The actual strength of Darwin’s theory (sic)

[Glenn]

"Coyne is quite the prominent evolutionary biologist, and has been antagonistic to intelligent design arguments for decades. If Darwin’s theory were actually the powerful idea it’s claimed to be, Coyne should have been able to counter design easily, simply by summarizing its arguments and showing how Darwin deals with them. Yet he can’t even bring himself to mention what those arguments are. Instead he tries to whip up hysteria against a book that argues for what most people already believe. That speaks volumes about the actual strength of Darwin’s theory."

https://evolutionnews.org/2019/03/bullet-points-for-jerry-coyne/

Reminds me of scientist's climate hysteria. Hmm. Would the credibility of science and scientists be on topic in a discussion of origins?

[Alan Kleinman MD PhD]

Glenn, this isn't the crowd that will discuss Darwinian evolution. First, they don't understand the subject other than to claim that it turns reptiles into birds and second, they don't understand how to do the mathematics of the different components of Darwinian evolution. Where you and I differ on this subject is that I think it ought to be taught in school but taught correctly because Darwinian evolution is the mechanism that causes drug resistance and cancer treatments to fail. Once the student understands correctly how Darwinian evolution works, it will be clear why the ToE is mathematically irrational.

[Glenn]

I don't know what led you to think I don't want evolutionary theory to be taught. And frankly, I am disappointed to hear you make such a claim.

[Alan Kleinman MD PhD]

It was a post you made a few days ago. I got a sense that you thought that Darwinism equated with the ToE. I posted a quote from Darwin's book which gave the essential concepts of Darwinism, the struggle for existence and adaptation. If you want to understand how drug resistance occurs or why cancer treatments fail, you need to correctly describe and quantitate these concepts. The problem is that biologists don't do this. Instead, they grossly over-extrapolate these concepts. So how would you want to see evolution taught?

[Glenn]

Although I don't equate Darwinism with the ToE, there are certain parallels. Not sure what you regard the ToE to be, but evolution has different connotations.
But basically, I am skeptical of about everything, including random mutation and natural selection to account for what we see today. You say you want it taught "correctly"; others say the same. As for me, I would rather students were allowed to make their own decisions after being shown all the "correct" stories.

[Alan Kleinman MD PhD]

On Tuesday, March 12, 2019 at 4:55:03 PM UTC-7, Glenn wrote:
> On Tuesday, March 12, 2019 at 4:30:02 PM UTC-7, Alan Kleinman MD PhD wrote:
> > On Tuesday, March 12, 2019 at 4:05:02 PM UTC-7, Glenn wrote:
> > > On Tuesday, March 12, 2019 at 3:20:03 PM UTC-7, Alan Kleinman MD PhD wrote:
> > > > On Tuesday, March 12, 2019 at 1:40:03 PM UTC-7, Glenn wrote:
> > > > > "Coyne is quite the prominent evolutionary biologist, and has been antagonistic to intelligent design arguments for decades. If Darwin’s theory were actually the powerful idea it’s claimed to be, Coyne should have been able to counter design easily, simply by summarizing its arguments and showing how Darwin deals with them. Yet he can’t even bring himself to mention what those arguments are. Instead he tries to whip up hysteria against a book that argues for what most people already believe. That speaks volumes about the actual strength of Darwin’s theory."
> > > > >
> > > > > https://evolutionnews.org/2019/03/bullet-points-for-jerry-coyne/
> > > > >
> > > > > Reminds me of scientist's climate hysteria. Hmm. Would the credibility of science and scientists be on topic in a discussion of origins?
> > > >
> > > > Glenn, this isn't the crowd that will discuss Darwinian evolution. First, they don't understand the subject other than to claim that it turns reptiles into birds and second, they don't understand how to do the mathematics of the different components of Darwinian evolution. Where you and I differ on this subject is that I think it ought to be taught in school but taught correctly because Darwinian evolution is the mechanism that causes drug resistance and cancer treatments to fail. Once the student understands correctly how Darwinian evolution works, it will be clear why the ToE is mathematically irrational.
> > >
> > > I don't know what led you to think I don't want evolutionary theory to be taught. And frankly, I am disappointed to hear you make such a claim.
> > It was a post you made a few days ago. I got a sense that you thought that Darwinism equated with the ToE. I posted a quote from Darwin's book which gave the essential concepts of Darwinism, the struggle for existence and adaptation. If you want to understand how drug resistance occurs or why cancer treatments fail, you need to correctly describe and quantitate these concepts. The problem is that biologists don't do this. Instead, they grossly over-extrapolate these concepts. So how would you want to see evolution taught?
>
> Although I don't equate Darwinism with the ToE, there are certain parallels. Not sure what you regard the ToE to be, but evolution has different connotations.

I regard the ToE to be the theory that some simple replicator from the primordial soup through a process of different forms of of genetic transform and common descent gave life as we see it today. That is mathematically irrational hogwash.

> But basically, I am skeptical of about everything, including random mutation and natural selection to account for what we see today.

rmns does happen, I have to deal with the consequences of this phenomenon on a regular basis in my medical practice. But you should be skeptical of the gross over extrapolation of this phenomenon. rmns cannot evolve hiv efficiently when subject to 3 selection pressures. Every biologist and physician should understand why but you don't get the correct explanation either in your biology classes or in medical school.

> You say you want it taught "correctly"; others say the same. As for me, I would rather students were allowed to make their own decisions after being shown all the "correct" stories.

Yes, "correctly". Take real, measurable and repeatable examples of the phenomenon, show by derivation from first principles the correct mathematics which governs the phenomenon and show how the empirical evidence correlates with the mathematics. The Lenski and Kishony experiments demonstrate all the features of evolution (without recombination). The Kishony experiment demonstrates adaptation in an essentially competition free environment and the Lenski experiment demonstrates adaptation in a competitive environment. When you understand these two experiments, you will understand the fundamentals of evolution. There is a reason why the reptifeatharians don't want to talk about these experiments, they spell bad news for the ToE. When it takes a billion replications for each evolutionary step under ideal conditions, what does that say for evolution for populations that can't attain these kinds of numbers (and that includes humans and virtually every other large replicator)? The numbers only get worse when you have more than a single selection pressure acting on the population, even hiv can't evolve efficiently to just 3 selection pressures targeting only 2 genes and this is the fastest evolving replicator known.

[erik simpson]

That's the most sensible-sounding thing I've ever seen you say. But there is a
problem with showing students all the "correct" stories. There are so many
stories (each though to be correct by somebody) that you'd never get through
anything. Some triage is necessary to weed out abovious nonsense. But what's
that? Do you really think that DrDr should have his day in school?

[Alan Kleinman MD PhD]

If you want students to understand evolution, they will have to learn this math.

[*Hemidactylus*]

Did someone hijack Glenn’s account and post something reasonable?

[Glenn]

Should someone assume you could determine what is reasonable?

[*Hemidactylus*]

Most definitely yes. That is why I am awestruck by your recent output. Are
you an imposter from Htrae or a result of a transporter malfunction during
an ion storm? Is the other Glenn now in cahoots with a Creationist Hemi
against a Dawkins worshipping DrDr who has a love of feathered dinosaurs
and understands the importance of lateral gene transfer in evolution of
antibiotic resistance?

[Alan Kleinman MD PhD]

On Tuesday, March 12, 2019 at 8:35:02 PM UTC-7, *Hemidactylus* wrote:
> Glenn <GlennS...@msn.com> wrote:
> > On Tuesday, March 12, 2019 at 7:10:02 PM UTC-7, *Hemidactylus* wrote:
> >> Glenn <GlennS...@msn.com> wrote:
> >>> On Tuesday, March 12, 2019 at 3:20:03 PM UTC-7, Alan Kleinman MD PhD wrote:
> >>>> On Tuesday, March 12, 2019 at 1:40:03 PM UTC-7, Glenn wrote:

> >>>> Glenn, this isn't the crowd that will discuss Darwinian evolution.
> >>>> First, they don't understand the subject other than to claim that it
> >>>> turns reptiles into birds and second, they don't understand how to do
> >>>> the mathematics of the different components of Darwinian evolution.
> >>>> Where you and I differ on this subject is that I think it ought to be
> >>>> taught in school but taught correctly because Darwinian evolution is the
> >>>> mechanism that causes drug resistance and cancer treatments to fail.
> >>>> Once the student understands correctly how Darwinian evolution works, it
> >>>> will be clear why the ToE is mathematically irrational.
> >>>
> >>> I don't know what led you to think I don't want evolutionary theory to
> >>> be taught. And frankly, I am disappointed to hear you make such a claim.
> >>>
> >> Did someone hijack Glenn’s account and post something reasonable?
> >
> > Should someone assume you could determine what is reasonable?
> >
> Most definitely yes. That is why I am awestruck by your recent output. Are
> you an imposter from Htrae or a result of a transporter malfunction during
> an ion storm? Is the other Glenn now in cahoots with a Creationist Hemi
> against a Dawkins worshipping DrDr who has a love of feathered dinosaurs
> and understands the importance of lateral gene transfer in evolution of
> antibiotic resistance?

One wonders if reptifeatharians ever think through their claims. Where exactly do these resistance alleles come from that are laterally transferred? And how do bacteria know which alleles to transfer? You heard the same kind of argument for that recombination was the reason that hiv could so rapidly evolve resistance yet combination therapy still works for the treatment of that disease. Even if an allele can be laterally transferred, all that it would do is accelerate the amplification for a single evolutionary step. Consider what would happen in the Kishony experiment if a variant of e Coli is used that does conjugation. The initial innoculate is placed on the petri-dish. The wild-type grows in the drug-free region. What allele can be transferred to give resistance? None so far because the allele doesn't exist. Finally, a beneficial mutation occurs that allows that variant to grow in the lowest concentration region. Does that variant now do conjugation with the wild-type and give the correct allele to allow the wild-type to grow in the low drug concentration region? Or does a wild-type transfer an allele to the low drug concentration resistant variant and cause it to lose its drug resistance. Explain to us how lateral gene transfer will accelerate the evolutionary process in the Kishony experiment.
.
And Lenski just published a new paper on drug resistance and antibiotic susceptibility:
https://mbio.asm.org/content/10/2/e00189-19
In most cases, drug-resistance disappears when the population is not exposed to the antibiotic for as short a period of 2000 generations. This is because in most cases, drug-resistant variants have reduced fitness compared to wild-types in the drug-free environment. And when those alleles disappear from the population, there is nothing to be laterally transferred when the population is again exposed to that drug. That allele must be evolved once again as demonstrated by the Kishony experiment. Hemi, you are grossly overstating what LGT can do in an adaptation process. And since you are going to clarify your claims, you might as well explain to us how LGT works when 2 or 3 drug therapy is used. Do the bacteria magically know which 2 or 3 resistance alleles need to be lateral transferred?

[Bill Rogers]

Even the Lenski experiment you cite, some resistance genes had essentially no fitness cost. From the paper....

"Despite the general trend toward increased susceptibility, we saw diverse outcomes with different antibiotics. For streptomycin, which was ***the only drug to which the ancestral strain was highly resistant***, none of the evolved lines showed any increased susceptibility."

Many antibiotic resistance mutations do impose a fitness cost, because they are mutations in the essential genes targetted by the antibiotic. But over time compensatory mutations can emerge which reduce that fitness cost and allow the resistance gene to persist even in the absence of drug pressure.

Here's one example among many..

The genomic basis of adaptation to the fitness cost of rifampicin resistance in Pseudomonas aeruginosa

https://royalsocietypublishing.org/doi/pdf/10.1098/rspb.2015.2452

But more important than the examples of compensatory mutations in individual cases is the evidence for maintenance and spread of resistance genes in environmental bacteria, where antibiotic treatment is not a factor and the bacteria are exposed, at most, only to low levels of antibiotic contaminating the environment from wastewater. You can find lots of papers about this

Continental-scale pollution of estuaries with antibiotic resistance genes

https://www.researchgate.net/profile/Michael_Gillings/publication/313124948_Continental-scale_pollution_of_estuaries_with_antibiotic_resistance_genes/links/58bdcfb8a6fdcc2d14eb4f11/Continental-scale-pollution-of-estuaries-with-antibiotic-resistance-genes.pdf

"The widespread dissemination of ARGs (antibiotic resistance genes) into aquatic environmentsis alarming and has implications for controlling the spread of resistance. The movement of the MCR1 polymixin resistance gene onto a conjugative plasmid41allows it to move from cell to cell for the first time. The release of such plasmids into environmental compartments rapidly increases the diversity of species that can acquire such an element and increases the risk of ARG transfer, especially if those waters are also polluted with relevant antibiotics. In turn, this vastly increases the potential for rapid global dissemination and the emergence of resistant opportunistic pathogens."

