Annoying creationists

[Olowkow]

I'm taking bets that this thread will not hit 8000 posts.

 

[m_huber]

Alan, I'm almost convinced that you're really an award-winning novelist, working on a new novel about your experience baiting scientists into defending evolution against ridiculous arguments.

Nevertheless, you do have one point.


This doesn't look anything like a fossil horse. (name: Equus simplicidens)

As for selection pressures, they can go both ways. The amount of available food is a selection pressure. If there is too little, diversity will decrease as species go extinct and fill specific niches. If there is too much, diversity will increase as a wider variety of morphologies will survive to reproduce. This really isn't either hard or necessarily mathematical. What's your problem here?

I would like to know something specific, though. You obviously have an emotional attachment to evolution being wrong. When people come here and are not emotional about a subject, they say "yeah, whatever" and back off. You have persisted for some time. What is your reason for wanting evolution to be wrong? How does it benefit you? Do you think the Genesis account is the ultimate correct answer, or do you discount it?

Just wondering.

 

[Belz...]

the fossil Rorschach record

Yeah. Sure. Those aren't wings and teeths and a tail...

 

[joobz]

I need to repeat this, becuase it's a new funny that kleinman made.

When asked how he explains nylon-eating bacteria evolving.

17.) nylon-eating bacteria-a polymerase evolves into a polymerase, what’s your point?

So his explanation that evolution doesn't occur is by admitting that bacteria evolves and evolves new functionality that it didn't not have before.

This is a clear admission to evolution occuring. and it is a macroscopic change. The ability for a bacteria to digest a food source that it previously couldn't can't possibly be labelled as "microscopic evolution". If it is, it renders the definitions meaningless.

 

[Belz...]

17.) nylon-eating bacteria-a polymerase evolves into a polymerase, what’s your point?

Did he just say it "evolves" ? I thought that was mathematically and empirically impossible !

 

[Shalamar]

Its almost sad that someone could fight so hard against something supported by evidence, just because their faith tells them it can't be true.

And its the lack of ANY evidence for creationism that makes creationists evil. They want to pollute and twist the minds of our children by telling them that science is wrong and evil. They don't see the damage that they're doing, or the results on how the rest of the world sees Americans these days.

And all Mr. Kleinman can do is yell 'Ha Ha. Evolution is stupid. You stupid evolutionists, look! I have no math to prove its mathematically impossible! Ha Ha!'

I weep for humanity.

 

[joobz]

Did he just say it "evolves" ? I thought that was mathematically and empirically impossible !

Yeah, I hope Dr. A gets a load of that one.

I'm sure kleinman will explain it as "microevolution", but that would simply be denying reality. This is a new gene that arose from a gene that did something completely different. And it used a frameshift mutation to do it.

 

[kjkent1]

Did he just say it "evolves" ? I thought that was mathematically and empirically impossible !

Kleinman is merely operating as a troll at this point, using the tried and true method of maintaining a debate without any substantive argument:

1. State an inflammatory proposition;
2. Ignore or ridicule opposing arguments;
3. Go to 1.

I wish forum moderators would prevent contributors from engaging in this behavior. It's such a waste of resources.

 

[Belz...]

Yes, but there is no rule against being stubborn, obtuse or stupid.

 

[m_huber]

What I find interesting is that Kleinman seems to treat us like enemies. We could easily agree to disagree and have a civil conversation. Even if we were to continue throwing jabs at each other, we could still learn something from one another.

I guess I don't always mind when someone has a false belief. What bothers me is when someone tries to either 1) force me to believe it or 2) use that belief for illegitimate personal gain. Kleinman has been unwilling to back down, choosing instead to come here and mock us and post segments of papers that talk about evolution. As a doctor, I'm sure that he knows both a tremendous amount of medical knowledge and a large number of interesting anecdotal stories. We will probably never know, as all we will ever see from him is his anti-evolution mode, which does neither him nor us any good.

 

[CriticalThanking]

I know I am going to regret posting in this thread. And no, I have not read all 7900 (and counting) posts in it. My apoligies if this has already been discussed. How could it not be after this many posts?

