Intelligent Design Natural selection

Is there evidence for natural selection?

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From a new book Otangelo Grasso is working on – comments welcome:

I am looking for comments, if my conclusion is sound, that evolution cannot be a theory. It cannot be tested, on how natural selection influences differential reproduction and the fitness landscape. 
Is there evidence for natural selection?

According to Darwin’s Theory, the main actors that drive evolution, is natural Selection, Genetic Drift, and Gene Flow. Natural selection depends on variation through random mutations. Inheritance,  differential survival, and reproduction ( reproductive success which permits new traits to spread in the population).   The genetic modification is supposed to be due to: Survival of the fittest, in other words, 1.  higher survival rates upon specific gene-induced phenotype adaptations to the environment, and 2. higher reproduction rates upon specific evolutionary genetic modifications. Keep in mind that these are two different, distinct factors. It’s a fact that harmful variants, where a mutation influences negatively health, fitness, and reproduction ability of organisms diminish. These are sorted out, or die through disease. In that regard, natural selection is a fact. That says nothing however about an organism gaining more fitness  ( reproductive success )  through the evolution of new advantageous traits.

Definitions of fitness:
J. Dekker (2007): 1. The average number of offspring produced by individuals with a certain genotype, relative to the numbers produced by individuals with other genotypes. 2: The relative competitive ability of a given genotype conferred by adaptive morphological, physiological, or behavioral characters, expressed and usually quantified as the average number of surviving progeny of one genotype compared with the average number of surviving progeny of competing genotypes; a measure of the contribution of a given genotype to the subsequent generation relative to that of other genotypes
A condition necessary for evolution to occur is variation in fitness of organisms according to the state they have for a heritable character. Individuals in the population with some characters must be more likely to reproduce, more fit. Organisms in a population vary in reproductive success. We will discuss fitness in Life History when we discuss competition, interference and the effects of neighbor plants.

Three Components of Fitness.  These different components are in conflict with each other, and any estimate of fitness must consider all of them:
1.  Reproduction
2.  Struggle for existence with competitors
3.  Avoidance of predators  2

S.El-Showk (2012): The common usage of the term “fitness” is connected with the idea of being in shape and associated physical attributes like strength, endurance or speed; this is quite different from its use in biology.  To an evolutionary biologist, fitness simply means reproductive success and reflects how well an organism is adapted to its environment.The main point is that fitness is simply a measure of reproductive success and so won’t always depend on traits such as strength and speed; reproductive success can also be achieved by mimicry, colorful displays, sneak fertilization and a host of other strategies that don’t correspond to the common notion of “physical fitness”.

What then are we to make of the phrase “survival of the fittest”? Fitness is just book-keeping; survival and differential reproduction result from natural selection, which actually is a driving mechanism in evolution. Organisms which are better suited to their environment will reproduce more and so increase the proportion of the population with their traits. Fitness is simply a measurement of survival (which is defined as reproductive success); it’s not the mechanism driving survival.  Organisms (or genes or replicators) don’t survive because they are fit; rather, they are considered fit because they survived. 3

The environment is not stable, but changes. Science would need to have the knowledge of what traits of each species are favored in a specific environment. Adaptation rates and mutational diversity and other spatiotemporal parameters, including population density, mutation rate, and the relative expansion speed and spatial dimensions. When the attempt is made to define with more precision what is meant by the degree of adaptation and fitness, we come across very thorny and seemingly intractable problems. 

As Evolution. Berkley explains: Of course, fitness is a relative thing. A genotype’s fitness depends on the environment in which the organism lives. The fittest genotype during an ice age, for example, is probably not the fittest genotype once the ice age is over. Fitness is a handy concept because it lumps everything that matters to natural selection (survival, mate-finding, reproduction) into one idea. The fittest individual is not necessarily the strongest, fastest, or biggest. A genotype’s fitness includes its ability to survive, find a mate, produce offspring — and ultimately leave its genes in the next generation. 1

Claim: Adam Eyre-Walker (2007): All organisms undergo mutation, the effects of which can be broadly divided into three categories. First, there are mutations that are harmful to the fitness of their host; these mutations generally either reduce survival or fertility. Second, there are ‘neutral’ mutations, which have little or no effect on fitness. Finally, there are advantageous mutations, which increase fitness by allowing organisms to adapt to their environment. Although we can divide mutations into these three categories, there is, in reality, a continuum of selective effects, stretching from those that are strongly deleterious, through weakly deleterious mutations, to neutral mutations and then on to mutations that are mildly or highly adaptive. The relative frequencies of these types of mutation are called the distribution of fitness effects (DFE)5

R. G. Brajesh et.al., (2019): Mutations occur spontaneously during the course of reproduction of an organism. Mutations that impart a beneficial characteristic to the organism are selected and consequently, the frequency of the mutant allele increases in the population. Mutations can be single base changes called point mutations like substitutions, insertions, deletions, as well as gross changes like chromosome recombination, duplication, and translocation 7

Reply:  How can random mutations give rise to higher fitness and higher reproduction of the individuals with the new allele variation favored by natural selection, and so spread in the population? This seems in fact to be a core issue that raises questions. The environmental conditions of a population, the weather, food resources, temperatures, etc. are random How do random events, like weather conditions, together with random mutations in the genome, provoke a fitness increase in an organism and a survival advantage over the other individuals without the mutation? 

T.Bataillon (2014): The rates and properties of new mutations affecting fitness have implications for a number of outstanding questions in evolutionary biology. Obtaining estimates of mutation rates and effects has historically been challenging, and little theory has been available for predicting the distribution of fitness effects (DFE); Future work should be aimed at identifying factors driving the observed variation in the distribution of fitness effects. What can we say about the distribution of fitness effects of new mutations? For the distribution of fitness effects DFE of beneficial mutations, experimentally inferred distributions seem to support theory for the most part. Distribution of fitness effects DFE has largely been unexplored and there is a need to extend both theory and experiment in this area. 4

The above confession demonstrates that a key question, namely how mutations in fact affect fitness has not been answered. I go further and say: Darwin’s Theory can in reality not be tested, nor quantified. The unknown factors in each case are too many, and the variations in the environment, and population and species behavior vary too. It cannot be defined what influence the given environment exercises in regard to specific animals and traits in that environment, nor how the environmental influence would change the fitness and reproduction success of each distinct animal species. Nor how reproduction success given new traits would change upon environmental changes.  What determines whether a gene variant spreads or not would depend theoretically on an incredibly complex web of factors – the species’ ecology, its physical and social environment, and sexual behavior. A further factor adding complexity is the fact that high social rank is associated with high levels of both copulatory behavior and the production of offspring which is widespread in the study of animal social behavior. 

As alpha males have on average higher reproductive success than other males, since they outcompete weaker individuals, and get preference to copulate if other (weaker)  males gain beneficial mutations (or the alphas’ negative mutations) as the alphas can outperform and win the battle for reproduction,  thus selection has an additional hurdle to overcome and spread the new variant in the population. This does not say anything about the fact that it would have to be determined what gene loci are responsible for sexual selection and behavior, and only mutations that influence sexual behavior would have an influence on fitness and the struggle to contribute more offspring to the next generation.   It is in praxis impossible to isolate these factors and see which is of selective importance,  quantify them, plug them in (usually in this context) to a mixed multivariate computational model, see what’s statistically significant, and get meaningful, real-life results. The varying factors are too many and nonpredictive. Darwin’s idea, therefore, depends on variable, unquantifiable multitude of factors that cannot be known, and cannot be tested, which turns the theory at best into a non-testable hypothesis, which then remains just that: a hypothesis. Since Darwin’s idea cannot be tested, it’s by definition, unscientific. 

If fitness is a relative thing, it cannot be detected and proven that natural selection is the mechanism that generates variations that produce more offspring, and therefore the new trait spreads in the population. Therefore, mutations and natural selection cannot be demonstrated to have the claimed effects. What is the relation between mutations in the genome, and the number of offspring? What mutations are responsible for the number of offspring produced? If the theory of evolution is true, there must be a detectable mechanism, that determines or induces, or regulates the number of offspring based due to specific genetic mutations. Only a specific section in the genome is responsible for this regulation.

There are specific regions in the genome responsible for each  mechanism of reproduction, being it sexual, or asexual reproduction, that is:  

1. Regulation and programming of sexual attraction ( hormones, pheromones, instinct, etc.)
2. Frequency of sexual intercourse and reproduction
3. The regulation of the number of offspring produced

What influence do environmental pressures have on these 3 points? What pressures induced organisms to evolve sexual, and asexual reproduction?  Are the tree mechanisms mentioned not amazingly various and differentiated, and each species have individual, species-specific mechanisms? Some have an enormous number of offspring that helps the survival of the species, while others have a very low reproduction rate ( whales  ? ) How could environmental pressures have induced this amazing variation, and why?  That means also on a molecular level, enormous differences from one species to the other exist.  how could accidental mutations have been the basis for all this variation? Would there not have to be SPECIFIC environmental pressures resulting in the selection of  SPECIFIC traits based on mutations of the organism to be selected that provide survival advantage and fitness? ( genome or epigenome, whatever )  AND higher reproduction rates of the organism at the same time?

What is the chance, that random mutations provoke positive phenotypic differences, that help the survival of the individual? What kind of environmental factors influence the survival of a species? What kind of mutations must be selected to guarantee a higher survival rate?

The lack of predictive power of natural selection is due to different environmental conditions that turn it impossible to quantify the effects and measure their outcome.

Ivana Cvijović (2015):Temporal fluctuations in environmental conditions can have dramatic effects on the fate of each new mutation, reducing the efficiency of natural selection and increasing the fixation probability of all mutations, including those that are strongly deleterious on average. This makes it difficult for a population to maintain specialist adaptations, even if their benefits outweigh their costs. Temporally varying selection pressures are neglected throughout much of population genetics, despite the fact that truly constant environments are rare. The fate of each mutation depends critically on its fitness in each environment, the dynamics of environmental changes, and the population size. We still lack both a quantitative and conceptual understanding of more significant fluctuations, where selection in each environment can lead to measurable changes in allele frequency. 6

More problems: R. G. Brajesh (2019): The genotypic mutational space of an organism is so vast, even for the tiniest of organisms like viruses or even one gene, that it becomes experimentally intractable. Hence, studies have limited to studying only small parts of the genome. For example, experiments have attempted to map the functional effect of mutations at important active site residues in proteins, like Lunzer et al. engineered the IDMH enzyme to use NADP as cofactor instead of NAD, and obtain the fitness landscape in terms of the mutational steps. Other experiments have attempted to ascertain how virulence is affected by mutations at certain important loci in viruses. However, due to the scale of the genotypic mutational space, it has been extremely difficult to experimentally obtain fitness landscapes of larger multicomponent systems, and study the statistical properties of these landscapes like the Distribution of Fitness Effects (DFE). Attempts have also been made to back-calculate the underlying DFE by experimentally observing how frequently new beneficial mutations emerge and of what strength, but the final results were inconclusive. As a result, how the beneficial, neutral, and deleterious mutations and their effects are distributed, when the organism genotype is at different locations on the fitness landscape, has remained largely intractable.7

And more problems: Adam Eyre-Walker (2007): The distribution of fitness effects DFE of deleterious mutations, in particular the proportion of weakly deleterious mutations, determine a population’s expected drift load—the reduction in fitness due to multiple small-effect deleterious mutations that individually are close enough to neutral to occasionally escape selection, but can collectively have important impacts on fitness. The DFE of new mutations influences many evolutionary patterns, such as the expected degree of parallel evolution, the evolutionary potential and capacity of populations to respond to novel environments, the evolutionary advantage of sex, and the maintenance of variation on quantitative traits, to name a few. Thus, an understanding of the DFE of mutations is a pivotal part of our understanding of the process of evolution.  Furthermore, the available data suggest that some aspects of the DFE of advantageous mutations are likely to differ between species5

Conclusion: The effects of natural selection on differential reproduction cannot be tested, since too many unknown variables have to be included, and that cannot lead to meaningful, quantifiable results that permit a clear picture. 

