Annoying creationists

[kleinman]

Annoying Creationists

How could I let the weekend go by without posting more mathematical data and empirical evidence which shows that the theory of evolution is both mathematically and empirically impossible?

Let’s summarize where our discussion on the theory of evolution stands. The spokesman for your theory makes the following two claims.

1. Inorganic chemicals cooperate to form life spontaneously. Now this happened billions of years ago because chemicals no longer cooperate these days. Why can’t these chemicals just get along these days and form life spontaneously again? We must not have enough energy around anymore. This spokesman has neither mathematical nor empirical evidence for this speculation.

2. The weather long ago transformed reptiles into birds. Can we put this concept into mathematical terms? Of course we can:

Lizards + Blizzards = Buzzards + Gizzards

Isn’t evolution a wizard? Now we don’t have weather anymore because lizards are still lizards and buzzards are still buzzards but someday, weather will return and blizzards will again turn lizards into buzzards with gizzards. An interesting speculation for the SciFi channel but no your spokesman has neither mathematical nor empirical evidence to back up this speculation either.

Enough of this illogical speculation of evolutionism and back to the mathematics of the mutation and selection sorting/optimization process and the empirical evidence which supports this mathematics. We have been looking at the peer reviewed and published mathematical model written by evolutionist Dr Tom Schneider and published in the evolutionist journal Nucleic Acids Research which mathematically models random point mutations and natural selection. This mathematical model maps out to an implicit multi-dimensional functional space given by the functional equation:

F(n,G,g,mr,nsp) = gfc

Where,

n = population size
G = genome length
g = number of sites
mr = mutation rate
nsp = number of selection pressures
gfc = generations for convergence.

We have been mapping out the 6-dimensional surface described by this functional equation by taking series of cuts along planes through this 6-dimensional surface and generating the data points which describes this surface. The first series we looked at were through the mr, gfc planes and we obtained the following points on the functional surface:

G=256, population=64, g=16, nsp=3:
mr|gfc to perfect creature
10^-7|95975841
10^-6|4278078
10^-5|1105535
10^-4|47279
10^-3|5029
1|662
2|572
3|12890
4|>1,000,000 did not converge

G=512, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|2412
2|1251
3|973
4|13251
5|22790
6|>1,000,000 did not converge

G=1024, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|18030
2|9701
3|4679
4|2991
5|1299
6|1979
7|3782
8|7254
9|16243
10|>1,000,000 did not converge

G=2048, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|42641
2|36817
3|11480
4|6049
5|10364
6|9708
7|3634
8|5382
9|5089
10|6170
11|9851
12|3952
13|10880
14|38738
15|6145
16|105799
17|259469
18|>1,000,000 did not converge

G=4096, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|163722
2|48755
3|57212
4|30316
5|19675
6|23306
7|17689
8|21947
9|13328
10|8935
11|16043
12|10225
13|17029
14|16052
15|17186
16|7715
17|14761
18|8772
19|12152
20|8806
21|7647
22|6724
23|4959
24|4096
25|13463
26|8325
27|8067
28|17877
29|46876
30|1000000 did not converge

These series of cases done in mr, gfc plane demonstrate a paraboloid shape to the surface. With lower mutation rates, the sorting process takes more generations, after all if the mutation rate was zero, there would be nothing to sort and if the mutation rate is too high, the genome is being scrambled too much and the sorting conditions can not be satisfied. What do you evolutionists think would happen to a population subjected to a mutagen like radiation or a chemical mutagen?

Now what happened when we varied g? We got the following data:

G=4096, population=64, mr=1 mutation per genome per generation, nsp=3:
g|gfc to perfect creature
2|140441
3|55585
4|52475
5|65441
6|26551
7|56496
8|79879
9|32391
10|59240
11|10684
12|53572
13|30162
14|35564
15|54498
16|42641
17|61064
18|54802
19|31806
20|45631
40|24544
80|28916
160|34389
200|28826

None of you evolutionists dared to offer an explanation of why gamma just seems to oscillate around without giving any particular direction to this variable. So here is the explanation why the curve behaves like this. g is the number of binding sites which are simply the portions of the genome where if the weight matrix does not find a match, it is counted as a mistake in the algorithm. Varying g simply changes whether a match of the weight matrix gives a mistake or does not give a mistake in that portion of the genome. Sorting must still be done based on the selection conditions at each locus in the genome, varying gamma only changes whether the conditions must match or not match the weight matrix at those particular portions of the genome.

Now then, how does population affect Dr Schneider’s model? Let’s start with Dr Schneider’s published case.