Here's a review...

Dissemination of Antimicrobial Resistance in Microbial Ecosystems through Horizontal Gene Transfer

https://www.frontiersin.org/articles/10.3389/fmicb.2016.00173/full

There's lots in this review, but, for example...

"The mobilization or transfer of ARGs by bacteriophages has been documented for various bacterial species: the transduction of erythromycin (Hyder and Streitfeld, 1978), tetracycline or multiple resistances between strains of S. pyogenes (Ubukata et al., 1975); the transfer of tetracycline and gentamicin resistance between enterococci (Mazaheri Nezhad Fard et al., 2011); the carriage of β-lactamase genes by bacteriophages in Escherichia coli (Billard-Pomares et al., 2014) and Salmonella (Schmieger and Schicklmaier, 1999); or the transfer of antibiotic resistance plasmids in MRSA (Varga et al., 2012)."

You are correct that antibiotic resistance genes often impose a fitness cost. But you are incorrect where you ignore the compensatory mutations that reduce those fitness costs.

You are correct when you note that, in theory, if resistance genes have fitness costs, that avoiding use of the drug, thereby removing the selection pressure, would lead to loss of the resistance gene and the need for it to evolve de novo once the selection pressure was applied again. But you are wrong to ignore the evidence that, in practice, this strategy usually does not work, because of the compensatory mutations that allow resistance genes to persist in the absence of drug pressure.

And you are just incorrect when you worry about "how the bacteria know which genes to transfer" in lateral gene transfer. They don't know anything. Selection just favors those cases in which they transfer the right genes (and of course many of those genes are found together on plasmids of mobile genetic elements anyway, and are therefore more likely to be transfered than chromosomal genes.

But don't worry, it's definitely true that to find the joint probability of independent events you multiply their individual probabilities. And yes, you ca still multiply probabilities if the events are not independent, as long as you use the correct conditional probabilities. Nobody can take that away from you.

[RonO]

Glenn, have you ever gotten anything from Behe that amounted to anything
in terms of your alternative? We are talking about the reason that you
are an IDiot. You know that you are an IDiot due to your religious
beliefs, so what have you ever gotten from Behe that was worth anything?

This should be something that you should be able to answer by now
because you have had decades to understand what Behe has been telling
you. Behe's IC made the "best" of IDiocy list, so why are you running
from the best that the ID perps have ever been able to give you? Why
would you keep going back to the ID perps for this kind of second rate
junk when you can't face the best?

Really, explain why this junk from Behe does you any good. Denial isn't
anything worth talking about at this point since Behe has told you that
biological evolution is a fact of nature. What do you think are the
postive aspects of what you just put up in terms of why you are an
IDiot? How does this type of IDiot denial help you?

Ron Okimoto

[Ernest Major]

In the same post (as quoted by Dr. Kleinmann's worse enemy) he seemed to
espouse both ultra-Darwinism and radical skepticism. Maybe the other bit
was an accident.

--
alias Ernest Major

[Alan Kleinman MD PhD]

What does "In most cases" mean to you?

>
> "Despite the general trend toward increased susceptibility, we saw diverse outcomes with different antibiotics. For streptomycin, which was ***the only drug to which the ancestral strain was highly resistant***, none of the evolved lines showed any increased susceptibility."
>
> Many antibiotic resistance mutations do impose a fitness cost, because they are mutations in the essential genes targetted by the antibiotic. But over time compensatory mutations can emerge which reduce that fitness cost and allow the resistance gene to persist even in the absence of drug pressure.

That's not what they found in the Lenski study:
"In summary, we examined changes in antibiotic-resistance profiles for
12 lineages of E. coli that evolved for 50,000 generations in antibiotic-free
medium. We observed a clear trend toward increased susceptibility, even though
the ancestor was already highly susceptible to all but one of the 15
antibiotics in this study. Most of the increases in susceptibility arose during
the first 2,000 generations, a period when adaptation to the experimental
environment was most rapid, and lineages that evolved hypermutability showed no
greater tendency to become more susceptible. These patterns suggest that the
increases in susceptibility were side effects of beneficial mutations in the
experimental environment, rather than resulting from the decay of unused genes
and functions. Against these overall trends, however, there were some exceptions, including small increases in resistance of some clones to a few
antibiotics and the retention of high-level resistance to streptomycin."
Most of the resistance alleles impose an energy burden on those variants giving them a fitness disadvantage in the low glucose (energy) environment. Only 1 of the 15 antibiotics tested showed "the retention of high-level resistance" and that was the case of streptomycin. And that is no guarantee that this allele will not cause fitness disadvantage in a different environment such as thermal stress or in the presence of other antibiotics. If these alleles had fitness advantage or were at least neutral in all environments, they would exist at all times in the wild-type, but they don't. If they did, antibiotics would never work but in the vast majority of cases they do work.

>
> Here's one example among many..
>
> The genomic basis of adaptation to the fitness cost of rifampicin resistance in Pseudomonas aeruginosa
>
> https://royalsocietypublishing.org/doi/pdf/10.1098/rspb.2015.2452

They only ran their experiment for 300 generations. And if rifampicin resistance is retained, why do I still see Pseudomonas aeruginosa infections in my medical practice that are still drug-sensitive.

>
> But more important than the examples of compensatory mutations in individual cases is the evidence for maintenance and spread of resistance genes in environmental bacteria, where antibiotic treatment is not a factor and the bacteria are exposed, at most, only to low levels of antibiotic contaminating the environment from wastewater. You can find lots of papers about this
>
> Continental-scale pollution of estuaries with antibiotic resistance genes
>
> https://www.researchgate.net/profile/Michael_Gillings/publication/313124948_Continental-scale_pollution_of_estuaries_with_antibiotic_resistance_genes/links/58bdcfb8a6fdcc2d14eb4f11/Continental-scale-pollution-of-estuaries-with-antibiotic-resistance-genes.pdf
>
> "The widespread dissemination of ARGs (antibiotic resistance genes) into aquatic environmentsis alarming and has implications for controlling the spread of resistance. The movement of the MCR1 polymixin resistance gene onto a conjugative plasmid41allows it to move from cell to cell for the first time. The release of such plasmids into environmental compartments rapidly increases the diversity of species that can acquire such an element and increases the risk of ARG transfer, especially if those waters are also polluted with relevant antibiotics. In turn, this vastly increases the potential for rapid global dissemination and the emergence of resistant opportunistic pathogens."

You clearly don't recognize the problem with these studies. I attended a conference last year where they presented a similar example. Two problems with these studies, first you need to demonstrate that the resistant bacteria didn't enter these waters as fecal bacteria from patients treated with antibiotics and second, you need to demonstrate that resistance can evolve in the water polluted with these antibiotics. The presenter at that conference demonstrated that resistance can evolve to the drug in growth media but not in the river water. River water presents a totally different environment to the bacteria than does a test tube of growth media in an incubator. I'll let you try to imagine the differences in the environments under these two conditions and explain to us how resistance can evolve in river water. Maybe you should do the experiment and demonstrate that it happens because that's what I suggested to the presenter at the conference. The presenter didn't look too happy with that suggestion.

>
> Here's a review...
>
> Dissemination of Antimicrobial Resistance in Microbial Ecosystems through Horizontal Gene Transfer
>
> https://www.frontiersin.org/articles/10.3389/fmicb.2016.00173/full
>
> There's lots in this review, but, for example...
>
> "The mobilization or transfer of ARGs by bacteriophages has been documented for various bacterial species: the transduction of erythromycin (Hyder and Streitfeld, 1978), tetracycline or multiple resistances between strains of S. pyogenes (Ubukata et al., 1975); the transfer of tetracycline and gentamicin resistance between enterococci (Mazaheri Nezhad Fard et al., 2011); the carriage of β-lactamase genes by bacteriophages in Escherichia coli (Billard-Pomares et al., 2014) and Salmonella (Schmieger and Schicklmaier, 1999); or the transfer of antibiotic resistance plasmids in MRSA (Varga et al., 2012)."

You still miss the point. Until the resistance allele evolves, there is nothing to laterally transfer. And if you use antibiotics correctly, you will drive the infective agent to extinction. If you use the antibiotics incorrectly, too low dosage, incomplete treatment, single drug therapy where resistant variants already exist in the population,..., you will introduce resistant variants into the environment and that environment starts with the patient. If you use the antibiotics correctly, there will be no resistance alleles to transfer laterally. If you think that the antibiotics eliminated from the patient and ending up in sewage water and rivers, demonstrate that resistant variants can evolve under the conditions provided by that environment.

>
> You are correct that antibiotic resistance genes often impose a fitness cost. But you are incorrect where you ignore the compensatory mutations that reduce those fitness costs.

So, are you claiming the drug sensitive Pseudomonas doesn't exist anymore? And where were the compensatory mutations in the Lenski study?

>
> You are correct when you note that, in theory, if resistance genes have fitness costs, that avoiding use of the drug, thereby removing the selection pressure, would lead to loss of the resistance gene and the need for it to evolve de novo once the selection pressure was applied again. But you are wrong to ignore the evidence that, in practice, this strategy usually does not work, because of the compensatory mutations that allow resistance genes to persist in the absence of drug pressure.

I think you mean loss of the resistance allele, not loss of the gene. From the Lenski paper:
"These patterns suggest that the increases in susceptibility were side effects of beneficial mutations in the experimental environment, rather than resulting
from the decay of unused genes and functions."
And the Lenski study is done with only a single selection condition, energy limitation. If your claim was correct, there would be no drug-sensitive bacteria at all. But that's not the case. Drug-resistance is a much bigger problem in the hospital environment where the patients tend to be more debilitated and immune compromised. I work in the community environment where patients tend to be healthier and generally have good functioning immune systems. Do you suggest that I deny them antibiotics when they come in with respiratory tract infections? If so, that would explain why pneumonia and sepsis are the most common medical reason for admission to the hospital. Too many medical providers are taking your bad advice.

>
> And you are just incorrect when you worry about "how the bacteria know which genes to transfer" in lateral gene transfer. They don't know anything. Selection just favors those cases in which they transfer the right genes (and of course many of those genes are found together on plasmids of mobile genetic elements anyway, and are therefore more likely to be transfered than chromosomal genes.

The "right genes" have to exist first. And your simple minded understanding of this problem and selection needs to be tested. What if you are treating someone with two drugs. What is the probability that the correct two alleles will be laterally transferred to some member of the population. Let "N" be the total population size, nA be the number of members of the population with resistance allele A to one drug and nB be the number of members of the population with resistant allele B to the second drug.

>
> But don't worry, it's definitely true that to find the joint probability of independent events you multiply their individual probabilities. And yes, you ca still multiply probabilities if the events are not independent, as long as you use the correct conditional probabilities. Nobody can take that away from you.

That's good that you understand this principle, now compute the joint probability of resistance allele A and resistance allele B be laterally transferred to some member of a population size "N". Don't forget to multiply these probabilities. We'll get you to understand the correct mathematics of evolution if we have to drag you kicking and screaming.

[Alan Kleinman MD PhD]

SlowO is now going to explain how sponges evolve livers, kidneys, hearts, brains, spleens and immune systems, endocrine organs including hypothalamus, pituitary, thyroid, parathyroids, adrenals, pineal body, and the reproductive organs (ovaries and testes), digestive organs including pancreas, salivary glands, gall bladder, musculoskeletal system, sensory organs, eyes, ears, sense of taste, smell and touch, and please include fossil intermediaries for each evolutionary step. Please include selection pressures, genes targeted and mutations required to do this transformation from sponge to SlowO. And since sponges still exist, please give examples of extant intermediaries and to assist SlowO, I'll help him with this by pointing out the existence of SpongeBob SquarePants.
.
If SlowO cannot do this, he can explain to us how the Kishony experiment works.

[jillery]

On Wed, 13 Mar 2019 07:03:01 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>> Many antibiotic resistance mutations do impose a fitness cost, because they are mutations in the essential genes targetted by the antibiotic. But over time compensatory mutations can emerge which reduce that fitness cost and allow the resistance gene to persist even in the absence of drug pressure.
>That's not what they found in the Lenski study:
>"In summary, we examined changes in antibiotic-resistance profiles for
>12 lineages of E. coli that evolved for 50,000 generations in antibiotic-free
>medium. We observed a clear trend toward increased susceptibility, even though
>the ancestor was already highly susceptible to all but one of the 15
>antibiotics in this study. Most of the increases in susceptibility arose during
>the first 2,000 generations, a period when adaptation to the experimental
>environment was most rapid, and lineages that evolved hypermutability showed no
>greater tendency to become more susceptible. These patterns suggest that the
>increases in susceptibility were side effects of beneficial mutations in the
>experimental environment, rather than resulting from the decay of unused genes
>and functions. Against these overall trends, however, there were some exceptions, including small increases in resistance of some clones to a few
>antibiotics and the retention of high-level resistance to streptomycin."
>Most of the resistance alleles impose an energy burden on those variants giving them a fitness disadvantage in the low glucose (energy) environment. Only 1 of the 15 antibiotics tested showed "the retention of high-level resistance" and that was the case of streptomycin. And that is no guarantee that this allele will not cause fitness disadvantage in a different environment such as thermal stress or in the presence of other antibiotics. If these alleles had fitness advantage or were at least neutral in all environments, they would exist at all times in the wild-type, but they don't. If they did, antibiotics would never work but in the vast majority of cases they do work.