1. Evolution.Berkley: Evolutionary fitness
2. J.Dekker: www.agron.iastate.edu/~weeds/AG517/Content/WeedEvol/NaturalSelection/natselect.html” target=”_blank” rel=”nofollow”>Natural Selection and its Four Conditions 2007
3. S.El-Showk: Natural selection: On fitness (2012)
4. Thomas Bataillon: Effects of new mutations on fitness: insights from models and data 2014 Jul
5. Adam Eyre-Walker: The distribution of fitness effects of new mutations August 2007
6. Ivana Cvijović: Fate of a mutation in a fluctuating environment August 24, 2015
7. R. G. Brajesh: Distribution of fitness effects of mutations obtained from a simple genetic regulatory network model 08 July 2019

91 Replies to “Is there evidence for natural selection?

  1. 1
    CuriousCat says:

    I think there’s sufficient evidence for suggesting natural selection to be an agent (or explanation; indeed it is difficult to assign the epistemical role of natural selection) for certain evolutionary phenomena, but this does not entail natural selection to be the ONLY agent for ALL evolutionary phenomena. I believe the problem rests on the latter argument, proposed by the (methodological) naturalist view, as an extrapolation of the former argument due to a naturalist worldview. Hence, the argument is something like this:

    i) Some (simple) biological phenomena can be explained referring to blind processes (although here blindness may refers to an epistemic blindness, not an ontic one, i.e. blindness is in the eye of the beholder), mutation+recombination+environmental pressure.

    ii) Everything in nature should stem from the nature itself.

    iii) Therefore, we have no option other than assuming that all biological evolution should be based on these blind processes (otherwise, naturalism is incorrect, since we cannot even imagine a “naturalistic” mechanism that would explain ALL the evolution).

    Here, naturalism acts as a very strong Bayesian prior, that is almost impossible to change using the likelihood function. Even an observation that seems highly unlikely to have been constructed by the blind processes would not be sufficient to change this belief (as it is usually seen); instead, “a research finding in the future will possibly solve this issue” will be reply. Hence, an ultimate belief in naturalism is the main source of the non-intellectual Darwinian approach.

  2. 2
    jerry says:

    Natural selection is alive and well.

    No serious person denies it. It is just very limited in what it can do. It leads to dead ends in biological change. Ask Michael Behe.

    It is most definitely is not in any way the cause for Evolution. Those who claim it is a factor are committing the fallacy of “Begging the Question.”

    Natural selection works in genetics. Genetics has nothing to do with Evolution. Genetics and natural selection should be a basic of ID. It is great design. Unfortunately this is not well understood by a large percentage of ID advocates.

  3. 3
    Alan Fox says:

    You are the best, Jerry. I promise I won’t let on! 😉

  4. 4
    martin_r says:

    Jerry, if natural selection would be real, there wouldn’t be such a life diversity ….

  5. 5
    martin_r says:

    From the-third-way-of-evolution website (founded by mainstream scientists, evolutionists, e.g. James Shapiro, Eugene Koonin and many others)

    Moreover, some Neo-Darwinists have elevated Natural Selection into a unique creative force that solves all the difficult evolutionary problems without a real empirical basis.

    This quote is right on their title page
    https://www.thethirdwayofevolution.com/

  6. 6
    Paxx says:

    Natural selection just means context pressures. Nothing more or less. So yes, it’s a valid concept.

    But random variation + context pressures cannot be extrapolated for the macro structures such as cell types, tissue types, organs and body plans.

    Any narrative that asserts such is simply blind evolution of the gaps. Not science.

  7. 7
    Otangelo says:

    The point I try to convey is not that natural selection does not act. But its effects cannot be predicted, tested, and quantified, and how it affects fitness. A theory or hypothesis that cannot be tested, is by definition, non-scientific.

    Increasing our ability to predict contemporary evolution 05 November 2020
    https://www.nature.com/articles/s41467-020-19437-x

  8. 8
    Alan Fox says:

    @ Otangelo

    You must have heard of Richard Lenski’s long term evolution experiment.

  9. 9
    hnorman42 says:

    The hard thing is testing the creative power of natural selection.

  10. 10
    jerry says:

    You must have heard of Richard Lenski’s long term evolution experiment

    You mean

    You must have heard of Richard Lenski’s long term genetic experiment

    Absolutely shows that natural selection contracts rather than expands a genome.

    hard thing is testing the creative power of natural selection

    There is no creative power.

    It’s zero. It contracts rather than expands.

  11. 11
    Paxx says:

    jerry @10,

    From an engineering standpoint, the progress of the bacteria is a helluva thing.

    It’s almost as if they were designed to adapt. 😉

  12. 12
    jerry says:

    the progress of the bacteria

    What progress?

  13. 13
    chuckdarwin says:

    CuriousCat/1
    You lost me at Bayesian…….

  14. 14
    Paxx says:

    Jerry: What progress?

    Adjusting to environmental change.

  15. 15
    jerry says:

    Adjusting to environmental change.

    Everybody (human or single cell organism) does that every day.

    Today, it is raining and cool so I will wear a rain jacket. Tomorrow it may be something different. My gut bacteria will adjust to my food intake each day. Is that progress? It could change tomorrow to something different.

    It’s trivial which is my point. Any change produced by natural selection is trivial over the long haul. It will make me or the organism better today but the change that does that will have to change shortly to some other environment if it can or else I/the organism will be bye-bye.

    Two things: the changes that happen through natural selection lead to dead ends by reducing variation. How is anything complex produce through reduced variation? When the geniuses of evolutionary biology figure that out, let me know?

    Second, if the change led to any significant improvement, it would destroy itself. It now makes the ecology in which it inhabits more unstable and thus likely to disappear, thus ending the organism with the significant improvement.

    In other words natural selection must be trivial or else it eliminates the organism that experience the significant change (if such a change is possible.)

    Besides, it is about genomic change and Evolution is the result of something other that produces changes in body plans.

    You lost me at Bayesian

    Don’t be upset Chuck.

    Lost is your natural state. Maybe someday you will find your way.

  16. 16
    bornagain77 says:

    Otangelo at 7:

    “The point I try to convey is not that natural selection does not act. But its effects cannot be predicted, tested, and quantified, and how it affects fitness. A theory or hypothesis that cannot be tested, is by definition, non-scientific.”

    Well, I think you are being just a little bit too charitable to Natural Selection is saying that it may ‘act’ (as a cause).

    As even the late William Provine himself honestly confessed, “Natural selection does not act on anything, nor does it select (for, or against), force, maximize, create, modify, shape, operate, drive, favor, maintain, push or adjust. Natural selection does nothing. Natural selection as a natural force belongs in the insubstantial category already populated by the Necker/Stahl phlogiston or Newton’s ‘ether’”,,,

    “Natural selection does not act on anything, nor does it select (for, or against), force, maximize, create, modify, shape, operate, drive, favor, maintain, push or adjust. Natural selection does nothing. Natural selection as a natural force belongs in the insubstantial category already populated by the Necker/Stahl phlogiston or Newton’s ‘ether’…Having natural selection select is nifty because it excuses the necessity of talking about the actual causation of natural selection. Such talk was excusable for Charles Darwin, but inexcusable for Darwinists now. Creationists have discovered our empty ‘natural selection’ language, and the ‘actions’ of natural selection make huge vulnerable targets.”
    – William B. Provine, The Origins of Theoretical Population Genetics (Chicago: University of Chicago Press, 2001), 199-200

    And although Darwinists, in their imaginary just-so stories, often speak as if Natural selection is “done consciously by the selecting agent”, in the real world Natural Selection is not an actual ’cause’ that acts on anything but, as Adam Sedgwick pointed out to Charles Darwin himself, Natural selection is merely “a secondary consequence of supposed, or known, primary facts.”

    From Adam Sedgwick – 24 November 1859 – Cambridge
    My dear Darwin,
    Excerpt: As to your grand principle—natural selection—what is it but a secondary consequence of supposed, or known, primary facts. Development is a better word because more close to the cause of the fact.,,,
    You write of “natural selection” as if it were done consciously by the selecting agent.,,,
    We all admit development as a fact of history; but how came it about?,,,
    https://www.darwinproject.ac.uk/letter/DCP-LETT-2548.xml

    In short, with Natural selection not being an actual ’cause’ that ‘acts’ on anything, but, in actuality, being nothing more than a ‘secondary consequence’ of supposed, or known, primary facts’, (and as Berlinski pointed out), “Natural selection disappears as a biological force and reappears as a statistical artifact.”

    The Strength of Natural Selection in the Wild – David Berlinski – April 25, 2005
    Excerpt: Natural selection disappears as a biological force and reappears as a statistical artifact. The change is not trivial. It is one thing to say that nothing in biology makes sense except in the light of evolution; it is quite another thing to say that nothing in biology makes sense except in the light of various regression correlations between quantitative characteristics. It hardly appears obvious that if natural selection is simply a matter of correlations established between quantitative traits, that Darwin’s theory has any content beyond the phenomenological, and in the most obvious sense, is no theory at all.
    – Berlinski
    http://www.discovery.org/a/2531/

    Moreover, (and unsurprisingly given that it is, in reality, a ‘secondary consequence’), Natural Selection, and/or fitness, cannot be rigorously measured, and/or even rigorously defined, so obviously Natural Selection, and/or fitness, can never be used as a useful scientific tool that we are able to make accurate, and testable, predictions with,

    Darwin’s Theory of Natural Selection Has Left a Legacy of Confusion over Biological Adaptation
    Brian Miller – September 20, 2021
    Excerpt: Evolutionary biologist Robert Reid stated:
    “Indeed the language of neo-Darwinism is so careless that the words ‘divine plan’ can be substituted for ‘selection pressure’ in any popular work in the biological literature without the slightest disruption in the logical flow of argument.”
    Robert Reid, Biological Emergences: Evolution by Natural Experiment, PP. 37-38 (2009)
    To fully comprehend the critique, one simply needs to imagine attempting to craft an evolutionary barometer that measures the selection pressure driving one organism to transform into something different (e.g., fish into an amphibian). The fact that no such instrument could be constructed highlights the fictitious nature of such mystical forces.
    https://evolutionnews.org/2021/09/darwins-theory-of-natural-selection-has-left-a-legacy-of-confusion-over-biological-adaptation/

    Evolutionary Fitness Is Not Measurable – November 20, 2021
    The central concept of natural selection cannot be measured. This means it has no scientific value.
    Excerpt:,, to measure something, it needs units. How is fitness to be measured? What are the units? Physicists have degrees Kelvin, ergs and Joules of energy and Faradays of electricity, but do 100 Spencers on a Haeckl-o-meter equal 10 Darwins of fitness?
    ,,, The term “fitness” becomes nebulous when you try to pin it down. Five evolutionists attempted to nail this jello to the wall, and wrote up their results in a preprint on bioRxiv by Alif et al. that asked, “What is the best fitness measure in wild populations?” (One might wonder why this question is being asked 162 years after Darwin presented his theory to the world.)
    ,,, The authors admit that their results do not necessarily apply to all living things. (they state),
    “A universal definition of fitness in mathematical terms that applies to all population structures and dynamics is however not agreed on.”
    Remember that this statement comes over 162 years after evolutionists began talking about fitness. If you cannot define something, how can you measure it? And if you can’t measure it, is it really scientific?,,,
    https://crev.info/2021/11/evolutionary-fitness-is-not-measurable/

    Where is the purposelessness of evolution? – 23 March 2012,
    Excerpt: The only way variation is seen as random is that it is random in respect to the effect variation has on fitness.
    The major problem with this is that the precise meaning of fitness has not been settled. There is still a major debate about what exactly fitness is supposed to mean (see this post for more on this issue).
    John O. Reiss notes also make the following interesting remark:
    “The rigor of this approach, however, is lessened because there is as yet no universally agreed upon measure of fitness; fitness is either defined metaphorically, or defined only relative to the particular model or system used. It is fair to say that due to this lack, there is still no real agreement on what exactly the process of natural selection is. This is clearly a problem.”
    Without a proper definition of fitness, we can’t really say what natural selection is in the first place.,,,
    https://www.news24.com/MyNews24/Where-is-the-purposelessness-of-evolution-20120322

    So thus Otangelo, you are completely correct in your observation that, “(Natural Selection’s) effects cannot be predicted, tested, and quantified, and how it affects fitness. A theory or hypothesis that cannot be tested, is by definition, non-scientific”,,,,

    ,,, the only place I take exception with your statement at 7 Otangelo is that you have given, (an ever so small), place that Natural Selection may ‘act’ (as a cause).,,, That simply is not the case.