If I recall some of this thread and understood the arguments, one of Kleinman's arguments is that multiple selection pressures cause would cause evolution to slow such that what we observe today could not have evolved in the time given. My musings:

1) There was a recent article noting that fishery policies of catch size restrictions (size of the individual fish, not the size/volume of total catch) have caused an observed accelleration of fish evolution. Specifically, the species are coming to sexual maturity faster and not growing as large. A new selection pressure (size selection during "predation") has resulted in an observable accelleration.

2) When is there ever only one selection pressure? Just thinking about the fish example, there are always many pressures. Preators that eat eggs, predators that eat fry, predators that eat large fish, predators that pick a specific size of fish (see #1), availability/seasonailty of food, changes in food types, bacteria, virii, changes in water temperature/sailnity/clarity/pollutants/depth/availability, AND CONSTANT CHANGES TO THE INTENSITY OF EACH OF THESE PRESSURES. And yet we observe evolutionary changes. It took me less than a minute to think of all items in this list. There must be more.

We now return you to your strawman burning already in progress.

CT

 

[Mr. Scott]

I know I am going to regret posting in this thread. And no, I have not read all 7900 (and counting) posts in it. My apoligies if this has already been discussed. How could it not be after this many posts?

I know exactly how those nitwit creationist loonies will answer.

If I recall some of this thread and understood the arguments, one of Kleinman's arguments is that multiple selection pressures cause would cause evolution to slow such that what we observe today could not have evolved in the time given.

Multiple selection pressures confound the process of evolution by mutation and natural selection. It's a sorting/optimization problem that becomes profoundly slowed by multiple sorting conditions.

1) There was a recent article noting that fishery policies of catch size restrictions (size of the individual fish, not the size/volume of total catch) have caused an observed accelleration of fish evolution. Specifically, the species are coming to sexual maturity faster and not growing as large. A new selection pressure (size selection during "predation") has resulted in an observable accelleration.

They're still fish, aren't they?

2) When is there ever only one selection pressure? Just thinking about the fish example, there are always many pressures. Preators that eat eggs, predators that eat fry, predators that eat large fish, predators that pick a specific size of fish (see #1), availability/seasonailty of food, changes in food types, bacteria, virii, changes in water temperature/sailnity/clarity/pollutants/depth/availability, AND CONSTANT CHANGES TO THE INTENSITY OF EACH OF THESE PRESSURES. And yet we observe evolutionary changes.

The intensity of the selection pressure has no effect on the sorting/optimisation problem. The more pressures, the longer it takes.

It took me less than a minute to think of all items in this list. There must be more.

It took me less than a minute to guess how the nut cases would respond.

We now return you to your strawman burning already in progress.

CT

Ah, the all-powerful strawman argument. Have you evolutionists figured out the mathematics and empirical facts about mutation and natural selection, or are you still responsible for the deaths of millions with your monotherapies based on the evolution fairy tale?[/mockery]

 

[Dr Adequate]

I think it worthwhile ...

<1500 words of kleinmania deleted for pointlessness>

Yes, you do find it worthwhile.

No-one knows why.

It's not as if you've deceived anyone, ever, during the course of the last fifteen months.

I wouldn't find fifteen months of failure at anything to be "worthwhile", least alone failure at something so stupid and pointless as lying to people about basic biology, but then we are two very different people.

 

[kleinman]

Annoying Creationists

Some evolutionists think that I view them as enemies. On the contrary, I view of you evolutionists as very confused and wrong about how the mutation and selection sorting/optimization process actually works both mathematically and empirically. Instead, you substitute illogical and irrational speculations that obfuscate how this process works in reality and as a consequence millions of people have and will continue to die prematurely from diseases subject to the mutation and selection sorting/optimization process. For example, several evolutionists on this thread have speculated that in some cases selection pressures increase the diversity of populations and in other cases selection pressures decrease the diversity of populations.