G=256, mr=1 mutation/genome-generation, g=16, nsp=3:
n|gfc to perfect creature
64|662
128|741
256|569
512|492
1024|451
2048|296
4096|167
8192|154
16384|162
32768|186

Wait a minute; I thought you evolutionists said that increasing population accelerates evolution? What’s happening here? Dr Schneider’s model is showing that increasing population accelerates evolution slightly but then the curve flattens out? How could this be? Is Dr Schneider’s mathematics wrong? Let’s try Dr Schneider’s model with a mutation rate of mr=1 mutation per million bases per generation

G=256, mr=1 mutation/million bases-generation, g=16, nsp=3:
n|gfc to perfect creature
64|4278078
128|2587709
256|5968438
512|4429939
1024|4510187
2048|1638610
4096|685196
8192|694504
16384|917748
32768|380032

Anyone want to make a guess how large the lizard population was that you assert transformed into a bird population by mutation and selection?

Next week we’ll look at this further. While you are waiting for the next episode in the story of the mutation and selection sorting/optimization process, here are some more empirical examples of how mutation and selection actually works.

http://www.malariaandhealth.com/professional/abstracts.htm

The aim of this workshop was to issue updated practical recommendations for the rational use of the QingHaoSu (QHS) derivatives, (i.e. medicines really in use and not molecules still under development). 54 malariologists and other experts from Europe, Africa, Latin America and Asia were invited, from research centers, universities, national administrations, military research centers or hospitals, pharmaceutical companies, NGOs, etc., together with WHO and international agency observers. Thanks to working papers including the most recent available data, and particularly the Cochrane Center meta-analysis of clinical trials, several practical conclusions were agreed on by the participants (they are views of individuals and do not represent the opinions or recommendations of any official body or agency):

(1) In adults and children QHS derivatives are the most rapidly acting antimalarials against falciparum malaria, including multidrug resistant strains; (2) There has been no resistance identified so far, but this should not cause complacency in the use of QHS; (3) All the investigated QHS drugs have shown comparable efficacy. There is a serious practical risk associated with the appearance of substandard and inadequately labelled preparations on the international market; (4) QHS derivatives are well tolerated and there is no evidence so far of serious clinical toxicity in man. The neurotoxicity seen in animals after high doses of certain compounds has not been reported in man; (5) Whenever possible, these drugs should be used in combination with a second, longer-acting antimalarial to avoid or limit the risk of resistance; (6) QHS should not be used for chemoprophylaxis. It was agreed that for use in severe malaria IM artemether and probably IV or IM artesunate are at least as effective as quinine; rectal formulations of these drugs require further studies but seem very promising. Use in uncomplicated malaria or during pregnancy, pharmacokinetics, activity and tolerability, were also considered in detail.

The final conclusions were focused on GMP standards of quality, efficacy and safety and, in addition to their application to QHS derivatives and other antimalarials, they should be more generally employed to control all drugs used in Tropical Medicine.

And

Chlorproguanil-dapsone (Lapdap) is a novel antifolate combination which offers the potential for affordable treatment for Fansidar™-resistant falciparum malaria in Africa, and reduced selective pressure for drug resistance.

Laboratory work, which has underpinned the development of Lapdap, started in Kenya in the early 1980s. Chlorcycloguanil [CCG], the active metabolite of chlorproguanil [CPG], was shown to have high activity against both pyrimethamine-sensitive and -resistant parasites, and to act synergistically in combination with sulfonamides and sulphones. A pilot study of Lapdap at two sites in Kenya showed that parasitaemia was cleared by a single dose, although recrudescence was common. In 1987-88, the relationship between selective pressure for parasite resistance and elimination half-life was demonstrated at Kilifi, which established the potential advantage of a short half-life combination like Lapdap, and this was further supported by a comparison of the in vitro therapeutic indices of the available antifolate combination treatments, undertaken in Liverpool and Kenya in 1992. Current investigations aim to define the relationship between drug pharmacokinetics and susceptibility to antifolate action, of parasites with particular dhps and dhfr genotypes, and to define resistance to this class of drug at the molecular level.

To date, clinical trial work on Lapdap has been undertaken with scientific, rather than regulatory, aims in mind. The completed Kilifi trial compared Lapdap with pyrimethamine-sulfadoxine [PM/SD] in symptomatic childhood falciparum malaria. The trial studied both a single dose of Lapdap [1.2 mg kg-l and 2.4 mg kg-l of CPG and DDS respectively] and three doses at 24 hour intervals. A community control group was recruited to estimate the monthly incidence of new parasitaemia. Initial clinical response to Lapdap [both regimens] and PM/SD was similar. However, in comparison with the control group the relative risk of new parasitaemia was 2.10 [95%CI 1.66 to 2.65] after one dose of Lapdap, 1.31 [0.99, 1.73] after three doses and 0.63 [0.43, 0.93] after one dose of PM/SD. We interpret this trial to show that (a) one dose of this potent, but rapidly-eliminated, combination is inadequate, (b) three doses of Lapdap give an adequate response and (c) PM/SD provides a period of chemoprophylaxis with the disadvantage of high selection pressure for resistance. Pharmacokinetic work [done in parallel with this trial] suggested that, while the dose of DDS [2.4 mg kg- 1 daily] was probably satisfactory, the dose of CPG [1.2 mg kg- 1 daily] may have been too low, and rising dose tolerance studies subsequently established that a CPO dose of 2.0 mg kg-l was tolerable. Ongoing clinical trial work in Kenya, Malawi and Tanzania [using 2.0 and 2.5 mg kg-1 of CPG and DDS respectively, daily for 3 days] will study (a) whether the lack of chemoprophylaxis after Lapdap confers disadvantage to the individual patient in comparison with PM/SD, and (b) whether Lapdap is as effective a salvage therapy in patients with "PM/SD-failure", as in-vitro data would predict.