    Natural Selection simply is not a ’cause’ that can ‘act’ on anything but is only, and can only ever be, a ‘secondary consequence of supposed, or known, primary facts” (Sedgwick).

    In conclusion, Natural selection, (Darwin’s supposed ‘designer substitute’, (Dawkins, Mayr, Ayala)), functions far more in the realm of imagination, and fictional ‘just-so story’ telling, than it ever does, or ever will, in the real world of empirical science and cause and effect

    Why Do We Invoke Darwin?
    Evolutionary theory contributes little to experimental biology
    PHILIP S. SKELL AUGUST 29, 2005
    Excerpt: Darwinian explanations for such things are often too supple: Natural selection makes humans self-centered and aggressive, except when it makes them altruistic and peaceable. Or natural selection produces virile men who eagerly spread their seed, except when it prefers men who are faithful protectors and providers. When an explanation is so supple that it can explain any behavior, it is difficult to test it experimentally, much less use it as a catalyst for scientific discovery.
    Darwinian evolution, whatever its other virtues, does not provide a fruitful heuristic in experimental biology.
    https://www.discovery.org/a/2816/

    Sociobiology: The Art of Story Telling – Stephen Jay Gould – 1978 – New Scientist
    Excerpt: Rudyard Kipling asked how the leopard got its spots, the rhino its wrinkled skin. He called his answers “Just So stories”. When evolutionists study individual adaptations, when they try to explain form and behaviour by reconstructing history and assessing current utility, they also tell just so stories – and the agent is natural selection.
    Virtuosity in invention replaces testability as the criterion for acceptance.
    – per google books

    Verse:

    2 Corinthians 10:5
    Casting down imaginations, and every high thing that exalteth itself against the knowledge of God, and bringing into captivity every thought to the obedience of Christ;

  17. 17
    CuriousCat says:

    I do not believe that these two following methods (that I also see above in the discussion) work to discredit evolution:

    1. One cannot use logic to “show” that natural selection does not work, e.g. “..It will make me or the organism better today but the change that does that will have to change shortly to some other environment if it can or else I/the organism will be bye-bye.” Indeed, it is just the opposite. It is logically possible that a reproducing and varying “thing” MAY adapt to its surroundings, if the variations span a sufficiently large palette.

    2. Arguing that natural selection is NOT a cause is not a useful argument to discredit the role of natural selection. Proteins are composed of wiggling and jiggling atoms due to thermal energy, that is provided by the random collision to other atoms, yet they may change their conformations for catalysis. Hence, random events may be a CAUSE of an organized motion. If one does not like this epistemic view, one may argue a different wording instead of cause, i.e. the cause of the conformational change is the inherent design of the protein, activated by the thermal energy. However, both descriptions indicate identical phenomenon.

    As I have said in my post above, the convenient argument to discredit the role of natural selection in evolution , i.e. the adaptation to the environment as a result of reproduction and variation, shoud be to criticize its sufficiency. I believe that the real problem with Darwinian people lies in not feeling the requirement to show detailed pathways of how organisms have evolved, but leave these to “future” studies with their infinite belief (that’s what I’m calling a Bayesian prior) in the sufficiency of this mechanism. I think this part should be emphasized more to persuade people, instead of the logical and epistemological status of natural selection.

  18. 18
    bornagain77 says:

    “to criticize its (Natural Selection’s) sufficiency”

    To wit,

    The waiting time problem in a model hominin population – 2015 Sep 17
    John Sanford, Wesley Brewer, Franzine Smith, and John Baumgardner
    Excerpt: The program Mendel’s Accountant realistically simulates the mutation/selection process,,,
    Given optimal settings, what is the longest nucleotide string that can arise within a reasonable waiting time within a hominin population of 10,000? Arguably, the waiting time for the fixation of a “string-of-one” is by itself problematic (Table 2). Waiting a minimum of 1.5 million years (realistically, much longer), for a single point mutation is not timely adaptation in the face of any type of pressing evolutionary challenge. This is especially problematic when we consider that it is estimated that it only took six million years for the chimp and human genomes to diverge by over 5 % [1]. This represents at least 75 million nucleotide changes in the human lineage, many of which must encode new information.
    While fixing one point mutation is problematic, our simulations show that the fixation of two co-dependent mutations is extremely problematic – requiring at least 84 million years (Table 2). This is ten-fold longer than the estimated time required for ape-to-man evolution. In this light, we suggest that a string of two specific mutations is a reasonable upper limit, in terms of the longest string length that is likely to evolve within a hominin population (at least in a way that is either timely or meaningful). Certainly the creation and fixation of a string of three (requiring at least 380 million years) would be extremely untimely (and trivial in effect), in terms of the evolution of modern man.
    It is widely thought that a larger population size can eliminate the waiting time problem. If that were true, then the waiting time problem would only be meaningful within small populations. While our simulations show that larger populations do help reduce waiting time, we see that the benefit of larger population size produces rapidly diminishing returns (Table 4 and Fig. 4). When we increase the hominin population from 10,000 to 1 million (our current upper limit for these types of experiments), the waiting time for creating a string of five is only reduced from two billion to 482 million years.
    http://www.ncbi.nlm.nih.gov/pm.....MC4573302/

    When Darwin’s Foundations Are Crumbling, What Will the (Darwinian) Faithful Do?
    Excerpt: Here’s a summation of the evolutionary picture that has emerged, according to Behe (in his new book “Darwin Devolves”:
    • The large majority of mutations are degradatory, meaning they’re mutations in which the gene is broken or blunted. Genetic information has been lost, not gained.
    • Sometimes the degradation helps an organism survive.
    • When the degradation confers a survival advantage, the mutation spreads throughout the population by natural selection.
    In genetics, a loss of information generally translates into a loss of function, so it might seem counterintuitive to suppose that a degradatory mutation would confer a survival advantage. Behe gives several examples, though, of instances where damaged genes have been shown to aid survival. In the case of the sickle-cell gene, for example, a single amino acid change causes hemoglobin to behave in a way that inhibits growth of the malaria microbe. It’s a loss-of-function mutation, but it confers a survival advantage in malaria-prone regions.
    The upshot of all this is that Darwin was right in believing that natural selection operating on random variations can cause organisms to become adapted to their environments, but he was wrong in believing that the process was constructive. Nowhere has the Darwinian mechanism been shown to build a complex system. It has only been shown to modify an already-existing system, usually in a loss-of-function manner.
    This is significant enough to upend the Darwinian narrative, but it gets worse. The same factors that contribute to adaptation work to prevent a species from evolving much further. Random mutation and natural selection quickly adjust species to their environmental niches, Behe writes, and then they maroon them there. He cites results from the long-running experiment conducted by Michigan State microbiologist Richard Lenski, whose E. coli lineage has surpassed 65,000 generations (equivalent to more than a million years for a large, complex species like humans), as sound evidence that random mutations wreak havoc in a species—and then that havoc gets frozen in place by natural selection.
    Behe sums up his main argument like this: “beneficial degradative mutations will rapidly, relentlessly, unavoidably, outcompete beneficial constructive mutations at every time and population scale.”1 The only Darwinian examples of evolution that have been observed have followed this pattern and resulted in evolutionary dead ends. Darwin devolves.,,,,
    https://salvomag.com/article/salvo49/darwinism-dissembled

  19. 19
    jerry says:

    it is just the opposite

    Using non logic to refute logic especially to refute evidence plus logic never gets one anywhere.

    But if one’s ideology is an end result for which there is no proof, then what is one to do.

  20. 20
    PyrrhoManiac1 says:

    Denis Walsh (philosopher of biology @ University of Toronto) argues in Organisms, Agency, and Evolution that we’re better off thinking of natural selection as an effect than as a cause: natural selection is what tends to happen to populations over time as organisms do what they do. So the real business of evolution happens at the level of organisms, and natural selection is (in a sense) epiphenomenal.

    I mention this because what kind of evidence we’re looking for depends on what we think natural selection is. If we think of natural selection as a causal mechanism of evolution, we’ll be looking for one kind of evidence. If we think of natural selection as an effect on populations of what organisms tend to do, we’ll be looking for a very different kind of evidence.

  21. 21
    relatd says:

    PM1 at 20,

    I’m sure a precise definition is available. The sticking point involves randomness.

  22. 22
    Nonlin.org says:

    Of course there’s no such thing as “ns”. The first and only clue you need, is that “natural selection” was conjured by a clueless individual, aka Darwin.

  23. 23
    relatd says:

    The thing to keep in mind is no one knows what the early earth was actually like, not to mention the various catastrophes that occurred like asteroid strikes. I think too often that some view it like a movie set.

  24. 24
    kairosfocus says:

    PM1, good point again. Cross-population differential reproductive success such that some go extinct and others survive and reproduce implies SUBTRACTION of the less favoured races, so it is not the source of fresh biological info, that has to come from sources of chance, incremental variation. I also argue that Orgel-Wicken functionally specific, complex organisation and/or associated information [FSCO/I] implies a sort of fine tuning, i.e. organisation, orientation and coupling of the right parts to achieve configuration based function. This points to how clumped at random clusters of such parts are overwhelmingly functionless gibberish as we see with sentences in ASCII strings vs meaningless random strings gyiuogsdthjcxyrd and again vs simple crystal cell like repetition sdsdsdsds . A term that came from Dembski is islands of function, I like to set such in the midst of seas of non function. An assembled Abu 6500 CT reel is different from what happens with shaking up parts in a bait bucket or scattering them over the bottom of the river. KF

  25. 25
    PyrrhoManiac1 says:

    @21: “I’m sure a precise definition is available. The sticking point involves randomness.”

    Maybe, but then everything depends on what we mean by “randomness”. The evolutionists would tell us that evolution is “random” only in the following sense: there is no empirically detectable process that can foresee what traits would increase fitness and cause those traits to arise.

    There are, I would say, two main problems with the so-called “modern synthesis”: mistaking natural selection to be a causal mechanism rather than a population-level effect, and far too much emphasis on genetic changes as a source of phenotypic diversity. There are multiple levels and kinds of phenotypic diversity, some of them are genetic and some of them not. Organisms are, first and foremost, alive, and we have lost sight of what that means: sensitive (aware of their surroundings) and capable of responding to those surroundings in a variety of ways. (Even the simplest of bacteria can discriminate between environmental states that are good for it and bad for it!) Or, to use a somewhat contentious term, teleology is real.

    The reason why evolutionary histories appear to be teleologically organized is because those histories are just very high-level summaries of what organisms are doing, and the reality of each and every individual organism really is teleologically organized.

    The chief error of the Modern Synthesis is to ignore the essential reality of organismal teleology — and then assign quasi-magical powers to “mutation” and to “selection” to compensate.

  26. 26
    kairosfocus says:

    PM1, the first teleology is in the algorithms encoded in D/RNA. An algorithm being a finite, goal directed stepwise process that halts. As in, goal directed. So, to, as in, goal. KF

  27. 27
    kairosfocus says:

    PM1,

    maybe in studying physics, one becomes so familiar with random, randomising and stochastic patterns, effects, results that one forgets how it can be controversial. Temperature is a measure of average random kinetic energy per degree of freedom for molecules etc.

    There is even a definable negative temperature that is reflective of population inversion and some wag or other says that in physics a negative temperature [such as in a lasing medium] is higher than an infinite ordinary temperature. A bit of an in joke turning on definitions and molecular statistics.

    We can get randomness such as with a die by exploiting sensitive dependence on initial conditions with eight corners and twelve edges so the uppermost resting face is unpredictable reflective of flat random distribution; butterfly effect acting on the nominally mechanically necessary. Chain two or more dice and define outcome as sum of faces, voila, peaked distributions. Indeed a coin is a two sided die, chain 1,000 and flip at random, we get a peaked binomial distribution. Convert to paramagnetic domains in a mild field and we have a toy statistical mechanics physical case.