In all cases, selection pressures decrease the diversity of populations. This can be shown mathematically with Dr Schneider’s ev computer simulation of random point mutations and natural selection as well as empirically with as many examples as you like. First let’s look at how Dr Schneider’s computer model demonstrates that natural selection reduces the diversity of a population.

Dr Schneider’s computer model starts with an initial condition of a population of randomly distributed genomes. This is the most diverse condition you can have and represents an initial condition of maximum disorder. When the algorithm is initiated, the selection conditions reduces the disorder of the sequences of genomes (increase the information content) in the population. This decrease in disorder (increase in information) is demonstrated by the following graph from Dr Schneider’s web site:

Note that with the removal of the selection conditions, any information accumulated by the mutation and selection sorting/optimization process is lost until the genome returns to random sequences.

In real cases of the mutation and selection sorting/optimization process, selection pressures eliminate phenodeviants (members of the population who can only survive to reproduce in an environment without those selection pressures). This is clearly seen when an antimicrobials is used on a population sensitive to that antimicrobial, when cancer cells are subjected to anti-cancer therapy, when weeds are subjected to herbicides and so on.

Diversity of populations occurs when you remove selection pressures. The reason why the Madagascar rain forest has such diverse populations is the low selection pressures (abundant water, mild temperatures without extremes, abundant food), while environments like deserts have far fewer diverse forms of life because of the lack of water, much greater temperature extremes and lack of food. If you tamper with the rainforest, these diverse life forms are quickly killed off. On the other hand, put a house up in the desert and the rattlesnakes and scorpions are much more likely to survive this intrusion. Selection pressures reduce the diversity of the populations subjected to these selection pressures. A citation which demonstrates this empirically is:

http://www.conservationmedicine.org/papers/Kilpatrick/Kilpatrick_2006_BiolCons.pdf

In some cases it is the combination of multiple stressors that lead to the decline of species or groups of species; e.g., amphibians by nematodes (Johnson et al., 1999), increased UV radiation and pollutants (Hatch and Blaustein, 2003; Beebee and Griffiths, 2005), and disease (Collins and Storfer, 2003; Daszak et al., 2003). Conserving endangered species and facilitating their recovery is one the main environmental challenges of the 21st century. Unfortunately, history has shown that in most cases permanent removal of stressors has not been possible and species often need to be

managed indefinitely to ensure their persistence; of the 1263 species listed under the Endangered Species Act of the United States less than 2% have been de-listed (US Fish and Wildlfe Service, 2004).

Manage indefinitely means remove selection pressures.

Now I note that you evolutionists have posted some fossil Rorschach. Don’t just post your images; tell us what your imaginations give you.

I also note that the author of blizzards turns lizards into buzzards with gizzards and the author of the n+1 selection pressures evolve more rapidly than n selection pressures but he doesn’t have any reality to back up his mythematics. We all enjoy your blizzdom.

 

[m_huber]

Do you even read other people's posts?

 

[Mr. Scott]

Do you [Kleinman] even read other people's posts?

The evolutionists who post on this thread are mere props in Kleinman's act, the objective of which is to google-bomb his nitwit ideas. To him we are cardboard cutout targets for him to knock down in the hope of future fame. Quite a pathetic spectacle.

 

[kleinman]

Annoying Creationists

Some evolutionists don’t think that I read their posts, such as those evolutionists who think that variations in the weather is what turns lizards into buzzards or that n+1 selection pressures sort more rapidly than n selection pressures. Sure you evolutionists have lots of speculations, but your mathematical and empirical evidence is simply not there. Here are some more empirical evidence that combination selection pressures profoundly slow the mutation and selection sorting/optimization process.
http://homepages.ed.ac.uk/eang09/research.html

The development of combination antiretroviral therapy was an immense breakthrough in HIV treatment, turning a previously lethal infection into a chronic treatable condition. In the absence of a vaccine, combination therapy is the only way HIV infection can be controlled, but there are two major problems, side effects due to toxicity and the development of resistance. Almost all drug failure is associated with antiretroviral resistance, which for some drugs (eg 3TC monotherapy) can arise within days (Frost et al. 2000). Combination therapy extends the period of efficacy greatly, but resistance still appears in a majority of patients.