And

Antimalarial drug development depends on the clear recognition of the importance of the differential susceptibility both of different stages and species of Plasmodium to drugs and the genetic versatility of these protozoa. Unlike most antimicrobial agents, antimalarial drugs may be targeted against different life cycle stages. Most compounds have a limited range of stages against which they are effective. In antibacterial chemotherapy, especially against chronic infections such as tuberculosis, it has long been accepted that polytherapy is essential in order either to overcome or restrict the emergence of drug-resistant organisms. This principle, in spite of many warnings, has only just started to gain acceptance in the antimalarial field. Antimalarial combinations may (1) target different life cycle stages, (2) reinforce drug action against specific metabolic pathways, (3) block the emergence of genetic variants or (4) reverse the pharmacological sequelae resulting from the selection of drug-resistant mutants. The first principle which was originally proposed by Guttman and Ehrlich in 1891 has recently been resurrected with the use of the artemisinin family against drug-resistant falciparum malaria and is currently a novel focus of attention by WHO. It is also of major importance in the prevention and treatment of chloroquine-resistant P. vivax by, for example, etaquine. The second principle became of significance after Hurly showed in 1959 that pyrimethamine and sulphadiazine potentiate each other's action against P. falciparum. It is currently being pursued by such trials as that of dapsone plus chlorproguanil. The third principle is exemplified by laboratory studies of combinations containing novel endoperoxides and clinical trials of benflumetol with artemether. The fourth principle, which is of wide application in cancer chemotherapy, may shortly provide rational new ways to treat patients infected with multidrug-resistant parasites. The consistent reluctance of physicians and health authorities to deploy rationally designed antimalarial drug combinations must be abandoned.

And

Co-artemether is a fixed combination antimalarial containing the artemisinin derivative artemether and the aryl amino alcohol benflumetol (lumefantrine). The combination exploits the rapid actions of the artemisinins and the more prolonged actions of benflumetol. Artemether exerts its antimalarial actions via the generation of reactive free radical species within the parasite's digestive food vacuole. These species are produced by the iron-dependent catalytic breakdown of the unusual peroxide bridge in this molecule. Benflumetol shares structural and physicochemical characteristics with other so called '"Class II blood schizontocides" such as mefloquine. As such, it is assumed that these drugs interact with some component of the haemoglobin degradation pathway characteristic of intra-erythrocytic parasites. The central importance of this pathway to benflumetol action has been established using a specific inhibitor of the initial haemoglobin cleavage event. The use of the combination has additional advantages in that the drugs have been shown to interact synergistically both in vitro against P. falciparum and in vivo against P. berghei and the use of drug combinations should reduce the rate of resistance development. The artemisinins are rapidly eliminated in man with elimination half-lives in the order of hours, whereas benflumetol shows variable bioavailability and a long elimination half-life. These pharmacokinetic differences between the two drugs will limit the importance of the synergy between the two drugs and may have an influence on the rate of resistance development.

And

Benflumetol (lumefantrine) and artemether are two new antimalarials developed in China. Both have good therapeutic effects against chloroquine-resistant Falciparum malaria. Benflumetol is a fluoremethanol, and is an active schizonticidal drug. It is formulated for oral administration as a solution in linoleic acid in the form of capsules. In China it has cure rates of above 95% against P. falciparum infections, but its onset of action is slow. It has low toxicity. Artemether is a derivative of artemisinin. It is characterised by its rapid onset of schizonticidal action, but has a relatively high rate of recrudescence.

A combination of the two drugs was developed in China in order to maintain their strong points while averting their shortcomings. This combination of artemether and benflumetol is synergistic. The synergistic indices were more than 5 and 6, calculated from ED50 and ED90 respectively, when tested against P. berghei in mice. The combination delayed the emergence of drug resistance and reduced the resistance level.

A regimen for clinical use was established. A fixed combination tablet comprising one part of artemether (20 mg) and six parts of benflumetol (120 mg) is in use. Four doses of four tablets taken at 0, 8, 24 and 48 hours had a satisfactory effect in patients with Falciparum malaria infections.

The treatment combines the benefits of both drugs, with a relatively short therapeutic course, rapid onset of action and high cure rate. It has low toxicity and is a well-tolerated drug for the treatment of malarial infections.