    Radioactivity is a random process, often tied to quantum tunnelling by which barrier potentials become in effect porous, giving a statistical decay curve with steady half life. In radiation safety, the focus was on how H2O is the commonest molecule and how ionisation makes reactive radicals, that then tear up the organic molecules in the cell. Disruptions to metabolic networks and to information then follow, clearly without mechanical predictable necessity [already hit hard by the butterfly effect] or plausible intelligently directed configuration. If bad enough one gets radiation sick, can die. At lower dosages, information degradation can go to cancer. Another joke, you tell the physics students at the party as they are the ones faintly glowing blue-green in the dark.

    But, even our brains are significantly radioactive as are bananas, K-40.

    So randomness is not an occult reification.

    We can evaluate it through algorithmic compressibility of description of outcomes in some description language. and so forth.

    Randomness does not mean, a world of chaos.

    Ponder, statistical distributions.

    KF

  28. 28
    Paxx says:

    Jerry: Everybody (human or single cell organism) does that every day.

    Yes. It’s not evidence for “evolution” writ large. Tissue types, cell types, organs and body plans.

  29. 29
    Seversky says:

    Trying to educate a creationist (Otangelo Grasso)

    Otangelo Grasso is a creationist who’s convinced he can learn to understand biochemistry by reading what’s on the internet and copy-pasting it into his website. He then takes that limited knowledge and concludes that evolution is impossible. He often poses “gotcha” questions based on his flawed understanding.

    His behavior isn’t very different from most other creationists who suffer from Dunning-Kruger Disease but he happens to be someone who I thought could be educated.

    I was wrong.

    Over the years I’ve tried to correct a number of errors he’s made so we could have an intelligent discussion about evolution. You can’t have such a discussion if one side ignores facts and refuses to learn. Here’s an example of a previous attempt: Fun and games with Otangelo Grasso about photosynthesis. Here’s a post from yesterday showing that I wasted my time: Otangelo Grasso on photosynthesi.(sic)

    […]

  30. 30
    BobSinclair says:

    Sev, ^^^

    If you’ve nothing to add, just say so. No reason to be uncivil/childish.

  31. 31
    Alan Fox says:

    How is drawing our attention to Otangelo’s modus operandi uncivil or childish?

  32. 32
    BobSinclair says:

    Af,

    So rather than contribute to a conversation, all you have to do is supply someone else’s opinion or critique of the person in question and declare job done.

    Understood.

  33. 33
    jerry says:

    From the The Great Courses’ course on Physics and Philosophy.

    You might think that aesthetics, the study of beauty, which largely focuses on questions related to art, has nothing to do with physics. But you would be wrong.

    One of my favorite Einstein stories concerns when word of Arthur Eddington’s confirmation of general relativity arrived by telegram. It was given to Einstein who read it and with a completely flat affect handed it to a graduate student who was in the office. She realized that this was momentous news, yet Einstein was not excited.

    Baffled, she asked him what his reaction would have been if the result had been otherwise, falsifying his theory. His response was “I would have pity for the dear Lord, the theory is right”

    Why was Einstein certain that he had the right answer regardless what God thought? Because the theory was too beautiful to be wrong.

    Beauty, elegance, coherence, symmetry-these are marks of truth in physics. And Einstein is not the only one who argues this.

    And I’m not only speaking of Keats who wrote, “Beauty is truth, truth beauty that is all ye know on Earth and all ye need to know. ”

    The reason why so many people including scientists believe in Darwin’s theory of Evolution is that it is simple and elegant at the same time and explains everything. So obviously true!

    Before, someone recites the thousands of reasons why it is not true, whoever does is fighting a loosing battle. I agree it’s nonsense but nevertheless everyone believes it.

    So seek some other way to undermine it. Just ranting against natural selection doesn’t get it done.

  34. 34
    Alan Fox says:

    So rather than contribute to a conversation, all you have to do is supply someone else’s opinion or critique of the person in question and declare job done.

    Otangelo doesn’t do conversation. I think people should be aware that his routine has been repeated in numerous venues on many occasions. It saves time so that people who are unaware of his history don’t have to start from scratch.

  35. 35
    jerry says:

    How is drawing our attention to Otangelo’s modus operandi uncivil or childish?

    Because it is irrelevant.

    The MO of the anti ID person is to focus on some trivial irrelevant detail while failing to engage in the substance of an argument. The above is an example.

    So the comment above is actually very childish while making an uncivil irrelevant accusation about someone.

    Aside: I have no idea of Otangelo’s religious beliefs. However, his scientific beliefs should be based on whether they are justified or not. For example, we get this irrelevant comment

    There is no substance to Otelangelo’s outpourings. It’s a mix of plagiarism and straw men. What’s good isn’t original and what’s original isn’t good.

    So what isn’t good or a straw man? I am interested in what may be erroneous. That would be the way to educate Otangelo since he is obviously monitoring this thread.

    Aside2: immediate confirmation of my observation about anti ID commenters.

  36. 36
    Alan Fox says:

    The MO of the anti ID person is to focus on some trivial irrelevant detail while failing to engage in the substance of an argument. The above is an example.

    There is no substance to Otelangelo’s outpourings. It’s a mix of plagiarism and straw men. What’s good isn’t original and what’s original isn’t good.

  37. 37
    PyrrhoManiac1 says:

    @26:

    PM1, the first teleology is in the algorithms encoded in D/RNA. An algorithm being a finite, goal directed stepwise process that halts. As in, goal directed. So, to, as in, goal. KF

    I have two worries about this idea.

    The first is that it seems to commit a sort of “mereological fallacy”: to attribute to a part of the system a property that belongs to the whole. It is to say that the organism as a whole exhibits teleology because one part of that system (the genetic algorithm) does. In contrast, I would rather say that teleology is a property of the system as a whole, and that the smallest “unit” of teleology is a single cell.

    The second is that the use of engineering metaphors in molecular biology is really problematic. This is because microscopic systems are subjected to Brownian motion in ways that macroscopic systems simply are not. This means that microscopic systems are constantly engulfed in massive amounts of randomness that’s unlike what we see in human-built artifacts, esp because we isolate our systems from possible sources of noise, heat, etc. as much as we can. For example, although a specific nucleotide sequence corresponds to a specific amino acid sequence, the actual gene products can vary quite a bit from individual cell to individual cell — it’s just that the differences get washed out at large enough cell populations. We just don’t see the rigidity of inputs to outputs that we see in computer programs.

  38. 38
    Querius says:

    Back to the OP, there’s a problem with definition of Fitness. Point 2 reads:

    Struggle for existence with competitors

    * If any one competitor “wins” it begins to form a monoculture, which is more prone to catastrophic collapse. The Irish potato famine comes to mind.

    * If a predator consistently “wins,” its population collapses due to starvation.

    * If an herbivore “wins,” it damages or destroys the “carrying capacity” of an ecosystem. The spread of rabbits in Australia come to mind. https://www.rabbitfreeaustralia.org.au/rabbits-in-australia/

    Achieving and maintaining a stable ecosystem is not trivial. I once spent a lot of time programming an ecosystem simulation. I was discouraged that it always seemed to suffer increasingly wild fluctuations in its component species and then crash. Then, I found out that this is a typical result.

    The conclusion is that reproduction without constraints dooms an ecosystem. How can natural selection possibly keep this from happening?

    -Q

  39. 39
    Querius says:

    PyrrhoManiac1 @37,

    Good point–biological systems are not deterministic. A point can be made for “survival of the luckiest,” which is why a single mutation in a population is not enough for fixation within a population.

    Advances in the study of epigenetics indicate that environmental stimulii have a profound effect on gene expression. For example, it’s now believed that adaptive changes in Darwin’s finches have a strong epigenetic component, and that these are expressed in the next generation rather than hundreds or thousands of years.

    The supposed evolution of epigenetics is also a fascinating topic for the questions and issues it raises. For example
    https://academic.oup.com/icb/article/54/1/31/2797821?login=false

    -Q

  40. 40
    jerry says:

    reproduction without constraints dooms an ecosystem. How can natural selection possibly keep this from happening?

    Very easily.

    Because natural selection only works in genetics, whatever changes that come about are trivial. This understanding is the basis for my claim that Darwinian changes are self refuting as a means of Evolution.

    Behe shows this in the Lenski genetic experiments and in the wild with devolution. The reasons why Darwinian Evolution is accepted has to do with its seemingly obvious affect on changes in organisms. Changes that are morphologically based but in reality must be based on genetics which doesn’t have the power to make significant changes.

    Its acceptance has to do with its apparent beauty as an elegant theory. See #33 above.

  41. 41
    kairosfocus says:

    PM1, protein synthesis is absolutely central to the cell, and the cell to biological life. That we find complex coded algorithms there, where algorithms are inherently goal directed procedures reflective of purpose [and use of language, process logic etc] puts manifestations of purpose into the core of biology. Nor is this a mere readily dismissible metaphor or analogy, we are looking at recognisable cases of machine code in action. Yes, this is a four state system, the Russians had three state machines and digital goes far beyond binary. Digital means, discrete state. The genetic code is a code, rightly widely and generally recognised as such. The mRNA is a string data structure tape, the tRNA a transport unit and position arm element where the actual encoding is in what is attached to the CCA tip, the ribosome is a constructor unit, with code tape controlled start, extension, halt, all based on a prong height code similar to keys for a Yale type lock. Resistance to acknowledging this seems to be driven by realisation of the consequences, not the widely recognised facts on the ground that are on record all the way back to Crick’s March 19 1953 letter to his son where on p 5 he first says it is like a code then emphasises the is by underscoring in it IS a code. KF

  42. 42
    kairosfocus says:

    Q, the issue is about feedback loops, lags [so phase shifts] and degenerative vs regenerative feedback. The solution is well balanced robust tuning and with a complex situation that exponentiates with degree of interaction, coupling etc. In shoet, a complex organised system dependent on configuration has a question of where are the operating points, thence islands of function in a configuration space, possible attractors and more, especially if nonlinearities are present. Much of the objection to Orgel-Wicken functionally specific, complex organisation and/or associated information [FSCO/I] is driven by failure to recognise such systems issues. KF

  43. 43
    Querius says:

    Jerry @40,

    Querius: reproduction without constraints dooms an ecosystem. How can natural selection possibly keep this from happening?

    Jerry: Very easily.

    While I agree that Darwinian evolution is supposed to occur in tiny steps, how would it be advantageous to the survival of an individual organism to evolve a lower rate of reproduction than the other organisms of its same species?

    -Q

  44. 44
    jerry says:

    I am going to be brief because formulating my thesis is taking too much time

    While I agree that Darwinian evolution is supposed to occur in tiny steps, how would it be advantageous to the survival of an individual organism to evolve a lower rate of reproduction than the other organisms of its same species?

    I’m not sure I understand what you are asking.

    It doesn’t make sense to me.

    I am trying to say that all changes must be trivial, that is they will make the organism adapt better to a new environment but at the same time not out compete other organisms in its ecology. It’s hard to imagine how a species could be superior in a non trivial way when to do so would allow it to outcompete its competitors. It would have to out compete previous versions without out. competing other species. It would be a fine line.

    How would a superior characteristic arise, better sight, stronger, faster, or whatever without also out competing the other species in the ecology. So they must be trivial. Even if they did accumulate at a very slow rate, eventually they would reach a point that would be better than their competitors. The rate of change is anything but a constant and it would be absurd to say that improved characteristics of competing species would offset each other when there is no process to ensure this.

    Individual organisms do not evolve. They die off. Offspring of an individual organism will have a different genome (single cell organism may be an exception). Some times the genome of offspring are better adapted to the environment, and are more likely to survive and the characteristics of these gene pools that facilitate this will be more prevalent. We call the result natural selection. This has the result of reducing the variation in the species.

    But the changes are trivial, just some alleles more prevalent than before. That is they will not affect the structure of the organism very much.

    However, suppose the offspring’s genome had a major change due to some form of variation. Allan MacNeill used to say there were 47+ possible source for variation. Now the gene pool is expanded by the variation.