There are at least two different separate ways bacteria can develop
susceptibility to antibiotics:

1) loss of resistance alleles.

2) as a side-effect to gain of unrelated beneficial alleles.


In the monotonous environment Lenski provides, completely isolated
from any antibiotics, there are no selective pressures to maintain
resistance alleles, or to discourage unrelated beneficial alleles
which have a side-effect of reducing resistance. In that environment,
any resistance to antibiotics would be a consequence of genetic drift.

Your statement that resistance alleles don't exist in the wild-type is
incorrect. There are multiple non-human sources of antibiotics, as
illustrated by Fleming's original serendipitous discovery.

My understanding is most antibiotics are based on compounds first
identified from the environment. This is a consequence of a
biochemical arms-race between bacteria and their competition.
Wild-type bacteria in an environment containing sources of non-manmade
antibiotics necessarily have a fitness advantage.

--
I disapprove of what you say, but I will defend to the death your right to say it.

Evelyn Beatrice Hall
Attributed to Voltaire

[jillery]

GIYF
<https://en.wikipedia.org/wiki/Horizontal_gene_transfer >

>And how do bacteria know which alleles to transfer?

Really? Do you really assume they transfer only specific genes, as
opposed to the scattershot approach that actually happens?

>You heard the same kind of argument for that recombination was the reason that hiv could so rapidly evolve resistance yet combination therapy still works for the treatment of that disease. Even if an allele can be laterally transferred, all that it would do is accelerate the amplification for a single evolutionary step. Consider what would happen in the Kishony experiment if a variant of e Coli is used that does conjugation. The initial innoculate is placed on the petri-dish. The wild-type grows in the drug-free region. What allele can be transferred to give resistance? None so far because the allele doesn't exist.

And how you know the allele doesn't exist? Alleles don't appear only
when they're needed, that's your ID assumption. Most biologists don't
think that way.

>Finally, a beneficial mutation occurs that allows that variant to grow in the lowest concentration region. Does that variant now do conjugation with the wild-type and give
>the correct allele to allow the wild-type to grow in the low drug concentration region? Or does a wild-type transfer an allele to the low drug concentration resistant variant and cause it to lose its drug resistance. Explain to us how lateral gene transfer will accelerate the evolutionary process in the Kishony experiment.

A fundamental problem for asexual populations is that a beneficial
allele is otherwise limited to the lineage in which it first appeared,
which also may have harmful alleles that limit that lineage's
amplification. HGT moves beneficial alleles to other lineages with
different alleles, and so increases the number of lineages which can
amplify the beneficial allele. This is a similar explanation for how
recombination benefits sexual populations.

>And Lenski just published a new paper on drug resistance and antibiotic susceptibility:
>https://mbio.asm.org/content/10/2/e00189-19
>In most cases, drug-resistance disappears when the population is not exposed to the antibiotic for as short a period of 2000 generations.

So beneficial alleles *do* exist before populations are exposed to
antibiotics, refuting your claims above. Try to remember this.

>This is because in most cases, drug-resistant variants have reduced fitness compared to wild-types in the drug-free environment. And when those alleles disappear from the population, there is nothing to be laterally transferred when the population is again exposed to that drug. That allele must be evolved once again as demonstrated by the Kishony experiment.

One of the things the Kishony experiment showed is that resistance
alleles appeared in multiple lineages, and did so quickly. The
appearance of antibiotic only gave those lineages a fitness advantage,
which allowed them to amplify. This is a phenomenon your hard
mathematics neither predicts nor explains.

>Hemi, you are grossly overstating what LGT can do in an adaptation process. And since you are going to clarify your claims, you might as well explain to us how LGT works when 2 or 3 drug therapy is used. Do the bacteria magically know which 2 or 3 resistance alleles need to be lateral transferred?

Once again, you assume others are stuck with your ID assumptions. All
alleles are candidates for HGT, beneficial or not. There are multiple
lineages, some with resistance to one antibiotic, some with resistance
to another. HGT allows lineages to benefit from alleles in other
lineages, which makes it more likely (not guarantee) a lineage will
get multiple resistance alleles. How do you still not get this?

[jillery]

Drdr polypolymath shoots himself in the foot so often, he could be the
poster child for both sides of the gun control debate.

[Bill Rogers]

"In most cases" to me, in this paper, means "every case, except the case in which the ancestral strain actually started with high level resistance." You know, clinically important resistance.

> >
> > "Despite the general trend toward increased susceptibility, we saw diverse outcomes with different antibiotics. For streptomycin, which was ***the only drug to which the ancestral strain was highly resistant***, none of the evolved lines showed any increased susceptibility."
> >
> > Many antibiotic resistance mutations do impose a fitness cost, because they are mutations in the essential genes targetted by the antibiotic. But over time compensatory mutations can emerge which reduce that fitness cost and allow the resistance gene to persist even in the absence of drug pressure.
> That's not what they found in the Lenski study:
> "In summary, we examined changes in antibiotic-resistance profiles for
> 12 lineages of E. coli that evolved for 50,000 generations in antibiotic-free
> medium. We observed a clear trend toward increased susceptibility, even though
> the ancestor was already highly susceptible to all but one of the 15
> antibiotics in this study. Most of the increases in susceptibility arose during
> the first 2,000 generations, a period when adaptation to the experimental
> environment was most rapid, and lineages that evolved hypermutability showed no
> greater tendency to become more susceptible. These patterns suggest that the
> increases in susceptibility were side effects of beneficial mutations in the
> experimental environment, rather than resulting from the decay of unused genes
> and functions. Against these overall trends, however, there were some exceptions, including small increases in resistance of some clones to a few
> antibiotics and the retention of high-level resistance to streptomycin."
> Most of the resistance alleles impose an energy burden on those variants giving them a fitness disadvantage in the low glucose (energy) environment. Only 1 of the 15 antibiotics tested showed "the retention of high-level resistance" and that was the case of streptomycin. And that is no guarantee that this allele will not cause fitness disadvantage in a different environment such as thermal stress or in the presence of other antibiotics. If these alleles had fitness advantage or were at least neutral in all environments, they would exist at all times in the wild-type, but they don't. If they did, antibiotics would never work but in the vast majority of cases they do work.

Things aren't so black and white. It's quite possible for resistance alleles to persist without going to fixation (OMG there's that word again), given that there are many different environments in which the bugs live.

> >
> > Here's one example among many..
> >
> > The genomic basis of adaptation to the fitness cost of rifampicin resistance in Pseudomonas aeruginosa
> >
> > https://royalsocietypublishing.org/doi/pdf/10.1098/rspb.2015.2452
> They only ran their experiment for 300 generations. And if rifampicin resistance is retained, why do I still see Pseudomonas aeruginosa infections in my medical practice that are still drug-sensitive.
> >
> > But more important than the examples of compensatory mutations in individual cases is the evidence for maintenance and spread of resistance genes in environmental bacteria, where antibiotic treatment is not a factor and the bacteria are exposed, at most, only to low levels of antibiotic contaminating the environment from wastewater. You can find lots of papers about this
> >
> > Continental-scale pollution of estuaries with antibiotic resistance genes
> >
> > https://www.researchgate.net/profile/Michael_Gillings/publication/313124948_Continental-scale_pollution_of_estuaries_with_antibiotic_resistance_genes/links/58bdcfb8a6fdcc2d14eb4f11/Continental-scale-pollution-of-estuaries-with-antibiotic-resistance-genes.pdf
> >
> > "The widespread dissemination of ARGs (antibiotic resistance genes) into aquatic environmentsis alarming and has implications for controlling the spread of resistance. The movement of the MCR1 polymixin resistance gene onto a conjugative plasmid41allows it to move from cell to cell for the first time. The release of such plasmids into environmental compartments rapidly increases the diversity of species that can acquire such an element and increases the risk of ARG transfer, especially if those waters are also polluted with relevant antibiotics. In turn, this vastly increases the potential for rapid global dissemination and the emergence of resistant opportunistic pathogens."

> You clearly don't recognize the problem with these studies. I attended a conference last year where they presented a similar example. Two problems with these studies, first you need to demonstrate that the resistant bacteria didn't enter these waters as fecal bacteria from patients treated with antibiotics,

Why would that matter? Wherever they came from, they remain present in the environment.

and second, you need to demonstrate that resistance can evolve in the water polluted with these antibiotics. The presenter at that conference demonstrated that resistance can evolve to the drug in growth media but not in the river water. River water presents a totally different environment to the bacteria than does a test tube of growth media in an incubator. I'll let you try to imagine the differences in the environments under these two conditions and explain to us how resistance can evolve in river water. Maybe you should do the experiment and demonstrate that it happens because that's what I suggested to the presenter at the conference. The presenter didn't look too happy with that suggestion.

Perhaps you overlooked the real reason for the preenter's expression. In any case, it does not matter whether the resistance can evolve de novo in river water, only that whatever fitness cost is associated with the resistance doesn't make it disappear quickly.

> >
> > Here's a review...
> >
> > Dissemination of Antimicrobial Resistance in Microbial Ecosystems through Horizontal Gene Transfer
> >
> > https://www.frontiersin.org/articles/10.3389/fmicb.2016.00173/full
> >
> > There's lots in this review, but, for example...
> >
> > "The mobilization or transfer of ARGs by bacteriophages has been documented for various bacterial species: the transduction of erythromycin (Hyder and Streitfeld, 1978), tetracycline or multiple resistances between strains of S. pyogenes (Ubukata et al., 1975); the transfer of tetracycline and gentamicin resistance between enterococci (Mazaheri Nezhad Fard et al., 2011); the carriage of β-lactamase genes by bacteriophages in Escherichia coli (Billard-Pomares et al., 2014) and Salmonella (Schmieger and Schicklmaier, 1999); or the transfer of antibiotic resistance plasmids in MRSA (Varga et al., 2012)."
> You still miss the point. Until the resistance allele evolves, there is nothing to laterally transfer. And if you use antibiotics correctly, you will drive the infective agent to extinction. If you use the antibiotics incorrectly, too low dosage, incomplete treatment, single drug therapy where resistant variants already exist in the population,..., you will introduce resistant variants into the environment and that environment starts with the patient. If you use the antibiotics correctly, there will be no resistance alleles to transfer laterally. If you think that the antibiotics eliminated from the patient and ending up in sewage water and rivers, demonstrate that resistant variants can evolve under the conditions provided by that environment.
> >
> > You are correct that antibiotic resistance genes often impose a fitness cost. But you are incorrect where you ignore the compensatory mutations that reduce those fitness costs.
> So, are you claiming the drug sensitive Pseudomonas doesn't exist anymore? And where were the compensatory mutations in the Lenski study?

Of course not. And, I don't know.

> >
> > You are correct when you note that, in theory, if resistance genes have fitness costs, that avoiding use of the drug, thereby removing the selection pressure, would lead to loss of the resistance gene and the need for it to evolve de novo once the selection pressure was applied again. But you are wrong to ignore the evidence that, in practice, this strategy usually does not work, because of the compensatory mutations that allow resistance genes to persist in the absence of drug pressure.
> I think you mean loss of the resistance allele, not loss of the gene.

Yes, you're right, I meant loss of the resistance allele.

>From the Lenski paper:
> "These patterns suggest that the increases in susceptibility were side effects of beneficial mutations in the experimental environment, rather than resulting
> from the decay of unused genes and functions."
> And the Lenski study is done with only a single selection condition, energy limitation. If your claim was correct, there would be no drug-sensitive bacteria at all.

No. It's not that there are no metabolic costs to resistance. Only that those costs are mitigated enough that the resistance alleles can persist for quite a while in the absence of drug pressure.

>But that's not the case. Drug-resistance is a much bigger problem in the hospital environment where the patients tend to be more debilitated and immune compromised. I work in the community environment where patients tend to be healthier and generally have good functioning immune systems. Do you suggest that I deny them antibiotics when they come in with respiratory tract infections?

Neither I nor any of the professional societies with whom you disagree about antibiotic usage guidelines think you should deny patients antibiotics when they are appropriate.