And

Antimalarial drug resistance is increasing throughout the tropical world. In some parts of Southeast Asia and South America there is complete resistance of P. falciparum to chloroquine and the combination of sulphadoxine-pyrimethamine. There is also partial resistance to quinine and mefloquine in some areas. Resistance to artemisinin and its derivatives has not been reported, although when used alone, these compounds are associated with high recrudescence rates, particularly if used in courses of less than 5 days. In 1994, the combination of mefloquine plus artesunate was introduced on the western border of Thailand and since then it has retained excellent efficacy. In vitro tests have confirmed that there has been no further decline in P. falciparum sensitivity to mefloquine.

Drug resistance arises as a result of genetic mutation(s), which are selected under drug pressure and then transmitted from one host to another. Combining unrelated drugs reduces the chance that a resistant mutant will be selected by (i.e. survive) drug treatment. The artemisinin derivatives are the most active antimalarials available and will reduce the infecting parasite biomass by 10,000-fold each cycle (2 days).

There is evidence from laboratory and field studies that the rate of gametocyte carriage increases with declining antimalarial efficacy. A recrudescent (i.e. resistant) infection is more likely to present with patent gametocytaemia, and as a consequence more drug-resistant strains are more likely to be transmitted. The artemisinin derivatives markedly reduce gametocyte carriage. Combination treatment regimens that include artemisinin derivatives reduce the emergence of resistance, the transmission, and thus the spread of, drug-resistant strains of P. falciparum.

The empirical evidence is clear and in the coming weeks, the mathematical evidence will become clear to you as well as we continue to investigate the mathematical behavior of Dr Schneider’s peer reviewed and published mathematical model of random point mutations and natural selection which show that combination selection pressures profoundly slow the mutation and selection sorting/optimization process.

Dr Schneider, I continue to support your model and the results it gives despite the fact that your fellow evolutionists continue to discredit your model. Dr Schneider, your model shows mathematically what has been observe empirically about the mutation and selection sorting/optimization process for more than 50 years.

Hopefully we can avert another generation from being confused on how this process works and it will not take 5 years to figure out that combination therapy should be used for diseases like HIV and other diseases subject to the mutation and selection sorting/optimization process and that we can prevent evolutionists from propagating the erroneous, illogical and irrational teaching of how the mutation and selection process works and their contribution to the premature death of millions of people with diseases subject to mutation and selection. All you evolutionists need to do is use some 21st century mathematics to bring your 19th century theory up to date. Of course when you do that, you would realize that it is mathematically impossible to transform a lizard into a bird by the mutation and selection sorting/optimization process no matter what the weather is like.

You all have a good weekend pondering these facts of how the mutation and selection sorting/optimization process actually works.

 

[Belz...]

Have you spoken about this obsession of yours to your local psychologist, Kleinman ? I'm sure he'd be very interested.

This is getting a little cheesy. Let's keep the armchair psychoanalysis to a minimum.

Replying to this modbox in thread will be off topic  Posted By: Paul C. Anagnostopoulos

 

[kjkent1]

How could I let the weekend go by without posting more mathematical data and empirical evidence which shows that the theory of evolution is both mathematically and empirically impossible?

Well, for starters, you could actually post some evidence supporting your position.

What would life be without at least a daily dose of kleinmania?

 

[m_huber]

Alan, the human body is not the best environment to model evolution. But if that is what you choose, then at least look at what the good doctors are trying to do. They are adding something to the environment that would not otherwise be there in an attempt to slow the evolution of an organism. Without an intelligent design, evolution runs rampant. Only when an intelligence acts on the system does it completely (and quite unnaturally) stabilize.

Even if lack of evolution was a reasonable conclusion to reach from the data that you have been looking at, it does not speak at all about organisms larger than bacteria (and perhaps not even that large). Life behaves somewhat differently on different scales. If you show evolution not to work in a specific case on a micro scale, you have not defeated evolution.

 

[Dr Adequate]

How could I let the weekend go by without posting more mathematical data and empirical evidence which shows that the theory of evolution is both mathematically and empirically impossible?

Let’s summarize where our discussion on the theory of evolution stands. The spokesman for your theory makes the following two claims.

1. Inorganic chemicals cooperate to form life spontaneously. Now this happened billions of years ago because chemicals no longer cooperate these days. Why can’t these chemicals just get along these days and form life spontaneously again? We must not have enough energy around anymore. This spokesman has neither mathematical nor empirical evidence for this speculation.

2. The weather long ago transformed reptiles into birds. Can we put this concept into mathematical terms? Of course we can:

Lizards + Blizzards = Buzzards + Gizzards

Isn’t evolution a wizard? Now we don’t have weather anymore because lizards are still lizards and buzzards are still buzzards but someday, weather will return and blizzards will again turn lizards into buzzards with gizzards. An interesting speculation for the SciFi channel but no your spokesman has neither mathematical nor empirical evidence to back up this speculation either.