    Suppose some combination of these variations led to a new characteristic that made the organisms superior to the previous organisms. Then this organism would out compete the previous gene pool and eliminate the previous organisms as well as other organism using the same ecology and thus, itself.

    There can be no magic rate of improvement without eventually eliminating other elements of the ecology and then itself.

    Not very clear but I do not have time now to express it more clearly.

    This leads to the possibilities of the fine tuning of ecologies. Nothing as precise as the fine tuning of the universe or the Earth but are ecologies such that they cannot continue unless the variation in the members are restricted with certain ranges?

  45. 45
    Otangelo says:

    Remind you, guys, that the only point of the OP is that the effects of natural selection in regards to differential reproduction, and fixation rate of different, supposedly beneficial allele variants in the genome, of animals living in the wild, CANNOT BE TESTED, and quantified, since unquantifiable variables are involved, like unstable ecological conditions, hierarchy and differentiated sexual behaviors, like alpha males copulating more frequently than other males, responsible for more offspring, etc. My observation has been confirmed by further science papers, that I have encountered, after posting the OP.

    L.Bromham (2017): The search for simple unifying theories in macroevolution and macroecology seems unlikely to succeed given the vast number of factors that can influence a particular lineage’s evolutionary trajectory, including rare events and the weight of history. Patterns in biodiversity are shaped by a great many factors, both intrinsic and extrinsic to organisms. Both evidence and theory suggests that one such factor is variation in the mutation rate between species. But the explanatory power of the observed relationship between molecular rates and biodiversity is relatively modest, so it does not provide anything like the predictive power that might be hoped for in a unifying theory. However, we feel that the evidence is growing that, in addition to the many and varied influences on the generation of diversity, the differential rate supply of variation through species-specific differences in mutation rate has some role to play in generating different rates of diversification.
    https://www.frontiersin.org/articles/10.3389/fgene.2017.00012/full

    Z. Patwa (2008): To date, the fixation probability of a specific beneficial mutation has never been experimentally measured.
    https://royalsocietypublishing.org/doi/10.1098/rsif.2008.0248#d3e1489

  46. 46
    Querius says:

    Jerry @44,

    This leads to the possibilities of the fine tuning of ecologies. Nothing as precise as the fine tuning of the universe or the Earth but are ecologies such that they cannot continue unless the variation in the members are restricted with certain ranges?

    Yes, fine tuning is exactly what occurred to me when I was adjusting (and failing at) my ecosystem simulations.

    However, it’s also likely that there’s an equivalent in biological ecosystems to something like Le Chatelier’s principle in chemistry, which maintains equilibria by counteracting changes in parameters.

    My point is that optimization of an organism in an ecosystem can easily run counter to the survival of the ecosystem by reducing its carrying capacity.

    -Q

  47. 47
    Querius says:

    Otangelo @45,

    Thank you for the information.

    I’ve run across some interesting estimates regarding fixation of a trait in a population from my reading some years back. Unfortunately, I’ve not been able to locate the reference yet, but I’ll keep looking.

    -Q

  48. 48
    Alan Fox says:

    However, it’s also likely that there’s an equivalent in biological ecosystems to something like Le Chatelier’s principle in chemistry, which maintains equilibria by counteracting changes in parameters.

    Speculation. Living organisms temporarily maintain themselves out of equilibrium with their niche environment by exploiting available sources of energy (solar energy in green plants, for instance). It’s the key to being alive rather than dead.

  49. 49
    bornagain77 says:

    AF: “Speculation. Living organisms temporarily maintain themselves out of equilibrium with their niche environment by exploiting available sources of energy (solar energy in green plants, for instance). It’s the key to being alive rather than dead.”

    So how is this self-admitted ‘speculation’ suppose to work exactly? Were some chemotroph bacteria, (which are already very sophisticated in their ability to capture energy), just sitting around one day and said to themselves, “Hey, there is some really neat solar energy over there, why don’t we construct really elaborate photosynthetic processes as well so that we may be able ‘exploit’ that available source of solar energy?”,, In short, none of your teleological based ‘speculation’ on ‘exploiting’ available energy sources makes any scientific sense.

    Origin of life: heterotrophic or autotrophic , the emergence of the Basic Metabolic Processes
    https://reasonandscience.catsboard.com/t2173-origin-of-life-heterotrophic-or-autotrophic-the-emergence-of-the-basic-metabolic-processes

    Evolutionary biology: Out of thin air John F. Allen & William Martin:
    The measure of the problem is here: “Oxygenetic photosynthesis involves about 100 proteins that are highly ordered within the photosynthetic membranes of the cell.”
    http://www.nature.com/nature/j.....5610a.html

    Researchers Build Public “Library” To Help Understand Photosynthesis – March 19, 2019
    Excerpt: It isn’t easy being green. It takes thousands of genes to build the photosynthetic machinery that plants need to harness sunlight for growth. And yet, researchers don’t know exactly how these genes work.
    Now a team led by Princeton University researchers has constructed a public “library” to help researchers to find out what each gene does. Using the library, the team identified 303 genes associated with photosynthesis including 21 newly discovered genes with high potential to provide new insights into this life-sustaining biological process. The study was published online this week in Nature Genetics.
    “The part of the plant responsible for photosynthesis is like a complex machine made up of many parts, and we want to understand what each part does,” said Martin Jonikas, assistant professor of molecular biology at Princeton.
    https://uncommondescent.com/intelligent-design/researchers-build-public-library-to-help-understand-photosynthesis/

    etc.. etc..

  50. 50
    kairosfocus says:

    Jerry, I think Q is alluding to the wolves vs rabbits problem. Wolves have few offspring but care more for them, going on to dominate an environment through pack based predatory power. Rabbits have many offspring but this serves as wolf fodder, the wolves in turn keeping rabbits within limits of the ecosystem. We can extend to grass which everybody tramples and many eat. Mango trees make many sweet fruit and the seeds are protected by being hard coated — they will pass through a cow’s gut [and would then be deposited with a dose of fertiliser] — and while an obvious large nut, are apparently bitter. Which, BTW, is a common signal for toxicity. KF

    PS, Hitler inappropriately extended this to his doctrines that turned Germany into predators on their neighbours. The world united to defeat the threat.

  51. 51
    kairosfocus says:

    AF, homeostasis for cells and organisms is no mean feat. KF

  52. 52
    PyrrhoManiac1 says:

    @48:

    Living organisms temporarily maintain themselves out of equilibrium with their niche environment by exploiting available sources of energy (solar energy in green plants, for instance). It’s the key to being alive rather than dead.

    Right — that’s homeostasis — a principle so important that J. Scott Turner calls it “Biology’s Second Law”.

    I think it quite plausible that homeostasis has explanatory priority over selection (what Turner calls “Biology’s First Law”) because homeostasis demonstrates the empirical reality of teleology — not the world-governing principle of “cosmic teleology” but the intrinsic purposiveness of individual organisms.

    A widely held view in 20th century evolutionary theory is that teleology, to the extent that it exists at all, is explained by selection acting on genetic variation. (This is the whole point of Ernst Mayr’s idea that “teleonomy” is explained by the genetic program.) I think this was a plausible view at the time, given the emergence of cybernetics in the 1940s, but it’s turned out to be a mistake.

    Instead, we need to look to homeostasis as the key to self-maintaining functional structures in organisms, understand teleology in terms of homeostasis — homeostasis, that is, and neither selection nor variation. Selection is a super-organismal, population-level effect of what tends to happen over time as organisms attempt to meet their goals and satisfy their needs. Genetic variation is important, but it can happens after selection as well as before (e.g. the Baldwin effect), and I think it too has been exaggerated — especially in popular treatments of evolutionary theory.

    The neglect of homeostasis in favor of selection and variation became entrenched in 20th century biology when the Modern Synthesis cemented population genetics as the centerpiece of the whole theory, to the benign neglect of organismal biology (esp. embryology and paleontology). There’s been a huge resurgence of organism-centered biology in recent 21st century evolutionary theory.

  53. 53
    Alan Fox says:

    …homeostasis demonstrates the empirical reality of teleology…

    How so? I’d be interested to see some empirical (heh) support for that claim.

  54. 54
    jerry says:

    Not very clear but I do not have time now to express it more clearly.

    This is meant for myself but if anyone wants to comment, feel free.

    Change happens through variation. This is well documented. But significant change is rare at best.

    The change can be small or it can be a massive change. By massive, I mean the size of change in genome as opposed to the effect of the change.

    Natural selection, or the process of certain changes leaving more individuals with a specific gene pool will happen by definition. By definition I mean that if the allele assortment changes over time, that will indicate something affected this assortment and it could be just random accumulations or it could be one assortment is better suited for its environment and produced more offspring.

    This process tends to reduce variation in the gene pool as some assortment become better able to survive in the new environment. However, it is possible that some new alleles have developed through this process.

    Will these new alleles lead to changes that are dramatic or will they essentially be trivial, that is will not lead to any new significant characteristics or capabilities? I maintain that it is the latter. Because any changes that lead to something dramatic will enable the gene pool of the organisms to out compete its competitors and as such destroy the ecology it inhabits. Such changes could happen quickly or take eons to accumulate.

    Either way a significant change has taken place. The timing of such changes cannot be coorinated with changes in other organisms to reduce the effect of the change, since they are completely independent of each other in terms of capability and timing.

    Therefore, any changes that do happen must be trivial and not lead to anything that is dramatic. Or else the ecology will be destroyed.

    Therefore Darwinian Evolution is self refuting. Postulating that it happens leads to the destruction of the organism in which it is taking place.

    Darwinian processes do happen in genetics, most emphatically yes. Darwinian processes in Evolution, most emphatically no.

    If there is Evolution and that is pretty much a fact, it must have happened some other way.

    I have been capitalizing the word “Evolution” to distinguish it from small changes in genetics which everyone agrees with. The debate is over large changes not small changes. By saying small changes accumulate, one is avoiding the obvious problem of ecology destruction and thus, destruction of the gene pool of the organism that has experienced the large accumulation of changes. It makes no difference if it is fast or slow, the end result will be the same.

    I’m sure this could be made more clear. What I am interested in is there is a flaw in the logic. In other words how could an organism experience significant changes without destroying its ecology.

    I often use the following example to illustrate this point. People frequently point to supposed imperfections in humans to indicate the failure of the designer to make a better human. A good example, of this is one I have frequently brought up, namely strength in humans.

    Humans that were stronger would have been able to produce more food. Strength has been a limiting factor in producing food for all of history. So why didn’t humans evolve to be stronger since strength is definitely in the gene pool? Why didn’t it win out. through natural selection?

  55. 55
    PyrrhoManiac1 says:

    @41.

    protein synthesis is absolutely central to the cell, and the cell to biological life. That we find complex coded algorithms there, where algorithms are inherently goal directed procedures reflective of purpose [and use of language, process logic etc] puts manifestations of purpose into the core of biology. Nor is this a mere readily dismissible metaphor or analogy, we are looking at recognisable cases of machine code in action.

    Algorithms, if I understand the concept correctly, aren’t just processes with finitely many steps that come to a stop. They are recursive processes that systemically map inputs to outputs. If I understand the concept correctly, that means there must be a one-to-one correspondence between input strings and output strings. Yet that is not what we see in molecular biology: there are lots of epigenetic factors (methylation and de-methylation), post-transcriptional events, and post-translational events — the same nucleotide sequence can generate different protein products based on changes in the intracellular environment. There’s a sensitivity to context and circumstance that we just don’t find in macroscopic computing devices.

    Additionally, in the case of molecular biology, there’s no way of demarcating ‘software’ from ‘hardware’. We can represent the nucleotide-amino acid correspondences, but the details of those correspondence depends on specific facts about the geometry of binding sites. We just don’t know how to distinguish the ‘software’ from the ‘hardware’, and that’s crucial for being able to talk about an algorithmic process in the first place.

    For that matter, we don’t even know how to tailor-make a protein from nucleotide sequences: that is, given some functional configuration we want in a protein, what would be the right nucleotide sequence? If that’s right, that would seem to entail that protein synthesis is not a computable function. And if that’s true, then there isn’t “machine code” in the cell — regardless of whether Cricks said so or not.