>If so, that would explain why pneumonia and sepsis are the most common medical reason for admission to the hospital. Too many medical providers are taking your bad advice.
> >
> > And you are just incorrect when you worry about "how the bacteria know which genes to transfer" in lateral gene transfer. They don't know anything. Selection just favors those cases in which they transfer the right genes (and of course many of those genes are found together on plasmids of mobile genetic elements anyway, and are therefore more likely to be transfered than chromosomal genes.
> The "right genes" have to exist first.

And they do - they exist both in hospitals and in the natural environment.

>And your simple minded understanding of this problem and selection needs to be tested. What if you are treating someone with two drugs. What is the probability that the correct two alleles will be laterally transferred to some member of the population. Let "N" be the total population size, nA be the number of members of the population with resistance allele A to one drug and nB be the number of members of the population with resistant allele B to the second drug.

It need not happen in the patient during the course of treatment. Remember that the resistance genes are often present together on plasmids and can be transferred together. That's here you need conditional probabilities.

There's plenty of literature out there. You could learn about this if you wanted. I'm not interested in convincing you of anything, only in putting up entry points to the literature for anyone who has gotten interested in LGT as a mechanism for the spread of resistance.

[Alan Kleinman MD PhD]

In jillery's fantasy world, starvation is not a selection pressure.

>
> Your statement that resistance alleles don't exist in the wild-type is
> incorrect. There are multiple non-human sources of antibiotics, as
> illustrated by Fleming's original serendipitous discovery.

In jillery's fantasy world, antibiotics never work because of resistance alleles in the wild-type.

>
> My understanding is most antibiotics are based on compounds first
> identified from the environment. This is a consequence of a
> biochemical arms-race between bacteria and their competition.
> Wild-type bacteria in an environment containing sources of non-manmade
> antibiotics necessarily have a fitness advantage.

In jillery's fantasy world, penicillin never works because all bacteria have resistance to this non-manmade antibiotic.

[Glenn]

On Wednesday, March 13, 2019 at 3:45:03 AM UTC-7, Bill Rogers wrote:

Does no increased susceptibility to an antibiotic mean that an organism has not suffered an overall loss of fitness?

>
> Many antibiotic resistance mutations do impose a fitness cost, because they are mutations in the essential genes targetted by the antibiotic. But over time compensatory mutations can emerge which reduce that fitness cost and allow the resistance gene to persist even in the absence of drug pressure.

Did Lenski observe, study and document these "over time compensatory mutations"?

>
> Here's one example among many..
>

If you are moving away from discussing Lenski's work, then

snip

[Bob Casanova]

On Wed, 13 Mar 2019 08:27:04 -0700 (PDT), the following
appeared in talk.origins, posted by Alan Kleinman MD PhD
<klei...@sti.net>:

In DocDocWorld, lack of nutrients can be overcome by drug
resistance.

>> Your statement that resistance alleles don't exist in the wild-type is
>> incorrect. There are multiple non-human sources of antibiotics, as
>> illustrated by Fleming's original serendipitous discovery.

>In jillery's fantasy world, antibiotics never work because of resistance alleles in the wild-type.

In DocDocWorld, Penicillium notatum did not exist prior to
Fleming's work.

>> My understanding is most antibiotics are based on compounds first
>> identified from the environment. This is a consequence of a
>> biochemical arms-race between bacteria and their competition.
>> Wild-type bacteria in an environment containing sources of non-manmade
>> antibiotics necessarily have a fitness advantage.

>In jillery's fantasy world, penicillin never works because all bacteria have resistance to this non-manmade antibiotic.

In DocDocWorld, no natural antibiotic ever existed.

See, Sparky, I can "re-interpret" your posts, too; you don't
have a monopoly on that. The difference is that, unlike you,
I know I'm doing it.
--

Bob C.

"The most exciting phrase to hear in science,
the one that heralds new discoveries, is not
'Eureka!' but 'That's funny...'"

- Isaac Asimov

[Alan Kleinman MD PhD]

Do the authors give enough information to quantify what they mean?

>
> > >
> > > "Despite the general trend toward increased susceptibility, we saw diverse outcomes with different antibiotics. For streptomycin, which was ***the only drug to which the ancestral strain was highly resistant***, none of the evolved lines showed any increased susceptibility."
> > >
> > > Many antibiotic resistance mutations do impose a fitness cost, because they are mutations in the essential genes targetted by the antibiotic. But over time compensatory mutations can emerge which reduce that fitness cost and allow the resistance gene to persist even in the absence of drug pressure.
> > That's not what they found in the Lenski study:
> > "In summary, we examined changes in antibiotic-resistance profiles for
> > 12 lineages of E. coli that evolved for 50,000 generations in antibiotic-free
> > medium. We observed a clear trend toward increased susceptibility, even though
> > the ancestor was already highly susceptible to all but one of the 15
> > antibiotics in this study. Most of the increases in susceptibility arose during
> > the first 2,000 generations, a period when adaptation to the experimental
> > environment was most rapid, and lineages that evolved hypermutability showed no
> > greater tendency to become more susceptible. These patterns suggest that the
> > increases in susceptibility were side effects of beneficial mutations in the
> > experimental environment, rather than resulting from the decay of unused genes
> > and functions. Against these overall trends, however, there were some exceptions, including small increases in resistance of some clones to a few
> > antibiotics and the retention of high-level resistance to streptomycin."
> > Most of the resistance alleles impose an energy burden on those variants giving them a fitness disadvantage in the low glucose (energy) environment. Only 1 of the 15 antibiotics tested showed "the retention of high-level resistance" and that was the case of streptomycin. And that is no guarantee that this allele will not cause fitness disadvantage in a different environment such as thermal stress or in the presence of other antibiotics. If these alleles had fitness advantage or were at least neutral in all environments, they would exist at all times in the wild-type, but they don't. If they did, antibiotics would never work but in the vast majority of cases they do work.
>
> Things aren't so black and white. It's quite possible for resistance alleles to persist without going to fixation (OMG there's that word again), given that there are many different environments in which the bugs live.

That's right, there are many different environments in which bacteria live. And if resistance alleles don't give improved fitness in that environment, what do you think will happen to the relative frequencies of those variants?

>
> > >
> > > Here's one example among many..
> > >
> > > The genomic basis of adaptation to the fitness cost of rifampicin resistance in Pseudomonas aeruginosa
> > >
> > > https://royalsocietypublishing.org/doi/pdf/10.1098/rspb.2015.2452
> > They only ran their experiment for 300 generations. And if rifampicin resistance is retained, why do I still see Pseudomonas aeruginosa infections in my medical practice that are still drug-sensitive.
> > >
> > > But more important than the examples of compensatory mutations in individual cases is the evidence for maintenance and spread of resistance genes in environmental bacteria, where antibiotic treatment is not a factor and the bacteria are exposed, at most, only to low levels of antibiotic contaminating the environment from wastewater. You can find lots of papers about this
> > >
> > > Continental-scale pollution of estuaries with antibiotic resistance genes
> > >
> > > https://www.researchgate.net/profile/Michael_Gillings/publication/313124948_Continental-scale_pollution_of_estuaries_with_antibiotic_resistance_genes/links/58bdcfb8a6fdcc2d14eb4f11/Continental-scale-pollution-of-estuaries-with-antibiotic-resistance-genes.pdf
> > >
> > > "The widespread dissemination of ARGs (antibiotic resistance genes) into aquatic environmentsis alarming and has implications for controlling the spread of resistance. The movement of the MCR1 polymixin resistance gene onto a conjugative plasmid41allows it to move from cell to cell for the first time. The release of such plasmids into environmental compartments rapidly increases the diversity of species that can acquire such an element and increases the risk of ARG transfer, especially if those waters are also polluted with relevant antibiotics. In turn, this vastly increases the potential for rapid global dissemination and the emergence of resistant opportunistic pathogens."
> > You clearly don't recognize the problem with these studies. I attended a conference last year where they presented a similar example. Two problems with these studies, first you need to demonstrate that the resistant bacteria didn't enter these waters as fecal bacteria from patients treated with antibiotics,
>
> Why would that matter? Wherever they came from, they remain present in the environment.

The implication of these studies is that resistance is evolving in river water due to antibiotics showing up in that environment, not in patients being treated by these drugs. If that is true, there is a problem. But to prove that, you need to show that bacteria in river water can evolve resistance to antibiotics. River water is a completely different environment than a patient receiving treatment with antibiotics. There already is a lot of bad advice circulating around the usage of antibiotics. These types of claims don't help.

>
> and second, you need to demonstrate that resistance can evolve in the water polluted with these antibiotics. The presenter at that conference demonstrated that resistance can evolve to the drug in growth media but not in the river water. River water presents a totally different environment to the bacteria than does a test tube of growth media in an incubator. I'll let you try to imagine the differences in the environments under these two conditions and explain to us how resistance can evolve in river water. Maybe you should do the experiment and demonstrate that it happens because that's what I suggested to the presenter at the conference. The presenter didn't look too happy with that suggestion.
>
> Perhaps you overlooked the real reason for the preenter's expression. In any case, it does not matter whether the resistance can evolve de novo in river water, only that whatever fitness cost is associated with the resistance doesn't make it disappear quickly.

You need to measure that, and that is what Lenski did for his particular environment and only 1 of 15 antibiotics retained high resistance after only 2000 generations in a starvation environment.

>
> > >
> > > Here's a review...
> > >
> > > Dissemination of Antimicrobial Resistance in Microbial Ecosystems through Horizontal Gene Transfer
> > >
> > > https://www.frontiersin.org/articles/10.3389/fmicb.2016.00173/full
> > >
> > > There's lots in this review, but, for example...
> > >
> > > "The mobilization or transfer of ARGs by bacteriophages has been documented for various bacterial species: the transduction of erythromycin (Hyder and Streitfeld, 1978), tetracycline or multiple resistances between strains of S. pyogenes (Ubukata et al., 1975); the transfer of tetracycline and gentamicin resistance between enterococci (Mazaheri Nezhad Fard et al., 2011); the carriage of β-lactamase genes by bacteriophages in Escherichia coli (Billard-Pomares et al., 2014) and Salmonella (Schmieger and Schicklmaier, 1999); or the transfer of antibiotic resistance plasmids in MRSA (Varga et al., 2012)."
> > You still miss the point. Until the resistance allele evolves, there is nothing to laterally transfer. And if you use antibiotics correctly, you will drive the infective agent to extinction. If you use the antibiotics incorrectly, too low dosage, incomplete treatment, single drug therapy where resistant variants already exist in the population,..., you will introduce resistant variants into the environment and that environment starts with the patient. If you use the antibiotics correctly, there will be no resistance alleles to transfer laterally. If you think that the antibiotics eliminated from the patient and ending up in sewage water and rivers, demonstrate that resistant variants can evolve under the conditions provided by that environment.
> > >
> > > You are correct that antibiotic resistance genes often impose a fitness cost. But you are incorrect where you ignore the compensatory mutations that reduce those fitness costs.
> > So, are you claiming the drug sensitive Pseudomonas doesn't exist anymore? And where were the compensatory mutations in the Lenski study?
>
> Of course not. And, I don't know.

Correct, drug-sensative Pseudomonas still exists. And there weren't compensatory mutations in 14 of the 15 cases that Lenski looked at. That's why drug susceptibility increased in those cases over 2000 generations.

> > >
> > > You are correct when you note that, in theory, if resistance genes have fitness costs, that avoiding use of the drug, thereby removing the selection pressure, would lead to loss of the resistance gene and the need for it to evolve de novo once the selection pressure was applied again. But you are wrong to ignore the evidence that, in practice, this strategy usually does not work, because of the compensatory mutations that allow resistance genes to persist in the absence of drug pressure.
> > I think you mean loss of the resistance allele, not loss of the gene.
>
> Yes, you're right, I meant loss of the resistance allele.
>
> >From the Lenski paper:
> > "These patterns suggest that the increases in susceptibility were side effects of beneficial mutations in the experimental environment, rather than resulting
> > from the decay of unused genes and functions."
> > And the Lenski study is done with only a single selection condition, energy limitation. If your claim was correct, there would be no drug-sensitive bacteria at all.
>
> No. It's not that there are no metabolic costs to resistance. Only that those costs are mitigated enough that the resistance alleles can persist for quite a while in the absence of drug pressure.

Only one case of where high level of resistance remained out of 15 drugs considered in the Lenski study after only 2000 generations. What Lenski has done is laid the foundation for measuring the sustainability of drug-resistance in a drug free environment. It's one thing for you to make your claim, it is quite another to measure it.

