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Good, you learned something. So tell everyone the mathematical reason why it takes a billion replications for each adaptive mutational step in that video.Again, you either fail to comprehend the context of the message or choose not to.
I do not feel like taking your "math quiz" as you assess my worthiness to discuss your work.
I learned more from the 3 minute video you posted about the Kishony experiment than 3+ days of your postings.
So you have observed macroevolution?If you really don't understand how observation and field work can be experiments, then there is really no hope for you to understand the nature of science, particularly as related to a science like evolution.
He may not have, but others have. I do believe that I already posted links on observing macroevolution. Perhaps you do not understand what macroevolution is.So you have observed macroevolution?
Good, you learned something. So tell everyone the mathematical reason why it takes a billion replications for each adaptive mutational step in that video.
There are journals that will publish almost anything as long as they are paid. Funny, they all seem to be open access journals. Hmm, isn't Statistics in Medicine open access?As I said, I'm not doing math performance for you.
Your paper tells me nothing I needed to know to estimate the probability of 1 billion events with 1 in 1 billion probability happening that I didn't already know. That's what really surprises me about the publication of that paper, I would think a journal titled "Statistics in Medicine" would have dismissed it as trivial.
I don't do trivial science.
How sad, you won't tell us what you learned.As I said, I'm not doing math performance for you.
They would have dismissed this paper because of its triviality except it demonstrated a trivial empirical fact of life of how adaptive evolution to a single selection pressure operates and drug resistance evolves. It's really pretty amazing when you think about it. Such a simple mathematical equation describes that on the surface seem such a confusing physical phenomenon. I can't say no one ever noticed this before me. My 5th-grade science teacher saw this mathematical relationship and started the derivation on the chalkboard. That was more than half a century ago. If it took me that long to fully understand that 5th-grade lecture, I guess I should understand why it takes so long for a macroevolutionist to understand it.Your paper tells me nothing I needed to know to estimate the probability of 1 billion events with 1 in 1 billion probability happening that I didn't already know. That's what really surprises me about the publication of that paper, I would think a journal titled "Statistics in Medicine" would have dismissed it as trivial.
Strange you would say that about this subject. Most people would say the evolution of drug resistance, herbicide resistance, pesticide resistance, and why cancer treatments fail is not trivial. The math may be trivial but not the physical consequences. But, to each his own, you go on and figure out your macro-science.I don't do trivial science.
They would have dismissed this paper because of its triviality except it demonstrated a trivial empirical fact of life of how adaptive evolution to a single selection pressure operates and drug resistance evolves. It's really pretty amazing when you think about it.
Hmm, perhaps the lack of evidence?Then why does nobody care? You still have next to no citations and seem to be reduced to pimping these papers on every single forum you can come across.
If your papers were really that correct/relevant/important, why are they being ignored?
Hmm, perhaps the lack of evidence?
It's better than pimping the lunacy of macroevolution.Then why does nobody care? You still have next to no citations and seem to be reduced to pimping these papers on every single forum you can come across.
If your papers were really that correct/relevant/important, why are they being ignored?
It's better than pimping the lunacy of macroevolution.
That explains why biologists can't properly explain the evolution of drug resistance and why cancer treatments fail. Build a field of study on a couple of courses in dumbbell math and a survey course in physics and that's what you get.Yet the "lunacy of macroevolution" is foundational to modern biology.
Funny, that.
Thank you for your interest in this discussion.
I really started learning something about the subject by studying a computer simulation of random mutation and natural selection written by a guy named Tom Schneider at the National Cancer Institute. He used to have a huge website sponsored by the NCI where you could run his model but it was taken down a few years ago. Schneider never did a thorough study with his model, he was just interested in showing that rmns could increase the system information. But he did make some really outrageous claims about what his model showed. What his model showed was that his 3 selection conditions only worked with extremely short genomes (256 bases long). If you tried to lengthen the genome in his model, the evolutionary process slowed markedly, even when you tried to evolve a virus-length genome of about 20,000 bases. You could evolve longer genomes if you set any 2 of 3 selection conditions to 0 and this was a big clue that the multiplication rule was at play. I saw the analogy between single drug and combination therapy for the treatment of HIV. I started looking at the literature and found numerous papers with empirical examples of this based on combination herbicides, pesticides, and of course, I found Edward Tatums Nobel lecture again more than 40 years after I was first told about this work in elementary school. One thing led to another and I started writing papers on the subject and they were getting published. I believe God led me on this path and revealed this to me. These atheists don't know what they are missing.
I actually went in the opposite direction from you. I originally thought that Darwin was completely wrong, but when I read what he wrote, I saw his logic. Darwin just didn't have any idea how many replications it takes for there to be an adaptive improvement. DNA was unknown to him. Darwin (and most biologists) were/are not aware that competition slows adaptation. Once you understand the physics of the process, it is obvious why.