    Most generally: I think that microscopic domains in liquid environments (including but not limited to molecular biology) are so replete with the randomness caused by Brownian motion that engineering metaphors are wholly misleading.

  56. 56
    PyrrhoManiac1 says:

    @53:
    “How so? I’d be interested to see some empirical (heh) support for that claim.”

    What I had in mind is the idea of “biological autonomy”: that we can describe biological systems as self-maintaining, goal-oriented systems. There’s a long video here, which is quite good but somewhat dry.

    Matteo Mossio and his colleagues Alvaro Moreno, Maël Montévil, and Leonardo Bich have many papers available free online that explain their ideas. Here are a few:

    Biological Organization as Closure of Constraint
    Organisational Closure in Biological Organisms
    What Makes Biological Organization Teleological?

  57. 57
    Alan Fox says:

    Apologies, Pyrrhomaniac1, I get a bit triggered when the word “teleology” pops up. I see your comments are much more nuanced and deserve more than the cursory glance I gave them.

  58. 58
    Sandy says:

    PyrrhoManiac1JVL Most generally: I think that microscopic domains in liquid environments (including but not limited to molecular biology) are so replete with the randomness caused by Brownian motion that engineering metaphors are wholly misleading.

    🙂 What in the world are you saying ? That a cell builds the same protein or organizes a cell division or makes a repair with different/random chemical reactions? You must be a very desperate atheist.

  59. 59
    PyrrhoManiac1 says:

    @57:

    Apologies, Pyrrhomaniac1, I get a bit triggered when the word “teleology” pops up. I see your comments are much more nuanced and deserve more than the cursory glance I gave them.

    No worries, I know that “the T word” can be ‘triggering’ for lots of people. My view is, since we know that we can’t do biology without teleology, we had better figure out how to think about teleology!

    @58:

    What in the world are you saying ? That a cell builds the same protein or organizes a cell division or makes a repair with different/random chemical reactions? You must be a very desperate atheist.

    I’m saying that if one compares gene products across individual cells, or the same gene product in the same cell over time, there are going to be subtle variations in how the intracellular environment affects transcription and translation. Those variations are caused by Brownian motion in liquid environments that aren’t computable in advance. And that’s why the engineering metaphors don’t work.

    (Also, not an atheist.)

  60. 60
    bornagain77 says:

    Pyr, FYI, ‘Brownian motion’ in cells is now shown to be far more constrained in cells than was first believed.

    For instance, in the following 2016 paper, it was found that “crowding in cells doesn’t hamper protein binding as much as they thought it did.” In fact, finding a lack of ‘collisions’ in the crowded cell was a ‘counterintuitive surprise’ for the researchers: Specifically one of the researchers stated: “This was a surprise,” “It’s counterintuitive, because one would think collisions between a protein and other molecules on DNA would slow it down. But the system is so dynamic, it doesn’t appear to be an issue.”

    Proteins put up with the roar of the crowd – June 23, 2016
    Excerpt: It gets mighty crowded around your DNA, but don’t worry: According to Rice University researchers, your proteins are nimble enough to find what they need.
    Rice theoretical scientists studying the mechanisms of protein-DNA interactions in live cells showed that crowding in cells doesn’t hamper protein binding as much as they thought it did.,,,
    If DNA can be likened to a library, it surely is a busy one. Molecules roam everywhere, floating in the cytoplasm and sticking to the tightly wound double helix. “People know that almost 90 percent of DNA is covered with proteins, such as polymerases, nucleosomes that compact two meters into one micron, and other protein molecules,” Kolomeisky said.,,,
    That makes it seem that proteins sliding along the strand would have a tough time binding, and it’s possible they sometimes get blocked. But the Rice team’s theory and simulations indicated that crowding agents usually move just as rapidly, sprinting out of the way.
    “If they move at the same speed, the molecules don’t bother each other,” Kolomeisky said. “Even if they’re covering a region, the blockers move away quickly so your protein can bind.”
    In previous research, the team determined that stationary obstacles sometimes help quicken a protein’s search for its target by limiting options. This time, the researchers sought to define how crowding both along DNA and in the cytoplasm influenced the process.
    “We may think everything’s fixed and frozen in cells, but it’s not,” Kolomeisky said. “Everything is moving.”,,,
    Floating proteins appear to find their targets quickly as well. “This was a surprise,” he said. “It’s counterintuitive, because one would think collisions between a protein and other molecules on DNA would slow it down. But the system is so dynamic, it doesn’t appear to be an issue.”
    http://phys.org/news/2016-06-p.....crowd.html

    In fact, instead of a biological systems being “dominated by randomly colliding individual protein molecules” (B. Alberts, C. Zimmer), the fact of the matter is that biological systems are now shown to be extremely resistant to random background noise. As the following article on photosynthesis stated, ‘These biological systems can direct a quantum process,,, in astoundingly subtle and controlled ways – showing remarkable resistance to the aggressive, random background noise of biology and extreme environments.’

    Unlocking nature’s quantum engineering for efficient solar energy – January 7, 2013
    Excerpt: Certain biological systems living in low light environments have unique protein structures for photosynthesis that use quantum dynamics to convert 100% of absorbed light into electrical charge,,,
    “Some of the key issues in current solar cell technologies appear to have been elegantly and rigorously solved by the molecular architecture of these PPCs – namely the rapid, lossless transfer of excitons to reaction centres.”,,,
    These biological systems can direct a quantum process, in this case energy transport, in astoundingly subtle and controlled ways – showing remarkable resistance to the aggressive, random background noise of biology and extreme environments. “This new understanding of how to maintain coherence in excitons, and even regenerate it through molecular vibrations, provides a fascinating glimpse into the intricate design solutions – seemingly including quantum engineering – ,,, and which could provide the inspiration for new types of room temperature quantum devices.”
    http://phys.org/news/2013-01-n.....nergy.html

    Likewise the following article on human vision stated that, “Research,, has shown that humans can detect the presence of a single photon, the smallest measurable unit of light”.,,, “it is remarkable: a photon, the smallest physical entity with quantum properties of which light consists, is interacting with a biological system consisting of billions of cells, all in a warm and wet environment,”,, and the researched added, “The response that the photon generates survives all the way to the level of our awareness despite the ubiquitous background noise. Any man-made detector would need to be cooled and isolated from noise to behave the same way.”,,, “What we want to know next is how does a biological system achieve such sensitivity? How does it achieve this in the presence of noise?”

    Study suggests humans can detect even the smallest units of light – July 21, 2016
    Excerpt: Research,, has shown that humans can detect the presence of a single photon, the smallest measurable unit of light. Previous studies had established that human subjects acclimated to the dark were capable only of reporting flashes of five to seven photons.,,,
    it is remarkable: a photon, the smallest physical entity with quantum properties of which light consists, is interacting with a biological system consisting of billions of cells, all in a warm and wet environment,” says Vaziri. “The response that the photon generates survives all the way to the level of our awareness despite the ubiquitous background noise. Any man-made detector would need to be cooled and isolated from noise to behave the same way.”,,,
    The gathered data from more than 30,000 trials demonstrated that humans can indeed detect a single photon incident on their eye with a probability significantly above chance.
    “What we want to know next is how does a biological system achieve such sensitivity? How does it achieve this in the presence of noise?”
    http://phys.org/news/2016-07-humans-smallest.html

    Moreover, instead of proteins randomly colliding into each other, (C. Zimmer), proteins instead are found to be “analogous to the way wine glasses tremble”,,, “If you tap on a bell, it rings for some time, and with a sound that is specific to the bell. This is how the proteins behave,”,,, “Many scientists have previously thought a protein is more like a wet sponge than a bell: If you tap on a wet sponge, you don’t get any sustained sound.”

    Symphony of Life, Revealed: New Imaging Technique Captures Vibrations of Proteins, Tiny Motions Critical to Human Life – Jan. 16, 2014
    Excerpt: To observe the protein vibrations, Markelz’ team relied on an interesting characteristic of proteins: The fact that they vibrate at the same frequency as the light they absorb.
    This is analogous to the way wine glasses tremble and shatter when a singer hits exactly the right note. Markelz explained: Wine glasses vibrate because they are absorbing the energy of sound waves, and the shape of a glass determines what pitches of sound it can absorb. Similarly, proteins with different structures will absorb and vibrate in response to light of different frequencies.
    So, to study vibrations in lysozyme, Markelz and her colleagues exposed a sample to light of different frequencies and polarizations, and measured the types of light the protein absorbed.
    This technique, , allowed the team to identify which sections of the protein vibrated under normal biological conditions. The researchers were also able to see that the vibrations endured over time, challenging existing assumptions.
    “If you tap on a bell, it rings for some time, and with a sound that is specific to the bell. This is how the proteins behave,” Markelz said. “Many scientists have previously thought a protein is more like a wet sponge than a bell: If you tap on a wet sponge, you don’t get any sustained sound.”
    http://www.sciencedaily.com/re.....084838.htm

    Moreover, in the following article subtitled ‘how bio-molecular machines can generate nontrivial quantum states’, the authors state that entanglement can be maintained even in the presence of very intense noise,

    Persistent dynamic entanglement from classical motion: how bio-molecular machines can generate nontrivial quantum states
    Gian Giacomo Guerreschi, Jianming Cai1, Sandu Popescu and Hans J Briegel
    Published 29 May 2012
    Excerpt: Very recently (Cai et al 2010 Phys. Rev. E 82 021921), a simple mechanism was presented by which a molecule subjected to forced oscillations, out of thermal equilibrium, can maintain quantum entanglement between two of its quantum degrees of freedom. Crucially, entanglement can be maintained even in the presence of very intense noise, so intense that no entanglement is possible when the forced oscillations cease. This mechanism may allow for the presence of nontrivial quantum entanglement in biological systems. Here we significantly enlarge the study of this model. In particular, we show that the persistent generation of dynamic entanglement is not restricted to the bosonic heat bath model, but can also be observed in other decoherence models, e.g. the spin gas model, and in non-Markovian scenarios. We also show how conformational changes can be used by an elementary machine to generate entanglement even in unfavorable conditions. In biological systems, similar mechanisms could be exploited by more complex molecular machines or motors.
    http://iopscience.iop.org/arti.....53043/meta

    And in the following article, the authors even go on to state that ‘this reverses the previous orthodoxy, which held that quantum effects could not exist in biological systems because of the amount of noise in these systems’,,, Environmental noise here drives a persistent and cyclic generation of new entanglement.

    Quantum entanglement in hot systems – 2011
    Excerpt: The authors remark that this reverses the previous orthodoxy, which held that quantum effects could not exist in biological systems because of the amount of noise in these systems,,,
    Environmental noise here drives a persistent and cyclic generation of new entanglement.
    http://quantum-mind.co.uk/quan.....t-systems/

    etc.. etc.. etc…

    Of related note:

    At the 6:52 minute mark of the video, Jim Al-Khalili states:

    “To paraphrase, (Erwin Schrödinger in his book “What Is Life”), he says at the molecular level living organisms have a certain order. A structure to them that’s very different from the random thermodynamic jostling of atoms and molecules in inanimate matter of the same complexity. In fact, living matter seems to behave in its order and its structure just like inanimate cooled down to near absolute zero. Where quantum effects play a very important role. There is something special about the structure, about the order, inside a living cell. So Schrodinger speculated that maybe quantum mechanics plays a role in life”.
    Jim Al-Khalili – Quantum biology – video
    https://www.youtube.com/watch?v=zOzCkeTPR3Q

    And via the ‘way back’ machine to 1998, “instead of a cell dominated by randomly colliding individual protein molecules, we now know that nearly every major process in a cell is carried out by assemblies of 10 or more protein molecules.”