>
> >But that's not the case. Drug-resistance is a much bigger problem in the hospital environment where the patients tend to be more debilitated and immune compromised. I work in the community environment where patients tend to be healthier and generally have good functioning immune systems. Do you suggest that I deny them antibiotics when they come in with respiratory tract infections?
>
> Neither I nor any of the professional societies with whom you disagree about antibiotic usage guidelines think you should deny patients antibiotics when they are appropriate.

The debate then becomes over the word "appropriate". If someone has a fever and sore throat and you make a clinical decision that it is a viral infection, the medical provider has a responsibility to do close follow-up to confirm rapid resolution of symptoms. Obviously this is not being done based on the data showing that the main reason for hospital admission is pneumonia and sepsis. Many of these cases could easily be treated in the out-patient environment if treatment was initiated earlier in the disease process.

>
>
> >If so, that would explain why pneumonia and sepsis are the most common medical reason for admission to the hospital. Too many medical providers are taking your bad advice.
> > >
> > > And you are just incorrect when you worry about "how the bacteria know which genes to transfer" in lateral gene transfer. They don't know anything. Selection just favors those cases in which they transfer the right genes (and of course many of those genes are found together on plasmids of mobile genetic elements anyway, and are therefore more likely to be transfered than chromosomal genes.
> > The "right genes" have to exist first.
>
> And they do - they exist both in hospitals and in the natural environment.

Sure, if you use selection pressures improperly, you can expect that these alleles to evolve.

>
> >And your simple minded understanding of this problem and selection needs to be tested. What if you are treating someone with two drugs. What is the probability that the correct two alleles will be laterally transferred to some member of the population. Let "N" be the total population size, nA be the number of members of the population with resistance allele A to one drug and nB be the number of members of the population with resistant allele B to the second drug.
>
> It need not happen in the patient during the course of treatment. Remember that the resistance genes are often present together on plasmids and can be transferred together. That's here you need conditional probabilities.

I hear that story. It's a wonder that antibiotics ever work but they do. And if they are used properly, they work in most cases.

>
> There's plenty of literature out there. You could learn about this if you wanted. I'm not interested in convincing you of anything, only in putting up entry points to the literature for anyone who has gotten interested in LGT as a mechanism for the spread of resistance.

You don't have to give me the entry point to this literature. Just show how to compute the probability of 2 different resistance alleles (not on the same plasmid) to be laterally transferred to some member of a population. You said you did this math in med school. Show how to do it for this case you claim is the major reason for drug resistance

[jillery]

On Wed, 13 Mar 2019 08:27:04 -0700 (PDT), Alan Kleinman MD PhD

In drdr polypolymath's fantasy world, his nonsense non-sequiturs and
asinine ad-hominems are coherent arguments. drdr polypolymath is a
quacker.

[Alan Kleinman MD PhD]

You still haven't taken that introductory course in probability theory so that you could understand something about stochastic processes (like evolution).

[jillery]

On Tue, 12 Mar 2019 17:39:51 -0400, jillery <69jp...@gmail.com>
wrote:

>On Tue, 12 Mar 2019 13:35:19 -0700 (PDT), Glenn <GlennS...@msn.com>

>wrote:
>
>>"Coyne is quite the prominent evolutionary biologist, and has been antagonistic to intelligent design arguments for decades. If Darwin’s theory were actually the powerful idea it’s claimed to be, Coyne should have been able to counter design easily, simply by summarizing its arguments and showing how Darwin deals with them. Yet he can’t even bring himself to mention what those arguments are. Instead he tries to whip up hysteria against a book that argues for what most people already believe. That speaks volumes about the actual strength of Darwin’s theory."
>>
>>https://evolutionnews.org/2019/03/bullet-points-for-jerry-coyne/
>>
>>Reminds me of scientist's climate hysteria. Hmm. Would the credibility of science and scientists be on topic in a discussion of origins?
>
>

>Michael Behe should have read Coyne's "Why Evolution Is True" before
>he again proved he has no idea what he's talking about.


Here's another WEIT article about Behe and his new book:

<https://whyevolutionistrue.wordpress.com/2019/03/13/behes-book-sliced-and-diced-again-by-members-of-his-own-department/>

<http://tinyurl.com/y3n2ypp2>

************************************
Behe and his Discovery Institute can’t abide this criticism, and have
struck back, but their blows are ineffectual. Just today their flaccid
house organ, Evolution News, issued four distinct attacks on me alone.
I’m bursting with pride!

[...]

Now today a new review appeared in the prestigious journal Evolution.
The kicker is that it’s by two members of Behe’s own department:
assistant professor Gregory Lang, who works on microbial evolution,
and assistant professor Amber Rice, an organismal evolutionist.
***********************************

I wonder if Evolution New's flaccid house organ would be helped by an
organismal evolutionist

[Alan Kleinman MD PhD]

You would certainly be helped by an introductory course in probability theory so that you might understand something about stochastic processes (like evolution). Your stupid foul mouth certainly doesn't explain it.

[Bob Casanova]

On Tue, 12 Mar 2019 13:35:19 -0700 (PDT), the following
appeared in talk.origins, posted by Glenn
<GlennS...@msn.com>:

>"Coyne is quite the prominent evolutionary biologist, and has been antagonistic to intelligent design arguments for decades. If Darwin’s theory were actually the powerful idea it’s claimed to be, Coyne should have been able to counter design easily, simply by summarizing its arguments and showing how Darwin deals with them. Yet he can’t even bring himself to mention what those arguments are. Instead he tries to whip up hysteria against a book that argues for what most people already believe. That speaks volumes about the actual strength of Darwin’s theory."
>
>https://evolutionnews.org/2019/03/bullet-points-for-jerry-coyne/

To be expected, given the known bias of the source.

>Reminds me of scientist's climate hysteria. Hmm. Would the credibility of science and scientists be on topic in a discussion of origins?

Possibly. Do you have a reputable source you'd like to cite
regarding the credibility of science and/or scientists?

[jillery]

Your nonsense non-sequiturs and asinine ad-hominems don't help
anything.

>Your stupid foul mouth certainly doesn't explain it.

I presume it's Jerry Coyne's words at which your blue nose is
sniffing. Take up your stupid foul mind with him.

[Alan Kleinman MD PhD]

Take a course in introductory probability theory and you might have a chance understanding stochastic processes (like evolution). But since you are choosing ignorance as a defense of your beliefs, it won't help.

>
>
> >Your stupid foul mouth certainly doesn't explain it.
>
>
> I presume it's Jerry Coyne's words at which your blue nose is
> sniffing. Take up your stupid foul mind with him.

No, it's your foul mouth. It shows whatever argument you had to defend your silly theory is long gone.

[jillery]

On Thu, 14 Mar 2019 13:04:30 -0700 (PDT), Alan Kleinman MD PhD

Nothing can help your stupid spam. Nobody needs a couse in
probability to know that as a certainty.

>> >Your stupid foul mouth certainly doesn't explain it.
>>
>>
>> I presume it's Jerry Coyne's words at which your blue nose is
>> sniffing. Take up your stupid foul mind with him.
>No, it's your foul mouth. It shows whatever argument you had to defend your silly theory is long gone.

I posted no argument here. You're just making up crap because you
know you have nothing intelligent to say.

[jillery]

On Wed, 13 Mar 2019 22:58:10 -0400, jillery <69jp...@gmail.com>

wrote:

>On Tue, 12 Mar 2019 17:39:51 -0400, jillery <69jp...@gmail.com>
>wrote:
>
>>On Tue, 12 Mar 2019 13:35:19 -0700 (PDT), Glenn <GlennS...@msn.com>
>>wrote:
>>
>>>"Coyne is quite the prominent evolutionary biologist, and has been antagonistic to intelligent design arguments for decades. If Darwin’s theory were actually the powerful idea it’s claimed to be, Coyne should have been able to counter design easily, simply by summarizing its arguments and showing how Darwin deals with them. Yet he can’t even bring himself to mention what those arguments are. Instead he tries to whip up hysteria against a book that argues for what most people already believe. That speaks volumes about the actual strength of Darwin’s theory."
>>>
>>>https://evolutionnews.org/2019/03/bullet-points-for-jerry-coyne/
>>>
>>>Reminds me of scientist's climate hysteria. Hmm. Would the credibility of science and scientists be on topic in a discussion of origins?
>>
>>
>>Michael Behe should have read Coyne's "Why Evolution Is True" before
>>he again proved he has no idea what he's talking about.
>
>
>Here's another WEIT article about Behe and his new book:
>
><https://whyevolutionistrue.wordpress.com/2019/03/13/behes-book-sliced-and-diced-again-by-members-of-his-own-department/>
>
><http://tinyurl.com/y3n2ypp2>
>
>************************************
>Behe and his Discovery Institute can’t abide this criticism, and have
>struck back, but their blows are ineffectual. Just today their flaccid
>house organ, Evolution News, issued four distinct attacks on me alone.
>I’m bursting with pride!
>
>[...]
>
>Now today a new review appeared in the prestigious journal Evolution.
>The kicker is that it’s by two members of Behe’s own department:
>assistant professor Gregory Lang, who works on microbial evolution,
>and assistant professor Amber Rice, an organismal evolutionist.
>***********************************
>

>I wonder if Evolution News' flaccid house organ would be helped by an
>organismal evolutionist


As if Behe needs yet another fish-slap in the face:

<https://whyevolutionistrue.wordpress.com/2019/03/14/the-evolution-of-irreducibly-complex-antifreeze-proteins-in-a-polar-fish-and-a-fish-slap-at-behe/>

<https://tinyurl.com/yyk39fs5>

Short version: Some arctic cod have a type of antifreeze in their
blood, which prevents ice crystals from forming in their bodies while
the fish swim in frigid Arctic waters. Phylogenetic studies show how
the DNA for the antifreeze protein, the DNA for a signal protein that
activates the antifreeze DNA, and a promoter DNA region that enables
the antifreeze transcription, all came from nonfunctional bits of the
fish genome and got cobbled together via translocations and
duplications.

This is a good refutation of Behe's "Devolved", and of his IC, which
claim that biological evolution can't assemble complex IC systems.
It's the kind of evidence which Behe and other IDiots can only wish
didn't exist.

[Glenn]

Suuure they did.

> nonfunctional bits of the
> fish genome and got cobbled together via translocations and
> duplications.
>
> This is a good refutation of Behe's "Devolved", and of his IC, which
> claim that biological evolution can't assemble complex IC systems.
> It's the kind of evidence which Behe and other IDiots can only wish
> didn't exist.
>

Right.

"There’s only one problem: it is all junk science."

https://evolutionnews.org/2019/02/at-last-the-details-of-how-proteins-evolve/

[Alan Kleinman MD PhD]

Take a course in introductory probability theory so you could understand something about stochastic processes (like Darwinian evolution). Then you could explain how the Kishony and Lenski experiments work. But you won't because that conflicts with your mathematically and empirically irrational belief system.

[jillery]

On Thu, 14 Mar 2019 20:27:48 -0700 (PDT), Glenn <GlennS...@msn.com>

Your mindless denials above show why you're a pseudo-skeptic, that you
deny without knowing what you're talking about. And then you cite an
article which uses the same mindless tactics. Take for example
Hunter's very first objection:
*****************************************
Why does a repeating genetic sequence “strongly suggest” that it
“evolved from repeated duplications?” What experiment revealed this
truth? What evidence gives us this profound principle? The answer, of
course, is that there is none. Nowhere do the evolutionists justify
this claim because there is no empirical justification.
******************************************

How does a repeating genetic sequence *not* suggest repeated
duplications? At the very least, it's plausible. And how does your
alleged skepticism *not* trip over Hunter's bald assertions of no
empirical justification? On what basis do you and Hunter presume the
scientists just made it up? Why do you mindlessly dismiss the
scientists' claims while at the same time mindlessly accept Hunter's
claims while Hunter mindlessly does exactly what he accuses the
scientists of doing?

In fact, the scientists' paper includes cites which support their
claims. Where are Hunter's cites? Where are your cites? Did you
even bother to check if maybe those scientists' cites do in fact
justify what Hunter claims has no justification? Based on your past
posts, my impression is you did not.

Hunter's article goes on to handwave away point after point, demanding
evidence for everything while at the same time providing no basis for
his own bald assertions.

Then Hunter really sticks his foot in his mouth:
*********************************
"We hypothesize that, upon the onset of selective pressure from cold
polar marine conditions, duplications of a 9-nt ancestral element in
the midst of the four GCA-rich duplicates occurred."