http://www.ajtmh.org/cgi/content/full/71/2_suppl/179

Increasing resistance of Plasmodium falciparum malaria to antimalarial drugs is posing a major threat to the global effort to "Roll Back Malaria". Chloroquine and sulfadoxine-pyrimethamine (SP) are being rendered increasingly ineffective, resulting in increasing morbidity, mortality, and economic and social costs. One strategy advocated for delaying the development of resistance to the remaining armory of effective drugs is the wide-scale deployment of artemisinin-based combination therapy. However, the cost of these combinations are higher than most of the currently used monotherapies and alternative non-artemisinin-based combinations.

How about this citation? You evolutionists think that recombination is the super mechanism which somehow transforms one species into another.
http://www.ethlife.ethz.ch/e/articles/sciencelife/hivrekombination.html

The immune deficiency syndrome, AIDS is a huge health problem worldwide – and will remain so for some time to come. One reason lies in the HI-viruses' ability to become resistant to specific drugs. Until now, scientists have supposed that the recombination of different viruses plays an important role here. But researchers at ETH now show that the recombination can in fact slow down the build-up of resistance and that it advances it under certain specific conditions. This throws light on the question of why sexuality exists.

and

So what are the possible consequences of this model for the ETH research team? Sebastian Bonhoeffer points to two aspects, the first of which is medical. If gene variants that are antagonistic to one another exist, then the build-up of resistance to a combination of drugs that favours such genes would be slowed down by recombination. What is missing from the picture is information on how strongly certain mutations in the HIV genome act synergistically or antagonistically on one another. Bonhoeffer now wants to turn his attention to this question using HI-virus data sequences, which he has in abundance.

However, such an analysis is not only relevant from a medical point of view. Bonhoeffer comes to his second point. It is highly possible that the results of such an investigation could also deliver insights into a far more fundamental question; why on earth does recombination exist? Because, as Bonhoeffer's model shows, in many cases this process has unfavourable consequences for HI-viruses. From an evolutionary point of view, it must be presumed that, under certain circumstances, the acquisition of recombination is advantageous. If these circumstances can be identified in the case of the HI-viruses then conclusions might be drawn on the reason – or reasons – for recombination in higher-order beings. Even though sexual reproduction and concomitant recombination is widespread, the advantages of sex as a means of reproduction is still one of biology's better kept secrets – despite numerous theories.

Could it be that recombination slows evolution? That can’t be, it doesn’t fit ridiculous evolutionists speculations. Who cares if millions of people die prematurely from diseases subject to the mutation and selection sorting/optimization process? The irrational and illogical theory of evolution is much more important than premature death of millions of people.

 

[m_huber]

You know, using the "Quote" button and responding to specific claims would make your case against "evolutionists" much more intelligible. Instead, you post large blocks of scientific articles that are moderately difficult to read, which you then claim support the belief that evolution doesn't happen. Instead, when those have been broken down, they only show that extinction prevents evolution. In other cases, evolution has been demonstrated at the bacterial and viral level, but instead of saying "oh, wow, reality exists!" you say, "But you don't have a mathematical proof!"

Math is trumped by reality. Always. Newton predicted that the world would end in 2060.

 

[kleinman]

Annoying Creationists

I’m not sure why evolutionists are having a hard time reading scientific articles. I thought the theory of evolution was based on science. Could it be that evolutionists have gotten so used to irrational and illogical speculations that when they are confronted with the mathematical and empirical evidence that multiple selection pressures profoundly slow the mutation and selection sorting/optimization process it confuses them? I have shown with Dr Schneider’s computer simulation that multiple selection conditions profoundly slow the sorting process in his algorithm. And now I am posting the empirical evidence which demonstrates the same effect when multiple selection pressures are applied to a population. Here are some more real example which show that combination selection pressures profoundly slow the mutation and selection sorting/optimization process.
http://www.annalsnyas.org/cgi/content/abstract/918/1/9