Enough of this illogical speculation of evolutionism and back to the mathematics of the mutation and selection sorting/optimization process and the empirical evidence which supports this mathematics. We have been looking at the peer reviewed and published mathematical model written by evolutionist Dr Tom Schneider and published in the evolutionist journal Nucleic Acids Research which mathematically models random point mutations and natural selection. This mathematical model maps out to an implicit multi-dimensional functional space given by the functional equation:

F(n,G,g,mr,nsp) = gfc

Where,

n = population size
G = genome length
g = number of sites
mr = mutation rate
nsp = number of selection pressures
gfc = generations for convergence.

We have been mapping out the 6-dimensional surface described by this functional equation by taking series of cuts along planes through this 6-dimensional surface and generating the data points which describes this surface. The first series we looked at were through the mr, gfc planes and we obtained the following points on the functional surface:

G=256, population=64, g=16, nsp=3:
mr|gfc to perfect creature
10^-7|95975841
10^-6|4278078
10^-5|1105535
10^-4|47279
10^-3|5029
1|662
2|572
3|12890
4|>1,000,000 did not converge

G=512, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|2412
2|1251
3|973
4|13251
5|22790
6|>1,000,000 did not converge

G=1024, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|18030
2|9701
3|4679
4|2991
5|1299
6|1979
7|3782
8|7254
9|16243
10|>1,000,000 did not converge

G=2048, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|42641
2|36817
3|11480
4|6049
5|10364
6|9708
7|3634
8|5382
9|5089
10|6170
11|9851
12|3952
13|10880
14|38738
15|6145
16|105799
17|259469
18|>1,000,000 did not converge

G=4096, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|163722
2|48755
3|57212
4|30316
5|19675
6|23306
7|17689
8|21947
9|13328
10|8935
11|16043
12|10225
13|17029
14|16052
15|17186
16|7715
17|14761
18|8772
19|12152
20|8806
21|7647
22|6724
23|4959
24|4096
25|13463
26|8325
27|8067
28|17877
29|46876
30|1000000 did not converge

These series of cases done in mr, gfc plane demonstrate a paraboloid shape to the surface. With lower mutation rates, the sorting process takes more generations, after all if the mutation rate was zero, there would be nothing to sort and if the mutation rate is too high, the genome is being scrambled too much and the sorting conditions can not be satisfied. What do you evolutionists think would happen to a population subjected to a mutagen like radiation or a chemical mutagen?

Now what happened when we varied g? We got the following data:

G=4096, population=64, mr=1 mutation per genome per generation, nsp=3:
g|gfc to perfect creature
2|140441
3|55585
4|52475
5|65441
6|26551
7|56496
8|79879
9|32391
10|59240
11|10684
12|53572
13|30162
14|35564
15|54498
16|42641
17|61064
18|54802
19|31806
20|45631
40|24544
80|28916
160|34389
200|28826

None of you evolutionists dared to offer an explanation of why gamma just seems to oscillate around without giving any particular direction to this variable. So here is the explanation why the curve behaves like this. g is the number of binding sites which are simply the portions of the genome where if the weight matrix does not find a match, it is counted as a mistake in the algorithm. Varying g simply changes whether a match of the weight matrix gives a mistake or does not give a mistake in that portion of the genome. Sorting must still be done based on the selection conditions at each locus in the genome, varying gamma only changes whether the conditions must match or not match the weight matrix at those particular portions of the genome.

Now then, how does population affect Dr Schneider’s model? Let’s start with Dr Schneider’s published case.

G=256, mr=1 mutation/genome-generation, g=16, nsp=3:
n|gfc to perfect creature
64|662
128|741
256|569
512|492
1024|451
2048|296
4096|167
8192|154
16384|162
32768|186

Wait a minute; I thought you evolutionists said that increasing population accelerates evolution? What’s happening here? Dr Schneider’s model is showing that increasing population accelerates evolution slightly but then the curve flattens out? How could this be? Is Dr Schneider’s mathematics wrong? Let’s try Dr Schneider’s model with a mutation rate of mr=1 mutation per million bases per generation

G=256, mr=1 mutation/million bases-generation, g=16, nsp=3:
n|gfc to perfect creature
64|4278078
128|2587709
256|5968438
512|4429939
1024|4510187
2048|1638610
4096|685196
8192|694504
16384|917748
32768|380032

Anyone want to make a guess how large the lizard population was that you assert transformed into a bird population by mutation and selection?

Next week we’ll look at this further. While you are waiting for the next episode in the story of the mutation and selection sorting/optimization process, here are some more empirical examples of how mutation and selection actually works.

http://www.malariaandhealth.com/professional/abstracts.htm

And

And

And

And

And

The empirical evidence is clear and in the coming weeks, the mathematical evidence will become clear to you as well as we continue to investigate the mathematical behavior of Dr Schneider’s peer reviewed and published mathematical model of random point mutations and natural selection which show that combination selection pressures profoundly slow the mutation and selection sorting/optimization process.