The above quote is an example of the non-empirical teleology that
pervades evolutionary thought. It was upon the onset of cold
conditions that the needed genetic duplications occurred. This is not
empirical; this is story-telling.
***********************************

Of course, the scientists made no teleological claim. They do *not*
say the mutations occurred *because* of cold polar conditions, as
Hunter misrepresents. Instead, they say the mutations appeared at the
time. Many other mutations appeared at the time, but those other
mutations provided no advantage at the time, but the mutations the
scientists identified *did* provide an advantage at the time. The
selective pressure amplified these mutations throughout the
population. That's how evolution works, not Hunter's imagined
teleology. Any storytelling here is strictly on Hunter's empty head.

[jillery]

On Fri, 15 Mar 2019 04:58:36 -0700 (PDT), Alan Kleinman MD PhD
<klei...@sti.net> wrote:

>Take a course in introductory probability theory

You first.

[Alan Kleinman MD PhD]

On Friday, March 15, 2019 at 6:00:04 AM UTC-7, jillery wrote:
> On Fri, 15 Mar 2019 04:58:36 -0700 (PDT), Alan Kleinman MD PhD
> <klei...@sti.net> wrote:
>
> >Take a course in introductory probability theory
>
>
> You first.

You are the one who needs it. Then you might have a chance to understand stochastic processes (like Darwinian evolution). And you might be able to explain simple evolutionary experiments like the Kishony and Lenski experiments. But you don't because it doesn't fit your mathematically and empirically irrational belief system.

[Glenn]

So much for anything else you blabber.

snip

[Percy Asknot]

If we agree that Creationism and/or ID is not science,
nothing's really settled. Both are specific and locked into
conclusions that are vigorously defended; there's no wiggle
room. The either-or nature of these defenses makes the whole
question of origins more complicated than it has to be.

Simply crying, "Science!" is not enough to settle anything
either. Since the whole question is reduced to two mutually
exclusive opposites, we may miss a third or even forth
alternative. The question is the origin and development of
life and, especially, intelligent life, not who gets to be
right.

There is nothing in our environment that demands a certain
answer. We first tell ourselves what must be true and then
pretend we can make the environment conform; we create a
bias. The history of philosophy provides the evidence that
we will believe what suits us. Dividing nature into just two
possible answers just means we only recognize two possible
questions.

Bill

[Alan Kleinman MD PhD]

If you want to understand how drug-resistance occurs and why cancer treatments fail, you had better correctly understand how Darwinian evolution works. And you won't get that correct explanation from someone who believes that reptiles can grow feathers.
>
> Bill

[jillery]

On Fri, 15 Mar 2019 06:13:16 -0700 (PDT), Alan Kleinman MD PhD

<klei...@sti.net> wrote:

>On Friday, March 15, 2019 at 6:00:04 AM UTC-7, jillery wrote:
>> On Fri, 15 Mar 2019 04:58:36 -0700 (PDT), Alan Kleinman MD PhD
>> <klei...@sti.net> wrote:
>>
>> >Take a course in introductory probability theory
>>
>>
>> You first.
>You are the one who needs it.

Really? So how come you can't explain your highly improbable
existence?

[jillery]

On Fri, 15 Mar 2019 08:51:06 -0700 (PDT), Glenn <GlennS...@msn.com>

<restore your dishonest and cowardly snip>

>>Your mindless denials above show why you're a pseudo-skeptic, that you

>So much for anything else you blabber.

Right here would have been a good place for you to have identified
what you think I "blabbered" and why you so think. That you didn't
shows you know you have no idea what you're talking about, and are
proud of it.

[Alan Kleinman MD PhD]

On Friday, March 15, 2019 at 3:35:03 PM UTC-7, jillery wrote:
> On Fri, 15 Mar 2019 06:13:16 -0700 (PDT), Alan Kleinman MD PhD
> <klei...@sti.net> wrote:
>
> >On Friday, March 15, 2019 at 6:00:04 AM UTC-7, jillery wrote:
> >> On Fri, 15 Mar 2019 04:58:36 -0700 (PDT), Alan Kleinman MD PhD
> >> <klei...@sti.net> wrote:
> >>
> >> >Take a course in introductory probability theory
> >>
> >>
> >> You first.
> >You are the one who needs it.
>
>
> Really? So how come you can't explain your highly improbable
> existence?

Do I have to explain everything to you? Isn't it enough that I explain how evolution works?

[Glenn]

On Friday, March 15, 2019 at 1:05:04 PM UTC-7, Bill wrote:

I think you're going in the right direction here. There are, though, other factors which should cause you to separate the "we" beside what you identify.
This doesn't mean that any "side" all wear white hats and play the ukulele.

[Mark Isaak]

On 3/15/19 1:01 PM, Percy Asknot wrote:
> Glenn wrote:
>
>> On Friday, March 15, 2019 at 5:55:03 AM UTC-7, jillery
>> wrote:
>>> On Thu, 14 Mar 2019 20:27:48 -0700 (PDT), Glenn
>>> <GlennS...@msn.com> wrote:
>>>
>>>> On Thursday, March 14, 2019 at 7:55:03 PM UTC-7, jillery
>>>> wrote:
>>>>>

>>>>> <https://tinyurl.com/yyk39fs5>
>>>>> [...]

>>>>> This is a good refutation of Behe's "Devolved", and of
>>>>> his IC, which claim that biological evolution can't
>>>>> assemble complex IC systems. It's the kind of evidence
>>>>> which Behe and other IDiots can only wish didn't
>>>>> exist.
>>>>>
>>>> Right.
>>>>
>>>> "There’s only one problem: it is all junk science."
>>>>
>>>> https://evolutionnews.org/2019/02/at-last-the-details-of-how-proteins-evolve/
>>>
>>> Your mindless denials above show why you're a
>>> pseudo-skeptic, that you deny without knowing what you're
>>> talking about.
>>
>> So much for anything else you blabber.
>>
>> snip
>
> If we agree that Creationism and/or ID is not science,

> nothing's really settled. [...]

No field of study is or is not science, dead stop. Whether what you are
doing is science or not depends on what questions you ask, how you
approach answering them, and how you interpret the data when you get it.
Creationism can include science (such as questions regarding flood
geology), and physics can include bullshit.

I had the opportunity of helping to judge a science fair yesterday, for
students in 8th grade. A pair of students for one project added varying
amounts of calcium to plants watered with fluoridated water, measured
growth, and concluded that calcium can help to overcome the unhealthy
effects of fluoride in plants and animals. That was not science. If
they had simply concluded that calcium can help plant growth, that would
be science, but they did not vary fluoride at all, much less look at
anything but one species of plant, so their conclusion did not match
their experiment. From talking to them, it was obvious that they were
dogmatic on the subject of fluoridated water, and that zeal apparently
affected their interpretation of their data. Other projects addressed
pretty much the same subject (factors affecting plant growth) and really
were decent science.

When creationists ask questions which can be answered by gathering and
examining data, and when they do not overinterpret the data into realms
far beyond what the data show, then I am happy to acknowledge
creationists doing science. It does happen, but it doesn't get a lot of
notice when it does (mostly, I think, because the findings are minor),
and it does not happen nearly as much as non-creationist science.

--
Mark Isaak eciton (at) curioustaxonomy (dot) net
"Omnia disce. Videbis postea nihil esse superfluum."
- Hugh of St. Victor

[jillery]

On Fri, 15 Mar 2019 16:11:59 -0700 (PDT), Alan Kleinman MD PhD

<klei...@sti.net> wrote:

>On Friday, March 15, 2019 at 3:35:03 PM UTC-7, jillery wrote:
>> On Fri, 15 Mar 2019 06:13:16 -0700 (PDT), Alan Kleinman MD PhD
>> <klei...@sti.net> wrote:
>>
>> >On Friday, March 15, 2019 at 6:00:04 AM UTC-7, jillery wrote:
>> >> On Fri, 15 Mar 2019 04:58:36 -0700 (PDT), Alan Kleinman MD PhD
>> >> <klei...@sti.net> wrote:
>> >>
>> >> >Take a course in introductory probability theory
>> >>
>> >>
>> >> You first.
>> >You are the one who needs it.
>>
>>
>> Really? So how come you can't explain your highly improbable
>> existence?
>Do I have to explain everything to you? Isn't it enough that I explain how evolution works?

Since you asked, no. Instead, try to explain what was asked. You're
welcome.

[Percy Asknot]

You reduce all non standard science to Creationism/ID as if
no other point of view either exists or is possible. Your
bete noire is just a tired old strawman. You contend with
the easiest opponent and fancy yourself the champion of
Science.

Bill

[Bob Casanova]

On Sat, 16 Mar 2019 10:25:35 -0500, the following appeared
in talk.origins, posted by Percy Asknot <fre...@gmail.com>:

Perhaps, while keeping in mind what science is (and what it
is not), you could explain how the content of Mark's post
was incorrect...?

And exactly what (again keeping in mind what science is and
what it is not) is "non standard science"?

Every post you make seems to show that you really don't
understand what science is and how it works to increase our
knowledge of the physical universe; you seem to think it's
"just another belief system", which is why I suspect you are
so adamant in your insistence that "everything is
subjective" and that we cannot know anything about reality.

[jillery]

On Sat, 16 Mar 2019 10:25:35 -0500, Percy Asknot <fre...@gmail.com>
wrote:

Not all, just the ones who assume a purposeful intelligent Creator.
And not the easiest, just the most evangelical. They may be the same
group, but your implied motives are incorrect.

[Edna Freon]

Bob Casanova wrote:

...

>
> Every post you make seems to show that you really don't
> understand what science is and how it works to increase
> our knowledge of the physical universe; you seem to think
> it's "just another belief system", which is why I suspect
> you are so adamant in your insistence that "everything is
> subjective" and that we cannot know anything about
> reality.

What I understand is the view that all matter is composed of
atoms. What we experience is how the atoms accumulate into
"things" that we perceive. These are vast clouds of atoms
and the clouds are perceptions, not things. This is all
based on conventional science.

The reality is the perception. What we believe about reality
is what we know, through science, is not "there" in any
physical sense; it is apparent. The reality we believe we
experience, only exists to beings having some suite of very
specialized perceptions. Why is this so problematic?

Bill

[*Hemidactylus*]

Edna Freon <fre...@gmail.com> wrote:
> Bob Casanova wrote:
>
> ...
>
>>
>> Every post you make seems to show that you really don't
>> understand what science is and how it works to increase
>> our knowledge of the physical universe; you seem to think
>> it's "just another belief system", which is why I suspect
>> you are so adamant in your insistence that "everything is
>> subjective" and that we cannot know anything about
>> reality.
>
> What I understand is the view that all matter is composed of
> atoms.
>

Where did “you” get that “idea”, which itself nothing more than
reverberation amongst atoms in a nervous system.

>
> What we experience is how the atoms accumulate into
> "things" that we perceive.

There is no “we” here. Just reverberation amongst “things” unworthy of
ontological status as neurons. Have you met our resident emergentist
jonathan? Your radical reductionism would seem fighting words to him.

> These are vast clouds of atoms
> and the clouds are perceptions, not things. This is all
> based on conventional science.
>

Neuroscience? Psychology? Sociology?

>
> The reality is the perception.

Thank you Bishop Berkeley. And we all know what sustains reality when we’re
not looking right?

> What we believe about reality
> is what we know, through science, is not "there" in any
> physical sense; it is apparent.

What tips the scales or registers on instruments? Water is a mere
perceptive cloud, yet I doubt you would jump from an illusory object
commonly referred to as a “cruise ship” into an ocean in the middle of the
night ( absence of sunlight blocked by the solid object called Earth
without a “floatation device”. That is reality encapsulated right there.
With any luck sunlight reflected back from an illusory object called the
moon would give you enough ambience to detect that ominous shark fin. But
relax, that shark isn’t really there or hungry as it is just a perceptive
cloud. And severe blood loss from a severed leg can’t really be fatal at
the level of quarks.

> The reality we believe we
> experience, only exists to beings having some suite of very
> specialized perceptions. Why is this so problematic?
>

Well since you are merely a perceptive cloud needing an Ultimate Mind to
sustain you between posts when we can’t infer your existence due to lack of
effect on the world, the rest of us can dismiss you as nothing more than an
ephemeral pond or mirage. Thus your “arguments” evaporate too, given they
imply your continued existence, intentionality, and capacity to marshal
evidence and reason. Or maybe you are truly a solipsist that argues with
itself.

[Percy Asknot]

You made no argument and applied no logic. All you've
contributed is yet another collection of baseless
assumption.

Bill

[Percy Asknot]

You reject a purposeful intelligent Creator without
explaining why. An assumption of atheism is not an argument,
just a bias. Since you, and those to whom you ally yourself,
adamantly deny the existence of such a entity, with no
evidence beyond your personal prejudices, no discussion is
possible.

Bill

[Burkhard]

quite possible- you would know - as it is merely a reformulation of the
point you yourself make

[*Hemidactylus*]

Ironymeter explosion rocks newsgroup. News at 11.