    “We have always underestimated cells. Undoubtedly we still do today. But at least we are no longer as naïve as we were when I was a graduate student in the 1960s. Then, most of us viewed cells as containing a giant set of second-order reactions: molecules A and B were thought to diffuse freely, randomly colliding with each other to produce molecule AB — and likewise for the many other molecules that interact with each other inside a cell. This seemed reasonable because, as we had learned from studying physical chemistry, motions at the scale of molecules are incredibly rapid. Consider an enzyme, for example. If its substrate molecule is present at a concentration of 0.5mM,which is only one substrate molecule for every 105 water molecules, the enzyme’s active site will randomly collide with about 500,000 molecules of substrate per second. And a typical globular protein will be spinning to and fro, turning about various axes at rates corresponding to a million rotations per second.
    But, as it turns out, we can walk and we can talk because the chemistry that makes life possible is much more elaborate and sophisticated than anything we students had ever considered. Proteins make up most of the dry mass of a cell. But instead of a cell dominated by randomly colliding individual protein molecules, we now know that nearly every major process in a cell is carried out by assemblies of 10 or more protein molecules. And, as it carries out its biological functions, each of these protein assemblies interacts with several other large complexes of proteins. Indeed, the entire cell can be viewed as a factory that contains an elaborate network of interlocking assembly lines, each of which is composed of a set of large protein machines.”
    – Bruce Alberts, “The Cell as a Collection of Protein Machines: Preparing the Next Generation of Molecular Biologists,” Cell, 92 (February 6, 1998): 291-294)
    https://brucealberts.ucsf.edu/publications/BAPub157.pdf
    Editor-in-Chief of Science (2009-2013). Dr Alberts served two six-year terms as the president of the National Academy of Sciences

  61. 61
    PyrrhoManiac1 says:

    @60: Thanks for those links, esp the link to the Shvets and Kolomeisky research. I would need to think a lot more about whether quantum-mechanical effects can mitigate Brownian motion, but on the face of it, it seems plausible if quantum effects can be somehow regulated.

    Still don’t see how that’s going to vindicate the use of engineering principles to describe molecular biology, though.

  62. 62
    kairosfocus says:

    PM1, I did not offer there a full orbed definition of algorithm. A short version would be a finite, goal directed stepwise process with start and halting. Start implies a beginning state, which embraces initial conditions, stepwise implies cumulative discrete stages which can include inputs, storage, processing, outputs, actuations etc. This implies a certain recursiveness i.e. a fetch decode execute cycle, but looping, branching or a program calling itself repeatedly are not necessary parts of an algorithm, never mind the 80% of time in loops issue. Halting and finite imply termination conditions for completion or failing or emergency etc. I need not go into Turing machines, the IPO framework etc, or even that programming is coding of algorithms that act on structured data. I excerpt below on protein synthesis, which of course shows the relevant naturally evident goal. I note that the algorithms in mind are those that form AA chains, based on codon sequences in mRNA in ribosomes and using tRNA. That is quite enough, whatever else may go on. KF

    PS, Wikipedia confesses by way of admitting the general consensus:

    Protein biosynthesis (or protein synthesis) is a core biological process, occurring inside cells, balancing the loss of cellular proteins (via degradation or export) through the production of new proteins [–> goal]. Proteins perform a number of critical functions [–> information and configuration based function] as enzymes, structural proteins or hormones. Protein synthesis is a very similar process for both prokaryotes and eukaryotes but there are some distinct differences.[1]

    Protein synthesis can be divided broadly into two phases – transcription and translation [–> language and code terms, of course there is also editing] . During transcription, a section of DNA encoding a protein [–> the coded algorithm], known as a gene, is converted into a template molecule called messenger RNA (mRNA) [–> in actuality mRNA is a string data structure used to stepwise start, elongate and terminate the AA chain, step by step per coded instruction] . This conversion is carried out by enzymes, known as RNA polymerases, in the nucleus of the cell.[2] In eukaryotes, this mRNA is initially produced in a premature form (pre-mRNA) which undergoes post-transcriptional modifications [–> editing] to produce mature mRNA. The mature mRNA is exported from the cell nucleus via nuclear pores to the cytoplasm of the cell for translation to occur. ,b>During translation, the mRNA is read by ribosomes which use the nucleotide sequence of the mRNA to determine the sequence of amino acids [–> tepwise is skiped over] . The ribosomes catalyze the formation of covalent peptide bonds between the encoded amino acids to form a polypeptide chain.

    Following translation the polypeptide chain must fold to form a functional protein; for example, to function as an enzyme the polypeptide chain must fold correctly [–> naturally evident goal, i.e. teleology] to produce a functional active site. In order to adopt a functional three-dimensional (3D) shape, the polypeptide chain must first form a series of smaller underlying structures called secondary structures. The polypeptide chain in these secondary structures then folds to produce the overall 3D tertiary structure. Once correctly folded, the protein can undergo further maturation through different post-translational modifications. Post-translational modifications can alter the protein’s ability to function, where it is located within the cell (e.g. cytoplasm or nucleus) and the protein’s ability to interact with other proteins.[3]

    Protein biosynthesis has a key role in disease as changes and errors in this process [–> bugs], through underlying DNA mutations or protein misfolding, are often the underlying causes of a disease. DNA mutations change the subsequent mRNA sequence, which then alters the mRNA encoded amino acid sequence. Mutations can cause the polypeptide chain to be shorter by generating a stop sequence which causes early termination of translation. [–> halting, through the three stop codons, this is also arguably a failsafe, misalignment or misframing or random change is fairly likely to trigger a halt so there will not be a runaway process] Alternatively, a mutation in the mRNA sequence changes the specific amino acid encoded at that position in the polypeptide chain. This amino acid change can impact the protein’s ability to function or to fold correctly.[4] Misfolded proteins are often implicated in disease as improperly folded proteins have a tendency to stick together to form dense protein clumps. These clumps are linked to a range of diseases, often neurological, including Alzheimer’s disease and Parkinson’s disease.[5]

  63. 63
    PyrrhoManiac1 says:

    @62 — it seems to me that you don’t distinguish between functions and goals. I infer this from your editorial insertion of “–> goal” after a description of protein synthesis.

    I would call that a function, and on my view, the difference between functions and goals is quite important.

    Would need to think about this for a bit about how I want to parse that distinction and why it matters.

  64. 64
    Seversky says:

    If you haven’t already seen them, you may find the series of posts on Larry Moran’s blog Sandwalk under the heading “The Function Wars” useful.

  65. 65
    jerry says:

    From Behe’s book, Darwin Devolves. The new Function Wars (Referred to above)

    A few years ago I reviewed research done on laboratory evolution of microbes

    (including the work of the Michigan State lab done to that point) for a journal called the Quarterly Review of Biology. The article was titled “Experimental Evolution, Loss-of-Function Mutations, and ‘The First Rule of Adaptive Evolution. “” The goal was to reexamine lab evolution work from the past four decades and evaluate it in terms of the mode in which the microbes evolved. As Darwin himself knew, there are three very general ways in which an organism can adapt: (1) it can gain a new ability; (2) it can lose an old one; or (3) it can tweak or modify something it already has. Because evolution can proceed in any one of those three ways, it’s a question of profound importance to science to determine which one tends to predominate.

    But when we try to categorize evolutionary events, we quickly run into a problem. What superficially looks like a gain or loss can actually be the opposite at the molecular level-a level Darwin and his contemporaries knew nothing about. To bring badly needed clarity to evaluating mutations, I divided them into three categories depending on how any particular change affected what I termed a “Functional Coded elemenT” or “FCT” (pronounced “fact”). A FCT is a stretch of information-bearing sequence that encodes a defined feature in either DNA or protein. Examples of FCTs are genes, control regions, protein-binding sites, protein modification sites, and other such features. A given mutation, then, can either make a new FCT (which I dubbed a gain-of-FCT mutation), destroy an old one (loss-of-FCT mutation), or do something else-either tweak an old FCT in a way that leaves it still working or affect some non coded feature of a cell (which I called a modification-of-function mutation). Some mutations can be ambiguous and hard to classify, but most are straightforward.

    Is Behe’s book, the ultimate guide to what’s possible through Darwinian natural selection?

  66. 66
    kairosfocus says:

    PM1, a goal is an end state that meets certain criteria of acceptable achievement, which may be as basic as restraining failure from ruinous consequences. Functions are different from goals, though they may be involved. I simply noted that “the production of new proteins ” implies the presence of a goal. As to producing endless hyperskeptical debates over the meaning of function, notice what Wiki confesses “Proteins perform a number of critical functions as enzymes, structural proteins or hormones” and, on the first, “to function as an enzyme the polypeptide chain must fold correctly to produce a functional active site” then noting “Misfolded proteins are often implicated in disease as improperly folded proteins have a tendency to stick together to form dense protein clumps.” where “These clumps are linked to a range of diseases, often neurological, including Alzheimer’s disease and Parkinson’s disease.” Hyperskeptical rhetorical games here run into observable and sometimes harsh realities. KF

  67. 67
    PyrrhoManiac1 says:

    @66:

    PM1, a goal is an end state that meets certain criteria of acceptable achievement, which may be as basic as restraining failure from ruinous consequences. Functions are different from goals, though they may be involved. I simply noted that “the production of new proteins ” implies the presence of a goal.

    I think of goals as (first and foremost) what organisms are attempting to achieve in order to satisfy their needs. Goals can be subordinate to one another, e.g. I’m going to store to buy some eggs in order to bake some cookies in order to do something nice for my co-workers in order to ____. (And as we know, the question of whether there is a final goal or summum bonum is one of the most important questions in Western philosophy.)

    Functions, then, are what sub-systems have that tend to contribute to the realization of a goal. So, I would say that the function of the heart is to pump blood, not that the heart has the goal of pumping blood. But the function of the heart is to pump blood, and not to make a thump-thump sound, because the pumping of blood contributes to the continued biological existence of the organism, and the thump-thump sound does not.

    (Some philosophers have argued that the heart has the function of pumping blood, and not a function of making a thump-thump sound, because in the evolutionary past, organisms with pumping hearts tended to be more fit and pass that trait along to subsequent generations. I’m deeply skeptical of the idea that selection can explain functions — though selection has other explanatory purposes. Put otherwise, I don’t think that evolution can explain teleology, and it was a colossal blunder of 20th century biology to think that it can.)

    If we’re OK with that, then I’d say that protein synthesis is much the same as the pumping of the heart — it has a function, and things that have functions can also malfunction, but the functions need to be understood in light of the goals — of the cell or of the organism as a whole.

    @64

    If you haven’t already seen them, you may find the series of posts on Larry Moran’s blog Sandwalk under the heading “The Function Wars” useful.

    Thanks for that! Very interesting. I guess I’m more sympathetic than Moran to the idea that we can figure out the explanatory priority between causal role accounts or selected effect accounts, but I’m open to agreeing with him that in many cases (e.g. genomics research) it doesn’t matter all that much.

  68. 68
    kairosfocus says:

    PM1, what you think of organisms has little to do with goal in the narrow context of algorithms. What does the executed algorithm end up at if correctly run on reasonable start points and inputs, and what does it do in event of failure or emergency are basic programming issues. KF

  69. 69
    PyrrhoManiac1 says:

    @68

    PM1, what you think of organisms has little to do with goal in the narrow context of algorithms. What does the executed algorithm end up at if correctly run on reasonable start points and inputs, and what does it do in event of failure or emergency are basic programming issues. KF

    Oh, sure, I pretty much agree with that — though it is worth a moment’s notice to realize that cybernetics in the 1940s-1960s was motivated by the idea that we can use the concept of an algorithm to give a mechanistic explanation of organismal teleology, and that’s what inspired Mayr’s concept of “the genetic program.”

    The reason I’ve been carrying on about organisms here is because I don’t think that organisms are like artifacts or machines, and that’s why engineering principles — not even computer science principles — can help us really understand what they’re doing and how they’re doing it.

    The idea that organisms are basically just really complicated machines is the conceptual basis of what Descartes got wrong and everything that’s followed from that error (including the assumption that biology is reducible to physics). I want us to go back to Aristotle’s clear-sighted recognition that organisms are fundamentally different from artifacts, and develop theoretical biology on that basis. This is the approach taken by Stephen Talbott and J. Scott Turner — names that I know are respected (if not admired) by the UD regulars.

