So when you say the Physics of Darwinian Evolution, to me, a physicist, that means that you are going to have Physics in it. Beyond simply mentioning the idea of the first and second law of thermodynamics, there is no physics. You have one equation that you type over and over again 1/(mutation rate). I will say that is not really the type of thing I’d expect if I was reading a paper on the Physics of Darwinian Evolution (a topic that is very interesting to me), so that was rather surprising. For example, here is a mini-conference from a few years back on the Physics of Evolution:
Here is a paper written by one of the presenters on what I was expecting your paper to look like:
You can see from Cook’s conclusion:
Beyond the chemical physics literature, frameworks related to ours have been used in evolutionary science,[43,44] where the cumulative fitness flux is maximized (like entropy production) subject to the trade-off that the speed of the allele change and magnitude of selective forces are minimized (like the conservative action). Therefore, our results suggest that states in evolutionary systems, which require greater cumulative fitness fluxes to reach, should be expected to be more stable. Exploring the application of our theory in ecology and evolutionary science with systems of multiple stable states will be an interesting way forward.
Now I don’t really know quite what this means, as I’m pretty tired and this isn’t my area of expertise, but it’s just an example of the sorts of things you probably should actually put in to a thermodynamical approach to evolution. Not just, “hey this is the first and second law,” make some assumptions, and then Dunning Kruger your way to disproving all of modern biology.
Here is also a recent book I haven’t gotten to check out yet but it seemed interesting and relevant:
I don’t know anything about the author, but reading and digesting some of the literature on the Physics of Evolution is my recommendation for a good place to start without me offering any other specific critiques of your paper.
Are you claiming that humans have a much greater reproductive fitness over chimpanzees because humans have a phage and chimpanzees don’t? Or are you claiming that chimpanzees don’t do sexual reproduction and humans do and therefore humans have much greater reproductive fitness?
My discussion of the physics of Darwinian evolution is very simple and intended for those that have no idea how thermodynamic principles apply to biological evolution. It starts with the understanding that it takes energy to replicate and that the carrying capacity of the environment supplies the total amount of energy to the population. This is the system, and the system and energy balance and the carrying capacity limit the total population size possible. On the other hand, descent with modification is a Markov random walk process. Markov processes are entropy-producing. This can be considered to be a disorganizing process or you can consider this a reduction in the certainty of a base at a given site in the genome if that is how you view entropy. Phylogeneticists use Markov models to try and determine the relatedness of different populations. The problem is they use a stationary model that quickly reaches equilibrium. (They also do their statistical analysis improperly). The reason why their model is incorrect is that they don’t use population size in their formulation. In reality, descent with modification operates far from equilibrium. If you include population size in the transition matrix, you can obtain a Markov formulation that correctly simulates descent with modification and gives results in agreement with experimental evidence.
It is very simple physics but I think if you study this a little, you will find this in agreement with the laws of thermodynamics.
I’ll let @T_aquaticus reply for himself as he wishes, but as both he and I already explained, one can’t compare the reproductive fitness of chimps to humans because they don’t share the same gene pool, so your question is nonsensical. Perhaps you mean to ask “Why is the population size of humans currently larger than that of chimps?” Answering that does not involve comparing their “fitnesses”, but rather comparing multiple factors including their different life history strategies, the breadth of their ecological niches, the carrying capacity of the habitat for that species, and potentially the competitive coefficient of each species if they happen to be consuming the same resources in the same habitat (e.g. see the classic Lotka-Volterra competition models). Did you ever take ecology classes at university?
I am a chemist, so I try to avoid detailed debates/arguments on Darwinian evolution; having said that, I find discussions on what is termed extended evolution (or a similar term) interesting. I have come across a discussion at the Templeton web site that may advance these discussions: a quote,… "A bewildering array of forces are at work, including epigenetic inheritance and developmental plasticity, as well as niche construction, microbiome transfer, and cultural behaviors.
While affirming the significant role of the gene in evolution, organism-centered approaches suggest that non-genetic factors are not merely footnotes but important drivers in the intricate feedback loops that affect how organisms grow and adapt."
Randy has sent me a message. I hope he is not offended by my posting of this part of his message but I think it is worth discussing this publically.
Thanks for the clarification, Randy. The transfer of genetic material by a bacteriophage is not the same as the transfer of genetic material by a plasmid through conjugation. It is thought by many that conjugation is a major factor in the evolution of drug resistance. I’m not so sure about this claim because the recovery rate of bacteria is so rapid as demonstrated by the Kishony experiment. It only takes about 30 doublings (generations) for a single member with a resistance allele to reach a population of a billion. And then, how do bacteria know to transfer any specific allele when doing conjugation? The only logical way that I can see for bacteria to make resistance alleles is by descent with modification and adaptation by accumulating random adaptive mutations. The carrying capacity of the human body for bacteria (or cancer cells) is more than large enough to support the population sizes needed for descent with modification and adaptation to operate. In my view of evolution, conjugation is not needed for the evolution of drug resistance.