Dr Schneider, I continue to support your model and the results it gives despite the fact that your fellow evolutionists continue to discredit your model. Dr Schneider, your model shows mathematically what has been observe empirically about the mutation and selection sorting/optimization process for more than 50 years.

Hopefully we can avert another generation from being confused on how this process works and it will not take 5 years to figure out that combination therapy should be used for diseases like HIV and other diseases subject to the mutation and selection sorting/optimization process and that we can prevent evolutionists from propagating the erroneous, illogical and irrational teaching of how the mutation and selection process works and their contribution to the premature death of millions of people with diseases subject to mutation and selection. All you evolutionists need to do is use some 21st century mathematics to bring your 19th century theory up to date. Of course when you do that, you would realize that it is mathematically impossible to transform a lizard into a bird by the mutation and selection sorting/optimization process no matter what the weather is like.

You all have a good weekend pondering these facts of how the mutation and selection sorting/optimization process actually works.

So ... you're still posting the same old crap?

I notice that you still haven't succeeded in deceiving anyone.

Have you noticed that?

 

[jimbob]

This cross forum post from Ambrielle at badscience could go here for some light relief:

There are two websites I check every day: Bad Science Forums and fstdt.com. Says it all really.
That first quote is probably my favourite, along with:

One of the most basic laws in the universe is the Second Law of Thermodynamics. This states that as time goes by, entropy in an environment will increase. Evolution argues differently against a law that is accepted EVERYWHERE BY EVERYONE. Evolution says that we started out simple, and over time became more complex. That just isn't possible: UNLESS there is a giant outside source of energy supplying the Earth with huge amounts of energy. If there were such a source, scientists would certainly know about it. [emphasis added]

Although this one has the advantage of being pithy:

I can sum it all up in three words: Evolution is a lie

 

[Zeuzzz]

One of the most basic laws in the universe is the Second Law of Thermodynamics. This states that as time goes by, entropy in an environment will increase.

Correct.

Evolution argues differently against a law that is accepted EVERYWHERE BY EVERYONE. Evolution says that we started out simple, and over time became more complex.

Correct. The effects of intention and consious thought can change the law of entropy, see Maxwell's demon. http://en.wikipedia.org/wiki/Maxwell's_demon

In other words, Maxwell imagines two containers, A and B. The containers are filled with the same gas at equal temperatures and placed next to each other. Observing the molecules on both sides, a little "demon" guards a trapdoor between the two containers. When a faster-than-average molecule from A flies towards the trapdoor, the demon opens it, and the molecule will fly from A to B. The average speed of the molecules in B will have increased while in A they will have slowed down on average. However, since average molecular speed corresponds to temperature, the temperature will have decreased in A and increased in B; this is contrary to the second law of thermodynamics.

That is just about the only time you will ever see that law broken, when conscious thought is input on a system to intentionally change it. Infact a lot of people define life as the reverse of entropy.

That just isn't possible: UNLESS there is a giant outside source of energy supplying the Earth with huge amounts of energy. If there were such a source, scientists would certainly know about it. [emphasis added]

Incorrect, and quite frankly, obsurd.

I can sum it all up in three words: Evolution is a lie

well, if thats true, you shoudn't exist then. I love self debunking crackpots

 

[jimbob]

Quote:
That just isn't possible: UNLESS there is a giant outside source of energy supplying the Earth with huge amounts of energy. If there were such a source, scientists would certainly know about it. [emphasis added]

Incorrect, and quite frankly, obsurd.

Quote:
I can sum it all up in three words: Evolution is a lie

well, if thats true, you shoudn't exist then. I love self debunking crackpots

er Zeuzzz...

FSDT.com, and Ambrielle were pointing out that the Sun is a "giant outside source of energy", a source of which, is needed for local entropy to decrease, though global entropy has to increase. If local entropy couldn't decrease, then fridges wouldn't work.

Ambrielle was also noting how many words there were in the phrase "evolution is a lie"

 

[Zeuzzz]

er Zeuzzz...

FSDT.com, and Ambrielle were pointing out that the Sun is a "giant outside source of energy", a source of which, is needed for local entropy to decrease, though global entropy has to increase. If local entropy couldn't decrease, then fridges wouldn't work.

Ambrielle was also noting how many words there were in the phrase "evolution is a lie"

Ah. Whoops.

Pardon me, I haven't had my weetabix yet today.

 

[jimbob]

Ah. Whoops.

Pardon me, I haven't had my weetabix yet today.

No dammit, this is the annoying creationists thread, it makes the train wrecks I have been more active in, seem exemplars of rationality and civility*. ;-)

Ah well...


* I don't tend to hang out on the CT subforum...

 

[Paul C. Anagnostopoulos]

Correct. The effects of intention and consious thought can change the law of entropy, see Maxwell's demon.

What does that have to do with evolution?

~~ Paul

 

[Dr Adequate]

Correct. The effects of intention and consious thought can change the law of entropy ...

No they can't.

 

[jimbob]

Originally Posted by Zeuzzz
Correct. The effects of intention and consious thought can change the law of

entropy ...
No they can't.