  70. 70
    kairosfocus says:

    PM1, we may debate organisms on the whole till the Egrets fly home to their roosts Saturday next week. Organisms start with cells, which are vastly beyond the tiny but crucial slice we are looking at, the process logic of chaining AA’s toward proteins based on a stepwise process that starts, extends, terminates based on as we all know a succession of codons in mRNA fed into a ribosome. This is based on the genetic code and is recognisably goal directed, stepwise, finite and halts. That is enough to see a crucial part of the architecture of the world of life, its use of code [so, language and logic], also the presence of goals, where yes it also reflects deep knowledge of polymer chemistry. This is a class of synthesis that dwarfs what we can do but we can recognise what it is. Onward, if we can keep from accidents and abuses it doubtless transforms chemistry and technology. KF

  71. 71
    Alan Fox says:

    Just a reminder for KF that sequence =/= function. Were I more computer-literate, I could devise a program that would write DNA sequences that begin with AUG, then a random choice of codons excluding TAA, TGA, TAG then adding a stop codon after a number of codons biased around an average protein sequence length, say 300 or so aa’s. There is no way as yet to discern putative function of the translated protein from a sequence length generated as I describe, other than synthesizing it and observing any biochemical activity. Sequence =/= function.

  72. 72
    bornagain77 says:

    “Were I more computer-literate”

    Yet ‘computer-literate’ Darwinists who have tried to simulate Darwinian evolution on computers “have either failed or inadvertently cheated.”

    Top Ten Questions and Objections to ‘Introduction to Evolutionary Informatics’ – Robert J. Marks II – June 12, 2017
    Excerpt: “There exists no model successfully describing undirected Darwinian evolution. Hard sciences are built on foundations of mathematics or definitive simulations. Examples include electromagnetics, Newtonian mechanics, geophysics, relativity, thermodynamics, quantum mechanics, optics, and many areas in biology. Those hoping to establish Darwinian evolution as a hard science with a model have either failed or inadvertently cheated. These models contain guidance mechanisms to land the airplane squarely on the target runway despite stochastic wind gusts. Not only can the guiding assistance be specifically identified in each proposed evolution model, its contribution to the success can be measured, in bits, as active information.,,,”,,, “there exists no model successfully describing undirected Darwinian evolution. According to our current understanding, there never will be.,,,”
    https://evolutionnews.org/2017/06/top-ten-questions-and-objections-to-introduction-to-evolutionary-informatics/
    Robert Jackson Marks II is an American electrical engineer. His contributions include the Zhao-Atlas-Marks (ZAM) time-frequency distribution in the field of signal processing,[1] the Cheung–Marks theorem[2] in Shannon sampling theory and the Papoulis-Marks-Cheung (PMC) approach in multidimensional sampling.[3] He was instrumental in the defining of the field of computational intelligence and co-edited the first book using computational intelligence in the title.[4][5]
    – per wikipedia

  73. 73
    kairosfocus says:

    AF, nowhere have I identified sequence with function. There are however functional sequences, of glyphs or of steps of procedure etc. It is those that are being discussed. That WE currently lack the depth of knowledge of polymer chemistry to predict fold, agglomeration, modifications and function also does not change the fact that we observe actual AA sequences constructed step by step on instructions and see that they become functional proteins, i.e. by algorithmic action. What we do not yet know does not remove what we do know. I still believe Dr Tour is pessimistic and within a century likely we will be able to synthesise new life from scratch, building on what Venter et al have done. KF

  74. 74
    Querius says:

    Otangelo @45,
    Miraculously, I found a reference in my first try this evening! In his book, Genetic Entropy, Cornell University research geneticist, J.C. Sanford, writes on pp 134-135

    Once the mutation arises in one individual, it has to become “fixed” (such that each individual in the population will eventually have a double dose of that mutation).

    so any specific desired mutation must arise many times before it “catches hold” in the population.

    Our numerical simulations suggest a substantially beneficial mutation will still be lost about 99 out of 100 times (Sanford et al., 2015). Such a beneficial mutation must happen about 100 times before it is likely to “catch hold” within the population.

    I’ve also run across other descriptions and estimates in other books, but I’m not going to press my luck,

    -Q

  75. 75
    Querius says:

    Kairosfocus @50,

    Jerry, I think Q is alluding to the wolves vs rabbits problem.

    Exactly. And grass. The wolf population always trails the population of rabbits, and we know what happens when the rabbits introduced to Australia don’t have enough population control. There’s a damping effect of a more diverse set of predators and prey, but reproduction rates need to change to prevent increasing population oscillations followed by a crash that severely damages the carrying capacity of the ecosystem.

    How did those reproductive adjustments evolve, since they are beneficial to the ecosystem but not beneficial to the evolution of individual organisms?

    -Q

  76. 76
    Querius says:

    PyrrhoManiac1,

    Thank you for your contributions.

    By Brownian motion, I assume you’re describing intracellular transport by means of diffusion, right? I’ve read that diffusion is a primary mechanism, but I’ve also heard of microtubules:

    Under Control Systems in the Living World, Nelson R. Cabej, in Building the Most Complex Structure on Earth, 2013, I read the following:

    Intracellular transport of molecules and organelles is responsible for their delivery to destination sites. Since the transport takes place primarily along microtubules, it is important that the free (plus) end of microtubules finds the correct destination site. Microtubules are dynamic polymers that continually growing or shortening in length to probe and explore many regions of the cell at random.

    Or are you suggesting that microtubules work through Brownian motion . . . or perhaps in concert with gradients in concentrations?

    -Q

  77. 77
    jerry says:

    How did those reproductive adjustments evolve, since they are beneficial to the ecosystem but not beneficial to the evolution of individual organisms?

    Good, but only part of what I am trying to express.

    Somehow there is something preventing the improvement of the species. I’m using the ecology as a limitation of change. The process of natural selection would not have the influence of the ecology in mind as a superior organism leaves offspring.

    But the real point is much, much bigger than this. Changes in the genome that lead to superior characteristics just won’t happen. They cannot possibly happen.

    A very interesting thing is that this claim has been made several times and no one disagrees. It is just ignored by both sides of the debate. Thus, the much more interesting thing is that no one is interested in a basic flaw of the supposedly main driver of Evolution.

    So is Darwinian Evolution self refuting or is the claim just pie in the sky? I find no logic against the claim.

    What are the forces preventing substantial change? Pointing to the ecology is just one piece of evidence that there is something that is limiting change. Is it the only reason why change must be trivial? Is there other evidence besides the ecology that shows that change must be limited?

    Then there is the obvious piece of evidence. That most people believe Darwinian Evolution is true. Using the atheist trope is bogus since most non-atheists believe it. Is the “beautiful theory” explanation at the root cause for this false belief?

  78. 78
    PyrrhoManiac1 says:

    @76 — in talking about Brownian motion I was referring only to diffusion (and osmosis, a kind of diffusion). Transport by microtubules and other elements of the cytoskeleton are far more constraining and constrained — and that’s necessary for a structure to be functional.

  79. 79
    Querius says:

    PyrrhoManiac1 @78,

    Ok. Thus, it now seems that most intracellular transport is through microtubules rather than diffusion, right?

    -Q

  80. 80
    Otangelo says:

    Here, as a syllogism:
    Large-scale evolution by natural selection is a non-testable hypothesis
    1. P. R. Ehrlich (1988): In modem evolutionary genetics, natural selection is defined as the differential reproduction of genotypes (individuals of some genotypes have more offspring than those of others) based on the mutations they carry and the environment in which they live. Organisms that are better suited to their environment will reproduce more and so increase the proportion of the population with their traits. ( More reproduction of a genotype = survival of the fittest = measure of fitness)
    2. T. Bataillon (2014): Obtaining estimates of mutation rates and effects has historically been challenging. I. Cvijovi? (2015): The fate of each mutation depends critically on its fitness in each environment, the dynamics of environmental changes, and the population size. We still lack both a quantitative and conceptual understanding of more significant fluctuations, where selection in each environment can lead to measurable changes in allele frequency.C. J. Graves (2019): Variable environments can cause the same allele to have differing effects on fitness depending on an individual’s environmental context. V. Ž. Alif (2021): Fitness is difficult to measure accurately. The metric of fitness is scarcely used because the estimation of an individual’s reproductive value requires long-term pedigree data, which is rarely available in wild populations where following individuals from birth to death is often impossible. D.Coppedge (2021): The central concept of natural selection cannot be measured. This means it has no scientific value.
    3. The key question, namely how mutations in fact affect fitness has not been answered. Darwin’s Theory can not be tested, nor quantified. The unknown factors are too many, the variations in the environment, and population and species behavior vary too. It cannot be defined what influence the given environment exercises in regard to specific animals and traits in that environment, nor how the environmental influence would change the fitness and reproduction success of each distinct animal species. Large-scale evolution is at best a non-testable hypothesis, which then remains just that: a hypothesis. Since Darwin’s idea cannot be tested, it’s by definition, unscientific, and anyone claiming that natural selection explains biodiversity makes that claim based on blind confidence and belief. Not evidence.

  81. 81
    whistler says:

    Otangelo
    Here, as a syllogism:
    Large-scale evolution by natural selection is a non-testable hypothesis

    Of course is not testable , why do you think they invented evolutionary /genetic “algorithms”? It’s easier to code a software to do what you want to prove than “to convince” the nature to sing the darwin’s song.

  82. 82
    jerry says:

    Since Darwin’s idea cannot be tested, it’s by definition, unscientific

    People have been saying that for years. No one cares.

    anyone claiming that natural selection explains biodiversity makes that claim based on blind confidence and belief. Not evidence.

    Again no one cares and this observation will go nowhere.

    They will say it’s cumulative over tens of millions of years. Then ignore it.

    Change the discussion and maybe it will go somewhere. The above have been standard objections for years.

  83. 83
    Seversky says:

    There is a difference between impractical to test and untestable even in principle.

  84. 84
  85. 85
    jerry says:

    29+ Evidences for Macroevolution

    Why don’t you take the best one or at least a very convincing piece of evidence and we can discuss it?

  86. 86
    Alan Fox says:

    Why don’t you take the best one or at least a very convincing piece of evidence and we can discuss it?

    Oh, disingenuous one. You’re on record here as refusing to look at any evidence for evolution, while at the same time being unable or unwilling to provide any evidence for “Intelligent Design”.

  87. 87
    Querius says:

    Alan Fox @86,

    . . . while at the same time being unable or unwilling to provide any evidence for “Intelligent Design”.

    Unfortunately, you seem to have ignored all the posts by Jerry and many others here in which we have provided evidence for Intelligent Design. There are also answers described here:
    https://uncommondescent.com/comment-policy/put-a-sock-in-it/
    See Intelligent Design is Not a Valid Theory Since it Does Not Make Predictions
    and Intelligent Design Makes No Scientific Observations

    How do you explain that even well-known scientists admit there’s evidence for design:

    Biology is the study of complicated things that have the appearance of having been designed with a purpose. – Richard Dawkins

    Your assertion that we haven’t provided any evidence for Intelligent Design doesn’t make it so.

    -Q

  88. 88
    Alan Fox says:

    Unfortunately, you seem to have ignored all the posts by Jerry and many others here in which we have provided evidence for Intelligent Design.

    Not true. I try and make a point of reading Jerry’s comments as I find them entertaining. It’s possible I’ve overlooked some that got sandwiched between comments by posters such as BA77, Kairosfocus, Related that I tend to scroll over.

    Jerry has never produced any evidence for “Intelligent Design” in the comments I’ve read. I keep asking for something, anything from ID proponents that would support ID as a valid, scientific hypothesis. I ask more specifically about FSCO/I and Dembski’s CSI. No substantive answers come forth.

  89. 89
    jerry says:

    never produced any evidence…

    No substantive answers come forth.

    What an absurd comment!

    Argument by assertion that all evidence I do not like is irrelevant. No honest person could make such a statement. Look to the Caine Mutiny defense for an answer.

    Signed – the opposite of disingenuous

  90. 90
    Alan Fox says:

    Jerry, you forget, as always, to produce, or link to empirical evidence supporting “Intelligent Design”.

  91. 91
    Querius says:

    Alan Fox @90,

    Here’s some empirical evidence against current OOL, which is strong evidence for Intelligent Design:
    https://youtu.be/v36_v4hsB-Y?t=139

    -Q

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