The mathematics of Darwinian evolution is pretty trivial when you look at the individual components. But when you consider superimposing the different processes (competition and adaptation), at first, it is not so obvious how the processes interact. What I think you recognized was that Darwinian cannot be extrapolated to large genetic transformations. It really helps when you can "run the numbers" because something that appears should work, doesn't work when you apply the correct mathematics or run an experiment that demonstrates the process. That's why it is important to correlate one's models with the experimental data.
Another way to look at it, if you live in an environment with disease, starvation, dehydration, predation, toxins, thermal stress,... If the disease doesn't get you, starvation might, or dehydration, or... long before you have a descendant with beneficial mutations to all these stressors.
That's the point. Antibiotics to treat infectious diseases, targeted cancer therapies, herbicides, pesticides, and insecticides are all-important selection pressures that people use in the fields of medicine and agriculture. But we are using these selection pressures on populations that are able to evolve. Understanding how this evolutionary process works is important so that we don't squander these difficult and costly to develop substances.
Strange you would say that about this subject. Most people would say the evolution of drug resistance, herbicide resistance, pesticide resistance, and why cancer treatments fail is not trivial. The math may be trivial but not the physical consequences. But, to each his own, you go on and figure out your macro-science.
Guy was talking about the evolution of bacteria into humans. Isn't that your concept of common descent? And I'm saying you don't even have the genetic evidence to show that humans and chimpanzees came from a common ancestor let alone this ludicrous idea that somehow we are descended from bacteria.
Fitness pertains to the fecundity of the variant. It can be measure in an absolute manner, the change in population size of the particular variant from one generation to the next. It is this measure that determines whether the variant has a reasonable probability of having a descendant with an adaptive mutation. Or it can be measured in a relative sense wherein in a competitive environment the variant with the highest relative fitness will usually take over the population and be "fixed"It's something of a catch-22 I found in modelling also; stable populations are stable populations, advantageous mutations are lost in the crowd. A small gene pool is easier to influence but provides far less probability of a significant advantageous mutation occurring in a generation. Where a new generation's genetic makeup leans only slightly deleterious- 'survival of the fittest' still applies- but it is a common fallacy to presume that 'fittest' somehow denotes 'fitter than' or even 'as fit as' the previous generation. Rather the gene pool succumbs to entropy; degradation, decline and eventual extinction.
It's not wise to squander the tools that we have.That's where the rubber meets the road. It's a fascinating academic debate, but clearly from common colds to cancer, we still lack the tools to wrestle these problems to the ground.
And what is that mechanism?As quantum mechanics unleashed a whole new dimension of technical possibilities concealed by classical physics- for better or worse- so too when Darwinism is finally superseded by a more enlightened understanding of the mechanisms.
Tour has good arguments against abiogenesis.James Tour for one, synthetic organic chemist and nano-tech pioneer is achieving some incredible things based on an assumption of intelligent design in cells rather than chance creation- it informs an entirely different set of questions, answers and solutions.
Fitness pertains to the fecundity of the variant. It can be measure in an absolute manner, the change in population size of the particular variant from one generation to the next. It is this measure that determines whether the variant has a reasonable probability of having a descendant with an adaptive mutation. Or it can be measured in a relative sense wherein in a competitive environment the variant with the highest relative fitness will usually take over the population and be "fixed"
And what is that mechanism?
For evolution in a single selection pressure environment, the description (math) is trivial. Evolution in a multi-selection pressure environment, the description becomes a little more complex. Still, the mathematics is quite straightforward.The things you claim to explain are not trivial, but you description seems to be.
I don't think your colleagues would have any problem with the triviality of the math if it didn't contradict the concept of macroevolution. I've heard many "scientists" over the years say that the multiplication rule of probabilities does not apply to biological evolution. It is this axiom that contradicts the notion of macroevolution.Since you clearly don't grasp what I am saying, a rephrase:
I don't bother doing science that is so trivial none of my colleagues have any interest in it. Though you don't seem to have any colleagues.
There is a distinction to be made between the theory and the observation though- i.e. I'm saying what we can observe and measure if breaking the laws of Darwinian evolution- as light waves disobeyed classical physics- the disparity shows that something else is at work
As above- apples still fall from trees, genetic apples will still fall not far from there's - but something beyond a handful of simple laws + time and random interaction is at work in both cases. Specifically- information.
Some secular scientists already already use pre-existing information as an argument against God- 'no divine intervention needed, the necessary genetic information already existed and just needed to be switched on'
Another clue that Newtonian physics was insufficient, was the observation that the universe itself did not develop in smooth incremental steps, but sudden explosive stages- speaking to more specific information driving these explosive events. And the observation of increasingly 'explosive events' are likewise a growing hurdle for ToE.
What does most of this have to do with evolution? (And are you implying that sudden stages of development in the universe were clues against Newtonian physics/for quantum mechanics, because that is just not historically correct?)
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