There is one confounding factor that should be considered. In an environment where two drugs are used to treat a disease, can conjugation cause the transfer of a resistance allele to one drug to a member having a resistance allele to the second drug? I think this is theoretically possible. The simplest way to model the probability calculation for this process would be to do it based on the frequencies of the variants in the population. Some variants would have resistance allele 1, other variants would have resistance allele 2 and the rest of the population would have neither resistance allele. This would be a simple trinomial distribution problem.
Another way of looking at this is by considering empirical evidence. HIV (though not a bacteria that can do conjugation) does recombination. Experience has shown that 3 drugs are necessary to give a durable treatment. This would stifle descent with modification because the virus would need vastly larger populations to get a member with resistance alleles by random mutation, and it would also stifle recombination because it would require 1 or 2 resistance alleles to be transferred to a member that already has 2 or 1 resistance alleles. Transferring a single resistance allele to one drug to a member with a resistant allele to the second drug will not help that offspring from the selection pressure of the third drug. I haven’t tried to model that process but it would probably take a multinomial distribution.
I think all biologists agree that we have become more knowledgeable about mechanisms of evolution since Darwin’s time. The debate is over the extent to which the mechanisms you mention are really novel or revolutionary–requiring a new “Extended Evolutionary Synthesis” called “EES”. Or whether this is just a part of a normal process of refining the existing theory at the edges. I am one of those in the latter camp. This view is articulated well by Jerry Coyne on his blog site, an excerpt of which I paste below FYI. (Dr. Coyne was responding to an article in the popular news hyping up the stance of EES supporters…
This article in the Guardian really says nothing new beyond what a dozen articles have said already: “There are things we know about evolution that Darwin never imagined, and we’ve made many discoveries that weren’t part of the ‘modern synthetic theory of evolution’ forged in the Thirties and Forties.” I’ve posted a ton about these issues already, many of which are said to form an “Extended Evolutionary Synthesis”, or EES. It turns out that yes, things like the neutral theory and epigenetics weren’t imagined by Darwin, who knew nothing about heredity, or even by the great Theodosius Dobzhansky, but the exponents of the EES sometimes try to pretend that it’s more than an extension of evolutionary biology, but a Kuhnian “revolution” mandating a “new theory of evolution”. Indeed that’s what the article below maintains. (The answer to the headline question is “yes.”)
But in fact we do not need a new theory of evolution: the basic theory proposed by Darwin in 1859, which includes gradualism, variation, natural selection as a critical factor responsible for adaptation, splitting of lineages, and the resultant common ancestry of all species and individuals, still holds. But we know a lot more now, and most of it can easily be incorporated into evolutionary biology. In fact, if you look at evolution textbooks from a few years ago, you’ll find phenomena like epigenesis, the neutral theory, “niche construction”, plasticity, and the like not only discussed, but shown to have been part of discussions about evolution for half a century or more. Now they’re simply part of “evolutionary biology”, which, yes, has expanded, but not in a manner that mandates replacing the old theory. Like cosmology, we just add new stuff to the field as it turns up, and ditch the stuff that turns out to be wrong
So, what is the ecologist’s explanation for why there are a lot more humans on Earth than chimpanzees though you claim they came from a common ancestor?
Welcome to the discussion GJDS. You bring up an important point. Up till now, we have only been discussing gene evolution and have discussed nothing about the feedback loops that control these genes. I think that much of this is due to the fact that a lot more is known about the genetic code for proteins than the genetic code(s) for the control system for these genes. It is incredible that a zygote stem cell has all the information necessary to control the differentiation of that cell into an adult with all its different organ systems and anatomical differences between one species and another. Only a small part of the genome codes for proteins. It is highly likely that the rest of the genome consists of the feedback control loops necessary for the expression of these protein-coding genes. I wouldn’t call this portion of the genome junk DNA.
Humans have a wider ecological niche (we have novel adaptations that have allowed us to exploit new habitats compared to chimps and expand our geographic range immensely). Also, a part of this is our intellectual adaptations (e.g. the ability for science and technology) which have allowed us to lower death rates and exploit resources efficiently, causing our population size to grow over time. At some point, though, humans will also reach their carrying capacity on earth because resources are limited. At their carrying capacities (when population size is stable), every sexually-reproducing female of any species leaves only 2 surviving offspring to the next generation (just replacing themselves in the population in the next generation). That would apply to mice and to men.