My favourite answer to the original statment by creationists is that local entropy can decrease in a fridge. But global entropy can only increase.

Local entropy can be only lowered by increasing global entropy.

I do wonder if the original quoted by FSDT was actually a parody...

"UNLESS there is a giant outside source of energy supplying the Earth with huge amounts of energy. If there were such a source, scientists would certainly know about it."

It almost seems too stupid even for a ctreationist...

 

[m_huber]

It almost seems too stupid even for a creationist...

Nah.

Seriously, we talk about creationists being stupid, but they are really better described as "deluded." They think they have reality figured out, and when someone points out that facts disagree with their view of reality, it puts them in a position of having to either dismiss their old version of reality or their new version of reality. The ones who come here generally have their minds made up already, and they reject any new version of reality, but there are many who are riding the fence, and just need to see evidence. It is instructive to those people to point out the lengths that creationists have to go to support their positions (such as arguing that the sun doesn't exist).

 

[Belz...]

Correct. The effects of intention and consious thought can change the law of entropy, see Maxwell's demon.

Nuh-huh.

 

[jimbob]

In case anyone was wondering: Here ie the thead where I got this quote from.

There are some gems...

 

[kleinman]

Annoying Creationists

Any of you evolutionists figure out how the mutation and selection sorting/optimization process works either mathematically or empirically? Of course not, because if you had, you would understand why five years of monotherapy was wasted on the treatment of HIV introducing huge numbers of resistant viruses into the gene pool despite a Nobel Laureate speech thirty years previous explained exactly what was needed and how years of sequential use of monotherapies produced MRSA, multidrug resistant gonorrhea and numerous other multidrug resistant microbes. You evolutionists have done an incredibly poor job of describing how the mutation and selection sorting/optimization process actually works and this has and will continue to contribute to the premature deaths of millions of people with diseases subject to the principles of mutation and selection. But I must admit, you have done an incredibly good job destroying the field of biology. So let’s see if we can reverse some of the massive damage you have done with your irrational and illogical speculations that have no place in the study of science.

We have been looking at the analytical geometric surface generated by the functional equation:

F(n,G,g,mr,nsp) = gfc

Where,

n = population size
G = genome length
g = number of sites
mr = mutation rate
nsp = number of selection pressures
gfc = generations for convergence.

And we have been examining the shape of this surface in the n, gfc plane. We have the following data so far:

G=256, mr=1 mutation/genome-generation, g=16, nsp=3:
n|gfc to perfect creature
64|662
128|741
256|569
512|492
1024|451
2048|296
4096|167
8192|154
16384|162
32768|186

And

G=256, mr=1 mutation/million bases-generation, g=16, nsp=3:
n|gfc to perfect creature
64|4278078
128|2587709
256|5968438
512|4429939
1024|4510187
2048|1638610
4096|685196
8192|694504
16384|917748
32768|380032

These cases do not show a rapid drop in the gfc. Let’s examine another series of case:

G=512, mr=1 mutation/genome-generation, g=16, nsp=3:
n|gfc to perfect creature
64|2412
128|1863
256|1836
512|1300
1024|1022
2048|632
4096|694
8192|610
16384|534

G=1024, mr=1 mutation/genome-generation, g=16, nsp=3:
n|gfc to perfect creature
64|18030
128|4446
256|4000
512|3896
1024|2710
2048|1793
4096|1140
8192|1182

G=1000, mr=1 mutation per 1000 bases per generation, g=16, nsp=3:
n|gfc to perfect creature
2 | failed to converge
4 | 66547
8 | 15916
16 | 17257
32 | 16416
64 | 9082
128 | 9378
256 | 4078
512 | 3685
1024 | 2793
2048 | 2080
4096 | 2565
6000 | 1541
8192 | 1798
16384 | 1001
32768 | 743
65536 | 633
131072 | 483
262144 | 702
524288 | 642
1048576 | 438

It is clear that large populations do not have a huge affect on the generations for convergence. This is one of the many speculations evolutionists assert for your mathematically illogical and irrational theory. Any of you evolutionists want to explain why continually doubling populations does not continually halve the generations for convergence?

Next, we will look at the affect of G, the genome length on the gfc. Any of you evolutionists want to speculate how this will affect the mutation and selection sorting/optimization process? While you are pondering this, here are some more empirical examples of how the mutation and selection sorting/optimization process actually works.

http://aidsinfo.nih.gov/contentfiles/AdultandAdolescentGL.pdf

Simultaneously stopping all drugs in a regimen containing these agents may result in functional monotherapy with the NNRTIs, because their half-lives are longer than other agents. This may increase the risk of selection of NNRTI-resistant mutations.

http://en.wikipedia.org/wiki/Pesticide

Tankmixing pesticides is the combination of two or more pesticides with different modes of action. This practice may improve individual pesticide application results in addition to the benefit of delaying the onset of or mitigating existing pest resistance.