[Percy Asknot]

Ridicule is not an argument. Can you explain the error in my
post that justifies the snarky reply? What is likelier is
that since my point cannot be cogently refuted, it must
simply be denied. Why burden yourself with thoughts you
can't understand or that might ramify in ways that challenge
your favorite prejudices? Ridicule might work of course,
especially in this newsgroup.

Bill

[*Hemidactylus*]

Bill has effectively evaporated himself out of the game as it takes more
than perception clouds of atoms to post an argument. He lacks substance and
coherence. It is an amazing feat that an ephemeral cloud named Bill bothers
to dress itself every morning. What’s the point lacking a solid perspective
above the subatomic level?

[*Hemidactylus*]

I am perceiving nothing more than a cloud of atoms, not output of a being
who has a cogent point to make. A cogent point would stand out as a salient
“thing” and those cannot exist by your reckoning.

Self-refutation is your strong suit. You do it so often and so thoroughly.

[Percy Asknot]

Odd that you see irony but can't explain how it applies to
my post. If my posts are really that weak, it should be no
great feat to refute them. They rarely are so it seems more
likely that they are simply being avoided. You would seem
somewhat less foolish if you said nothing at all.

Bill

[Percy Asknot]

So, matter is not made of smaller parts (atoms, for
instance)? All that we see is indivisible, there are no
constituent parts, no particles. Everything is exactly as it
appears to the observer. Do the physicists know this yet?

Bill

[*Hemidactylus*]

You’re not there in any physical sense. I think that pretty much nips it in
the illusory bud. Illusions can’t make arguments warranting a response.
They surely don’t share a common ontological or epistemic space with other
illusions they are for some reason trying to persuade by shooting
themselves in the foot with long dead idealistic nonsense.

[*Hemidactylus*]

I’m sorry. Is the quark trying to make a point given a brain is not a
“thing”?

[Percy Asknot]

As I pointed out above: you would do better saying nothing
rather than saying nothing so loudly that everyone knows you
have nothing to say. You weave and dodge, avoiding any reply
that might actually address my point(s), giving the
impression that you can't.

You would like to blame me for your shallow blather and,
lucky for you, this newsgroup is the perfect place to get
away with it.

Bill

Bill

[Glenn]

Are you sure you don't have brain cancer?

[*Hemidactylus*]

“You”’re the one who denies their own existence, albeit implicitly. You
said “vast clouds of atoms and the clouds are perceptions, not things” and
“What we believe about reality is what we know, through science, is not
"there" in any physical sense; it is apparent.” Therefore you don’t exist.
You implied it yourself in your own reality dismissive rhetoric. That you
can’t own it when called out is your problem not mine.

Now if you would merely admit you possess a physically instantiated object
call a brain that exists in an objective reality shared with other humans,
we may make some progress in being able to take you seriously. Even then
there will be a long road ahead as you will then need to admit your brain
functions to produce behavior that has effects on computer networks that
depend on electricity. Network cables and routers are real too, just like
brains. Baby steps.

[*Hemidactylus*]

What sort of person asks a question like that?

[Burkhard]

His post is an exact rendition of your post. If you find his post
snarky, then yours was as well.

[*Hemidactylus*]

Explain yourself Glenn!

[Percy Asknot]

Taking a baby step (for your benefit), I do not deny the
existence of brains or their various functions. That has not
been my point. I have said that the perceptions a brain
processes are of "things" that only exist as perceptions.

I suggest further, that since perceptions only occur in
living organisms, they are not fundamental nor absolute.
Perception is derivative, a consequence of life and not a
physical thing. We accept the perception as real which tells
us only that it creates its own reality.

For some obscure reason this confounds most posters here.
There is a kind of need to avoid admitting that what is
believed real, is merely appearance. Maybe the concept seems
supernatural (which of course, it is) and that scares some
people. Since this concept will not be discussed, the trend
is to ridicule whomever brings it up.

Bill

[Mark Isaak]

Who are you talking to? Not me, since I just did the exact opposite of
what you said.

[*Hemidactylus*]

Ok.

> That has not
> been my point. I have said that the perceptions a brain
> processes are of "things" that only exist as perceptions.
>

Are brains “things”?

>
> I suggest further, that since perceptions only occur in
> living organisms, they are not fundamental nor absolute.
> Perception is derivative, a consequence of life and not a
> physical thing.

I was with you up until that last bit. Yes perception is derivative. That
is actually an excellent point. But it is still physical.

> We accept the perception as real which tells
> us only that it creates its own reality.
>

Ok your crispness went soggy.

>
> For some obscure reason this confounds most posters here.
>

I wonder why. And we were making so much headway.

>
> There is a kind of need to avoid admitting that what is
> believed real, is merely appearance.

Science can peel the scales (appearances) from our eyes. Sure it has
limits, but damn you act as though we can’t pop our epistemic bubbles. The
Copernican revolution, evolution, germ theory, relativity, and QM were huge
leaps in our knowledge.

> Maybe the concept seems
> supernatural (which of course, it is) and that scares some
> people.

Ok you just left the field of play due to a flagrant foul right there.

> Since this concept will not be discussed, the trend
> is to ridicule whomever brings it up.
>

I wonder why.

[Percy Asknot]

Sorry. I aimed my remarks at those in the School of
Scientism, the Defenders of Unscientific Science. The same
folks who condemn just about everyone as Creationists. Or,
the majority of posters here.

Bill

[*Hemidactylus*]

I hate scientism.

[Percy Asknot]

Science improves the focus and sharpens the edges of
appearances but the appearances remain. Everything that's
been thought about it "The Copernican revolution,
evolution, germ theory, relativity, and QM" are about what
the appearances appear to be.

If everything is made of atoms and the forces that bind
them, then atoms are the only physical entities. That's
pretty obvious. We know what we perceive is a collection of
atoms yet call the collection real. How can that be?

>> Maybe the concept seems
>> supernatural (which of course, it is) and that scares
>> some people.
>
> Ok you just left the field of play due to a flagrant foul
> right there.

What's the foul? The word, "supernatural"? Consider that the
brain creates thought. Once created, it becomes "mind",
something other than the physical brain. Thinking is,
literally, supernatural.

Bill

[jillery]

On Sat, 16 Mar 2019 16:25:13 -0500, Percy Asknot <fre...@gmail.com>

wrote:

>jillery wrote:
>
>> On Sat, 16 Mar 2019 10:25:35 -0500, Percy Asknot
>> <fre...@gmail.com> wrote:
>>
>>>Mark Isaak wrote:
>>>
>>>> On 3/15/19 1:01 PM, Percy Asknot wrote:
>>>>> Glenn wrote:
>>>>>
>>>>>> On Friday, March 15, 2019 at 5:55:03 AM UTC-7, jillery
>>>>>> wrote:
>>>>>>> On Thu, 14 Mar 2019 20:27:48 -0700 (PDT), Glenn
>>>>>>> <GlennS...@msn.com> wrote:
>>>>>>>
>>>>>>>> On Thursday, March 14, 2019 at 7:55:03 PM UTC-7,
>>>>>>>> jillery wrote:
>>>>>>>>>
>>>>>>>>> <https://tinyurl.com/yyk39fs5>
>>>>>>>>> [...]
>>>>>>>>> This is a good refutation of Behe's "Devolved", and
>>>>>>>>> of his IC, which claim that biological evolution
>>>>>>>>> can't assemble complex IC systems. It's the kind of
>>>>>>>>> evidence which Behe and other IDiots can only wish
>>>>>>>>> didn't exist.
>>>>>>>>>
>>>>>>>> Right.
>>>>>>>>

>>>>>>>> "There?s only one problem: it is all junk science."

No, I didn't reject anything above. I just merely corrected your
overly broad generalities. But I have rejected a purposeful
intelligent Creator before, but usually accompanied by an explanation,
specifically that a purposeful intelligent Creator is a poor
explanation, poor in the sense that a purposeful intelligent Creator
as a cause is consistent with all possible effects and all possible
outcomes, and so doesn't distinguish among them.

Invoking a purposeful intelligent Creator might help with your warm
fuzzy feelings, but as a link in a coherent chain of reasoning, it's
useless.

>An assumption of atheism is not an argument,
>just a bias. Since you, and those to whom you ally yourself,
>adamantly deny the existence of such a entity, with no
>evidence beyond your personal prejudices, no discussion is
>possible.

There's your problem. I don't deny the existence of such an entity.
Instead, I do deny that invoking its existence has explanatory
utility. You like to pretend I deny its existence so you don't have
to explain how invoking its existence informs how the universe works.

Ok, I stipulate for argument's sake a purposeful intelligent Creator
exists. Now your turn. Where do you take the conversation from
there? You do want to have a conversation, don't you?

--
I disapprove of what you say, but I will defend to the death your right to say it.

Evelyn Beatrice Hall
Attributed to Voltaire

[jillery]

In the spirit of avoiding talking past each other, it would be helpful
if each of you posted at least one example of what you mean by
"scientism".

[*Hemidactylus*]

Going beyond the purview of science by jumping the tracks on what Gould
refers to masterfully in *Hedgehog, the Fox, and the Magister's Pox* as
magisteria. Sam Harris did so in *The Moral Landscape* by collapsing
science and morality. EO Wilson may have in the way he adapted Whelwell’s
term consilience to subsumption of humanities into science. I am following
Gould in the latter. Since Pinker enthusiastically endorses Wilson’s
approach in his strawman polemics against a bogeyman Second Culture of wine
drinking literati (fashioning himself as the Second Coming of CP Snow in
*Enlightenment Now*) he too crosses the line a bit.

TH Huxley was merely championing the cause for including science in the
curriculum in his showdown with classicist Matthew Arnold, though he was
characterized as devaluing classicism and collapsing the magisteria by
Lionel Trilling. Huxley was reacting to the Ancients who felt the
understanding of Greek and Roman language and culture were paramount and
sacred, an attitude going back to the Renaissance and Scholasticism who
thought Aristotle (and Galen) had said everything that needed to be known
of the natural world (OK that may be a characterization).

The parochial and arrogant attitude of some scientists (eg- Steven
Weinberg) toward philosophy is also scientism.

[Bill Rogers]

OK Here's the problem. You say "we know that what we perceive is a collection of atoms, yet call the collection real."

First, why wouldn't the collection be real? You have no trouble attributing reality to atoms, but they are just collections of protons, neutrons, and electrons.

Second, you yourself are a collection of atoms. If you are unwilling to attribute reality to collections of atoms, then you are not real yourself.

Third, how do you think you know that things are collections of atoms, anyway? If our macroscopic perceptions are unreal or totally subjective, how can you know about atoms in the first place? Everything you think you know about the reality of atoms comes from people using macroscopic perception to look at pieces of macroscopic lab equipment, doing experiments, thinking about evidence, building more lab equipment and looking at what it does, using their own regular perceptions. If our perceptions are totally subjective, how much moreso concepts like atoms which derive from a long chain of subjective perceptions of lab equipment and subjective reasoning about those perceptions.

That's the heart of the problem. If you are unwilling to say that our perceptions tell us something real and reliable about external reality, even if they are imperfect and don't give us the whole story, then you are stuck. You then have no basis to assert anything about anything except your own entirely subjective preferred belief.

[jillery]

On Sun, 17 Mar 2019 04:52:41 -0500, *Hemidactylus*
<ecph...@allspamis.invalid> wrote:

>jillery <69jp...@gmail.com> wrote:
>> On Sat, 16 Mar 2019 19:58:09 -0500, *Hemidactylus*
>> <ecph...@allspamis.invalid> wrote:
>>
>>> Percy Asknot <fre...@gmail.com> wrote:
>>>> Mark Isaak wrote:
>>>>
>>>>> On 3/16/19 8:25 AM, Percy Asknot wrote:

[...]

Ok, now let's see if Bill aka Percy agrees with your examples and/or
provides any of his own, assuming that he really wants to have a
discussion.

[Percy Asknot]

Your belief that nature is just accidental accumulations of
inert stuff forming a kind of machine, is a good example of
warm fuzzy feelings. It might feel good to believe that
everything is knowable and predictable and makes perfect
mechanistic sense but it's just substitute for some other
warm and fuzzy feelings.

>
>
>
>>An assumption of atheism is not an argument,
>>just a bias. Since you, and those to whom you ally
>>yourself, adamantly deny the existence of such a entity,
>>with no evidence beyond your personal prejudices, no
>>discussion is possible.
>
>
> There's your problem. I don't deny the existence of such
> an entity. Instead, I do deny that invoking its existence
> has explanatory
> utility. You like to pretend I deny its existence so you
> don't have to explain how invoking its existence informs
> how the universe works.
>
> Ok, I stipulate for argument's sake a purposeful
> intelligent Creator
> exists. Now your turn. Where do you take the
> conversation from
> there? You do want to have a conversation, don't you?
>

As I mentioned elsewhere, human reality is illusory, made of
human perceptions. We have built an elaborate complex of
interdependent concepts that we believe explains all the
important stuff. But concepts are not physical entities,
cannot be measured or quantified or otherwise verified, they
are literally, supernatural.