Large-cohort studies in North America, Europe, and Thailand have shown that zidovudine/azidothymidine (AZT) monotherapy, given at the late stages of pregnancy, is of proven benefit in reducing mother-to-infant HIV transmission by 51% to 68%. AZT monotherapy will not be of long-term benefit for mothers because no single drug can counteract viral infection; benefits to babies will be short-lived if HIV-1 is acquired through breastfeeding after birth. Unfortunately, ongoing mutation of HIV under conditions of drug pressure allows for the evolution and selection of AZT-resistant viruses. Emergence of AZT-resistant variants in pregnant mothers (7-29%) and their infected offspring (5-21%) has been described in several studies. Drug resistance arises more frequently in those mothers who received AZT therapy before pregnancy. Recent advances in combination chemotherapy may provide alternative strategies in prevention of vertical transmission and drug resistance. Genotypic screening of the HIV-1 isolated from pregnant mothers may provide rational modifications in antiretroviral (ARV) strategies to circumvent vertical HIV transmission. This may be of advantage for resource-rich nations but not for underdeveloped nations with limited access to ARVs. Public health programs are vital to have an impact on the tragic pandemic of pediatric AIDS.

http://www.who.int/infectious-disease-report/2000/ch5.htm

Drug combinations have long been recognised as critical in combating multi drug-resistant malaria.

And

It wasn't until the 1950s that effective treatment for leprosy was introduced into vulnerable populations. By the 70s, the organism had launched a major counter-offensive and had effectively disarmed and rendered obsolete the sulpha drug dapsone. By the 1980s, two drugs – rifampicin and clofazamine – cleared the way for viable treatment alternatives. The organism developed resistance to all three drugs when prescribed singly but in combination with dapsone, these new medications effectively trounced the leprosy bacilli and led the way to cure and – researchers hope – elimination by 2005. Wiser for the experience, scientists are holding back three alternative drugs in the event that resistance recurs. The only outstanding issue however is cost. Fortunately, a solution involving the private and public sectors working in tandem with corporate interests means patients need wait no longer. Blister packs containing multi-drug therapies are now being distributed to patients free of charge. Thanks to WHO-sponsored research grants, Nippon Foundation funds, and donations of medication from the Swiss pharmaceutical Novartis, leprosy is on the way out.

http://www.nyas.org/ebriefreps/main.asp?intSubsectionID=5103

"In the history of malaria disease, we lost all the single drugs by drug resistance."

and

For example, the best current treatments for malaria are clearly artemisinin-based combination therapies, or ACTs, which were develop in the early 1990s. These drugs exploit the effectiveness of artemisinin, to which resistance has not yet developed, but combine it with older antibiotics to sustain this effectiveness.

Now I know that there are evolutionists out there who have the ridiculous belief that variations in the weather like blizzards turn lizards into buzzards with gizzards and there are evolutionist mythematicians who believe that n+1 selection pressures cause a population to evolve more quickly than n selection pressures and this is good stuff for the SciFi channel but they simply do not have mathematical or empirical evidence of these ridiculous speculations. While on the other hand, we have posted and will continue to post the empirical evidence which substantiates the mathematics which show that combination selection pressures profoundly slow the mutation and selection sorting/optimization process.

 

[kleinman]

Annoying Creationists

You evolutionists continue to have difficulty understanding the mathematics of the mutation and selection sorting/optimization process. Let’s give a brief review how Dr Schneider (head of computational molecular biology at the National Cancer Institute) did his mathematical model and how accurately his mathematical model simulates the real behavior of the mutation and selection sorting/optimization process. Dr Schneider’s mathematical model is based on the following which is from his web site at http://www.lecb.ncifcrf.gov/~toms/paper/ev/evj/evj-guide.html :

Mutate each creature by changing its genome randomly. For example, the program might change the letter at position 82 from an A to a T. Mutation happens everywhere in the genome, both in the gene, in the binding sites, and in the spaces between. The location is random and the change is random.

Then

Evaluate each creature: count the number of mistakes each one makes.

This is the first step of selection.

Then

Sort the creatures by their mistakes.