http://www.weeds.iastate.edu/mgmt/2004/combination.shtml

The evolution of herbicide resistance within a weed population is based on selection pressure. The more frequently a herbicide is used, the more pressure placed on a weed population, and the sooner resistance will appear at a troublesome level in the population. Using alternative modes of action can reduce the potential for selecting resistant weeds by placing different selection pressures on weed populations. In a system relying only on glyphosate, a weed possessing a trait allowing it to survive glyphosate will rapidly increase in frequency. But if a second herbicide is used with glyphosate, this alternative herbicide may kill the weed with the glyphosate resistant trait and prevent it from increasing within the weed population. Theoretically this approach is sound and can reduce the potential for herbicide resistance.

http://72.14.253.104/search?q=cache:rHo5amSD9IAJ:digitalcommons.unl.edu/cgi/viewcontent.cgi%3Farticle%3D1047%26context%3Dvpc16+combination+rodenticide+resistance&hl=en&ct=clnk&cd=4&gl=us

Coumatetralyl (Racumin ) has been known since 1957 as a multiple dose anticoagulant and has been used successfully over many decades. In the seventies and especially the eighties, rats developed an increased resistance to anticoagulants in certain regions of Central Europe. Also, the addition of vitamin K to animal feed (especially to chicken feed) has reduced the efficacy against rats and mice in farm buildings. Combinations of anticoagulants with different types of vitamin D are generally described to increase the efficacy of action against rodents. It was found that especially the combination of coumatetralyl with cholecalciferol (vitamin D3) could overcome the above mentioned problems. Cholecalciferol causes hypercalcemia and, therefore, has a different mode of action compared to anticoagulants. The combination of these active ingredients leads to an obvious increase in efficacy against rodents, even under difficult conditions. The formulation with optimal rodenticidal efficacy contains 0.04 % coumatetralyl and 0.025 % cholecalciferol mixed in rolled oats.

How can this be? I thought you evolutionists said that increasing the number of selection pressures accelerates evolution. Something just doesn’t add up in your theory. We’ll continue studying the mathematics of ev and find out what it is. Of course, if you evolutionists want to give us an example of multiple selection pressures accelerating the mutation and selection sorting/optimization process, that would be interesting, but as one of you evolutionists has said that experiment just hasn’t been done. How many decades will it take for you evolutionists to figure out that mutationandselectiondidn’tdoit?

 

[kjkent1]

How can this be? I thought you evolutionists said that increasing the number of selection pressures accelerates evolution. Something just doesn’t add up in your theory. We’ll continue studying the mathematics of ev and find out what it is. Of course, if you evolutionists want to give us an example of multiple selection pressures accelerating the mutation and selection sorting/optimization process, that would be interesting, but as one of you evolutionists has said that experiment just hasn’t been done. How many decades will it take for you evolutionists to figure out that mutationandselectiondidn’tdoit?

First, kleinman sets up a strawman: evolutionists say that increasing the number of selection pressures accelerates evolution. I don't believe anyone who understands evolution will flatly claim that an organism beseiged by combinations of toxins will easily survive so as to have the opportunity to reproduce and evolve. So, kleinman's strawmen and his empirical examples are not an attempt to model anything close to the natural conditions under which organisms evolve. Instead, kleinman presents the scenario of: what happens when you conduct an intellitgent extermination of a species?

Answer: it dies.

Brilliant conclusion, kleinamn...brilliant.

What is somewhat more interesting, however, is that there are peer-reviewed studies showing that DESPITE the hostility of an all out toxic attact on an organism, the organism can sometimes manage to evolve so as to escape the intelligently designed deathtrap. This shows just how vital the process of evoluion really is.

In sum, we begin another week of watching repeated kleinman self immolations. It's a great spectacle, the first few times it's observed. But, then, it gets sooooooooooo booooooooooriiiiiiiiiiig.

Everybody...yawn.

 

[m_huber]

Any of you evolutionists figure out how the mutation and selection sorting/optimization process works either mathematically or empirically? Of course not, because if you had, you would understand why five years of monotherapy was wasted on the treatment of HIV introducing huge numbers of resistant viruses into the gene pool despite a Nobel Laureate speech thirty years previous explained exactly what was needed and how years of sequential use of monotherapies produced MRSA, multidrug resistant gonorrhea and numerous other multidrug resistant microbes.

Alan, you do realize that you are citing numerous examples of evolution taking place, don't you?

Before the State of the Union address tonight, I saw the Simpson's episode where Lisa opposes Creation Science in the classroom. What a great show. Too bad they didn't use hyperbole.

 

[Myriad]

In sum, we begin another week of watching repeated kleinman self immolations. It's a great spectacle, the first few times it's observed. But, then, it gets sooooooooooo booooooooooriiiiiiiiiiig.

Yes, but now there's a difference.

Last week, he was suspended, and came back after three days.

So now, he has a lot more in common with Jesus.

Respectfully,
Myriad