A Creator may not be required for the physical reality we
experience, but it is the only plausible cause of the
consciousness behind the concepts we take so seriously.
Consciousness is something you experience but not quantify
so it's not accessible to science and, probably not
something reducible to nature. We have to consider another
source.

Bill

[Percy Asknot]

As far as scientism goes, I agree. I might go further and
add that scientism is a reverence for Science, a plugin
replacement for deities. Add to that the militant disdain
for those who hold other views and scientism looks a lot
like a cult.

Bill

[Trolidan Troltar]

On 3/16/19 8:25 AM, Percy Asknot wrote:> Mark Isaak wrote:
>
>> On 3/15/19 1:01 PM, Percy Asknot wrote:
>>> Glenn wrote:
>>>
>>>> On Friday, March 15, 2019 at 5:55:03 AM UTC-7, jillery
>>>> wrote:
>>>>> On Thu, 14 Mar 2019 20:27:48 -0700 (PDT), Glenn
>>>>> <GlennS...@msn.com> wrote:
>>>>>
>>>>>> On Thursday, March 14, 2019 at 7:55:03 PM UTC-7,
>>>>>> jillery wrote:
>>>>>>>
>>>>>>> <https://tinyurl.com/yyk39fs5>
>>>>>>> [...]
>>>>>>> This is a good refutation of Behe's "Devolved", and
>>>>>>> of his IC, which claim that biological evolution
>>>>>>> can't assemble complex IC systems. It's the kind of
>>>>>>> evidence which Behe and other IDiots can only wish
>>>>>>> didn't exist.
>>>>>>>
>>>>>> Right.
>>>>>>

>>>>>> "There’s only one problem: it is all junk science."

>>>>>>
>>>>>>
https://evolutionnews.org/2019/02/at-last-the-details-of-how-proteins-evolve/
>>>>>
>>>>> Your mindless denials above show why you're a
>>>>> pseudo-skeptic, that you deny without knowing what
>>>>> you're talking about.
>>>>
>>>> So much for anything else you blabber.
>>>>
>>>> snip
>>>

> no other point of view either exists or is possible. Your
> bete noire is just a tired old strawman. You contend with
> the easiest opponent and fancy yourself the champion of
> Science.
>
> Bill

Also he is taking standard science and painting his own
viewpoint into it.

If the ones doing standard science aren't saying their own
viewpoints it is his bias to say that they are all
non-creationists without asking them.

As for whether any field of study can not be a 'science'
such as art, mathematics, religion, philosophy, law,
psychology, astrology, or others that depends on
what a 'science' is.

[Bob Casanova]

On Sat, 16 Mar 2019 13:38:14 -0500, the following appeared
in talk.origins, posted by Edna Freon <fre...@gmail.com>:

>Bob Casanova wrote:

>> Every post you make seems to show that you really don't
>> understand what science is and how it works to increase
>> our knowledge of the physical universe; you seem to think
>> it's "just another belief system", which is why I suspect
>> you are so adamant in your insistence that "everything is
>> subjective" and that we cannot know anything about
>> reality.

>What I understand is the view that all matter is composed of

>atoms. What we experience is how the atoms accumulate into
>"things" that we perceive. These are vast clouds of atoms

>and the clouds are perceptions, not things. This is all
>based on conventional science.
>

>The reality is the perception. What we believe about reality

>is what we know, through science, is not "there" in any

>physical sense; it is apparent. The reality we believe we

>experience, only exists to beings having some suite of very
>specialized perceptions. Why is this so problematic?

It's problematic because it's solely your opinion that
everything is subjective; you have zero evidence that this
is correct.

But let's restore the part you snipped (the referenced post
by Mark, the content of which you snipped, is still
available for anyone who cares to check what he posted):

"Perhaps, while keeping in mind what science is (and what it
is not), you could explain how the content of Mark's post
was incorrect...?

And exactly what (again keeping in mind what science is and
what it is not) is 'non standard science'?"

What is so difficult about those two questions that you have
to evade them?
--

Bob C.

"The most exciting phrase to hear in science,
the one that heralds new discoveries, is not
'Eureka!' but 'That's funny...'"

- Isaac Asimov

[Bob Casanova]

On Sat, 16 Mar 2019 16:28:56 -0500, the following appeared
in talk.origins, posted by Percy Asknot <fre...@gmail.com>:

>*Hemidactylus* wrote:
>
>> Edna Freon <fre...@gmail.com> wrote:
>>> Bob Casanova wrote:
>>>
>>> ...
>>>
>>>>

>>>> Every post you make seems to show that you really don't
>>>> understand what science is and how it works to increase
>>>> our knowledge of the physical universe; you seem to
>>>> think it's "just another belief system", which is why I
>>>> suspect you are so adamant in your insistence that
>>>> "everything is subjective" and that we cannot know
>>>> anything about reality.
>>>
>>> What I understand is the view that all matter is composed
>>> of atoms.
>>>

>> Where did “you” get that “idea”, which itself nothing more
>> than reverberation amongst atoms in a nervous system.
>>>

>>> What we experience is how the atoms accumulate into
>>> "things" that we perceive.
>>

>> There is no “we” here. Just reverberation amongst “things”
>> unworthy of ontological status as neurons. Have you met
>> our resident emergentist jonathan? Your radical
>> reductionism would seem fighting words to him.
>>

>>> These are vast clouds of atoms
>>> and the clouds are perceptions, not things. This is all
>>> based on conventional science.
>>>

>> Neuroscience? Psychology? Sociology?

>>>
>>> The reality is the perception.
>>

>> Thank you Bishop Berkeley. And we all know what sustains
>> reality when we’re not looking right?
>>

>>> What we believe about reality
>>> is what we know, through science, is not "there" in any
>>> physical sense; it is apparent.
>>

>> What tips the scales or registers on instruments? Water is
>> a mere perceptive cloud, yet I doubt you would jump from
>> an illusory object commonly referred to as a “cruise ship”
>> into an ocean in the middle of the night ( absence of
>> sunlight blocked by the solid object called Earth without
>> a “floatation device”. That is reality encapsulated right
>> there. With any luck sunlight reflected back from an
>> illusory object called the moon would give you enough
>> ambience to detect that ominous shark fin. But relax, that
>> shark isn’t really there or hungry as it is just a
>> perceptive cloud. And severe blood loss from a severed leg
>> can’t really be fatal at the level of quarks.
>>

>>> The reality we believe we
>>> experience, only exists to beings having some suite of
>>> very specialized perceptions. Why is this so problematic?
>>>

>> Well since you are merely a perceptive cloud needing an
>> Ultimate Mind to sustain you between posts when we can’t
>> infer your existence due to lack of effect on the world,
>> the rest of us can dismiss you as nothing more than an
>> ephemeral pond or mirage. Thus your “arguments” evaporate
>> too, given they imply your continued existence,
>> intentionality, and capacity to marshal evidence and
>> reason. Or maybe you are truly a solipsist that argues
>> with itself.
>
>You made no argument and applied no logic. All you've
>contributed is yet another collection of baseless
>assumption.

The irony, it *burns*!

[Bob Casanova]

On Sat, 16 Mar 2019 18:15:40 -0500, the following appeared
in talk.origins, posted by *Hemidactylus*
<ecph...@allspamis.invalid>:

The "Glenn sort".

[Bob Casanova]

On Sat, 16 Mar 2019 15:56:03 -0700 (PDT), the following
appeared in talk.origins, posted by Glenn
<GlennS...@msn.com>:

Nothing rational to add, as usual? OK.

[jillery]

On Sun, 17 Mar 2019 11:35:08 -0500, Percy Asknot <fre...@gmail.com>
wrote:

>>>adapted Whelwell?s term consilience to subsumption of

>>>humanities into science. I am following Gould in the

>>>latter. Since Pinker enthusiastically endorses Wilson?s

Ok then, since you and Hemidactylus have a rough agreement on what is
scientism, ISTM the next step is to explain how you accuse him of
scientism while he says he hates it. Clearly one or both of you
is/are incorrect.

[jillery]

On Sun, 17 Mar 2019 11:30:28 -0500, Percy Asknot <fre...@gmail.com>

I neither stated nor implied that I believe everything is knowable,
nor are my conclusions based on it. And you assert a false
equivalence. My confidence in explanations from material science is
not a belief, but is based on the ability of those explanations to
identify cause and effect and predict future outcomes. There is no
meaningful comparison between that and invoking the existence of a
purposeful intelligent Creator. Once again, you assert an equivalence
so you don't have to explain how invoking a Creator informs how the

How do you know a Creator is the *only* plausible cause of
consciousness? How is a purposeful intelligent Creator even
plausible? Presenting your opinions as facts not in evidence is a
poor way to start a conversation.

[*Hemidactylus*]

No answer? That figures.

[Alan Kleinman MD PhD]

On Friday, March 15, 2019 at 5:05:02 PM UTC-7, Mark Isaak wrote:
> On 3/15/19 1:01 PM, Percy Asknot wrote:
> > Glenn wrote:
> >
> >> On Friday, March 15, 2019 at 5:55:03 AM UTC-7, jillery
> >> wrote:
> >>> On Thu, 14 Mar 2019 20:27:48 -0700 (PDT), Glenn
> >>> <GlennS...@msn.com> wrote:
> >>>
> >>>> On Thursday, March 14, 2019 at 7:55:03 PM UTC-7, jillery
> >>>> wrote:
> >>>>>
> >>>>> <https://tinyurl.com/yyk39fs5>
> >>>>> [...]
> >>>>> This is a good refutation of Behe's "Devolved", and of
> >>>>> his IC, which claim that biological evolution can't
> >>>>> assemble complex IC systems. It's the kind of evidence
> >>>>> which Behe and other IDiots can only wish didn't
> >>>>> exist.
> >>>>>
> >>>> Right.
> >>>>

> >>>> "There’s only one problem: it is all junk science."

Does BookMark think that it takes a billion replications for each evolutionary step in the Kishony and Lenski experiments is "overinterpret"ing the data, especially in light of the fact the mutation rate is e-9? And what does BookMark think about the adaptation of any other replicator by rmns is suggested by this data?

[Alan Kleinman MD PhD]

On Saturday, March 16, 2019 at 10:35:02 AM UTC-7, Bob Casanova wrote:
> On Sat, 16 Mar 2019 10:25:35 -0500, the following appeared
> in talk.origins, posted by Percy Asknot <fre...@gmail.com>:

> >You reduce all non standard science to Creationism/ID as if
> >no other point of view either exists or is possible. Your
> >bete noire is just a tired old strawman. You contend with
> >the easiest opponent and fancy yourself the champion of
> >Science.
>

> Perhaps, while keeping in mind what science is (and what it
> is not), you could explain how the content of Mark's post
> was incorrect...?
>
> And exactly what (again keeping in mind what science is and
> what it is not) is "non standard science"?
>

> Every post you make seems to show that you really don't
> understand what science is and how it works to increase our
> knowledge of the physical universe; you seem to think it's
> "just another belief system", which is why I suspect you are
> so adamant in your insistence that "everything is
> subjective" and that we cannot know anything about reality.

dimmy didn't get anything out of his two courses in statistics but thinks he has mastered evolutionary science. Perhaps dimmy wants to describe the stochastic process that is occurring with the Kishony experiment based on his ignorance he has gathered in his failure to get anything out of his two courses in statistics.

[Bob Casanova]

On Mon, 18 Mar 2019 05:46:32 -0700 (PDT), the following
appeared in talk.origins, posted by Alan Kleinman MD PhD
<klei...@sti.net>:

Nothing relevant to contribute, as usual? OK.

[Alan Kleinman MD PhD]

Is this the greatest intellect that the reptifeatharians have to offer?

[Bob Casanova]

On Mon, 18 Mar 2019 11:14:32 -0700 (PDT), the following

It's not an "intellect", Sparky, it's an observation of the
lack of anything relevant from you. *Do* try to keep up.

[Alan Kleinman MD PhD]

If you had kept up on your two courses in statistics, you might understand this discussion.

[Bob Casanova]

On Tue, 19 Mar 2019 11:49:34 -0700 (PDT), the following

A-a-a-a-nd, we're back to the usual irrelevancies.

[Alan Kleinman MD PhD]

Just because you don't understand introductory probability theory doesn't make it irrelevant. But it does explain why you don't understand how stochastic processes work (like evolution).