This is the second step of selection.

then

Kill half of the creatures, the ones that make the most mistakes.

This is the final step of selection.

Then

Replicate (make another copy of) the creatures that make the least mistakes.

Then

The cycle is repeated every 'generation'.

Now, Dr Schneider has suggested the following in his publication on ev in Nucleic Acids Research http://nar.oxfordjournals.org/cgi/content/full/28/14/2794 .

Variations of the program could be used to investigate how population size, genome length, number of sites, size of recognition regions, mutation rate, selective pressure, overlapping sites and other factors affect the evolution. Another use of the program may include understanding the sources and effects of skewed genomic composition (4,7,30,31). However, this could be caused by mutation rates, and/or it could be the result of some kind(s) of evolutionary pressure that we don’t understand, so how one implements the skew may well affect or bias the results.

When you actually do the bookkeeping associated with the mutation and selection sorting/optimization process that Dr Schneider has mathematically modeled, it shows that increasing population sizes have only a small affect on the rate of information accumulation, increasing genome length markedly slow the rate of information accumulation, number of sites has only a minimal affect on the rate of information accumulation, mutation rate has an approximately linear affect on the rate of information accumulation (for realistic mutation rates) however, the number of selection pressures has a profound affect on the rate of information accumulation. A single selection condition can be sorted for very rapidly by Dr Schneider’s sorting algorithm while all three selection conditions can only be sorted for rapidly only on extremely tiny unrealistic length genomes. This mathematical behavior that Dr Schneider’s mathematical model demonstrates is reflected in reality as demonstrated by more of these real examples of the mutation and selection sorting/optimization process.
http://www.ctu.mrc.ac.uk/penta/abcpath.pdf

Abacavir (ABC) selects for four mutations (K65R, L74V, Y115F and M184V) in HIV-1 reverse transcriptase (RT), both in vitro and during monotherapy in vivo. The aim of this analysis was to compare the selection of these and other nucleoside reverse transcriptase inhibitor (NRTI)-associated mutations by ABC-containing therapies in the presence and absence of concurrent lamivudine (3TC) and/or zidovudine (ZDV) and to assess the effect of these mutations on phenotypic susceptibility to the NRTIs.

and

The results of this study demonstrate that ZDV is useful as a resistance modulator, at least in combination with ABC, effectively reducing the incidence of selection forK65R and L74V. This may increase the likelihood that agents such as ddI, TDF and others affected by these two mutations will remain efficacious in second-line regimens. The relevance of these findings to combinations including NRTIs other than ABC, 3TC and ZDV remains to be elucidated.

http://cancerres.aacrjournals.org/cgi/reprint/22/11_Part_1/1290.pdf

The possible application to chemotherapy of factors affecting the regulatory systems of cells has been considered. The extensive coordinate changes in intracellular enzyme concentrations which result from exposure to compounds interfering with the normal regulatory mechanisms suggest the possibility of combination therapy based upon the selective induction of quantitative changes in enzymatic activities. Such approaches would appear to be useful in circumventing two major problems of chemotherapy: finding sufficient metabolic differences between host and parasite to provide targets for selective drug toxicity, and preventing the eventual development of drug resistance.

It is concluded that a combination of two compounds affecting the same metabolic pathway, one producing feedback inhibition and the other effective through lethal synthesis, will show an enhanced differential toxicity greater than that from either drug alone. Similarly, pairs of compounds in which one member produces enzyme repression and the other is active through lethal synthesis should produce collateral sensitivity and thus prevent the development of drug-resistant populations.

The failure of evolutionists to understand and acknowledge this mathematical and empirical fact of life that combination selection pressures profoundly slow the mutation and selection sorting/optimization process contribute to the premature death of millions of people suffering from diseases subject to the mutation and selection phenomenon. This was sadly demonstrated by the many year delay in understanding that HIV requires combination therapy to slow the evolution of this virus despite the fact that this was known decades earlier. You evolutionists have blundered in your description of the mutation and selection sorting/optimization process because the basic science and mathematics of this process does not fit with your irrational and illogical world view.