness of nature as is designing the processes of plate tectonics. The fact that they are dangerous to humans is an unintended side effect of something that is good in itself. I hope this helped Pantrog, But this subject digresses from our main discussion; I wanted to show you a rather humorous antidote someone "an IDists" had for the supergerms: http://www.answersingenesis.org/creation/v11/i2/supergerms.asp Likewise, you contract a hospital infection only in a hospital. The hospitals are spraying disinfectants on every available surface to kill off their so-called supergerms, and, most importantly, dealing with serious clinical infections requiring powerful antibiotics. Maybe they would do better to bring in a few truckloads of dirt off the street every six months, and spread that around and sweep it off! Maybe the hospitals would do even better to do research on inoculating superinfection patients, not with more antibiotics, but with a competing infection that would crowd out the supergerms. (I doubt that this would work, but it’s worth exploring, especially when germs that kill by bacteriotoxins are concerned.) Now that should definitely be food for thought Pantrog! LOL bornagain77
The huge population size is a very poor substitute for a sufficient number of generations needed for anything complicated to evolve. Several thousand generations isn't enough to make any weakly selectable new trait prevalent, let alone a complicated sequence of improvements. Hu
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