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Is there evidence for natural selection ?

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1 Is there evidence for natural selection ? on Fri Mar 17, 2017 10:49 pm

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Is there evidence for natural selection ?

http://reasonandscience.heavenforum.org/t2458-is-there-evidence-for-natural-selection

According to Darwins Theory, what drives 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, higher survival rates upon specific gene-induced phenotype adaptations to the environment,  higher reproduction rates upon specific evolutionary genetic modifications. It's a fact that harmful variants, where a mutation influences negatively health, fitness, and reproduction ability of organisms diminishes. 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. The environment is not stable, but changes. Science would need to have the knowledge 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. It cannot be defined what influence given environment exercises in regard to specific animals and traits in that environment, nor how the environmental influence would change 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 influence in 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 model, and see what's statistically significant, and get meaningful, real life results. The varying factors are too many and nonpredictive. Darwin's idea, therefore, which depends on variable, unquantifiable multitude of factors that cannot be known, cannot be tested and is at best a hypothesis, which then remains just that: a hypothesis. Since Darwin's idea cannot be tested, it's by definition, unscientific.

Peter Smartt A mutation would need to be quite strongly positive to be visible to natural selection. If it only had a selection advantage of a few percent, it won't make any difference because it will be invisible among all the"white noise" of 1) randomness in which individuals survive to reproduce more, 2) other mutations at other loci, 3) epigenetics, 4) random genetic drift. Regarding 2), the vast majority of mutations either have no effect our are mildly deleterious, but can't be selected against because they are to mild to be seen by natural selection, so they can potentially accumulate in the genome. Regarding 4), in a stable population, each individual will have on average 2 offspring, and on average the mutation will be passed on to one of them. This individual will then pass the mutation on to one of its two offspring, so only 1 in 4 of the grandchildren will carry the mutation. So it is virtually inevitable that the mutation will eventually be lost in a stable population. Also regarding 2), very few traits are actually mendelian. Most are caused by thousands of SNPs throughout the genome, with each SNP only causing a miniscule but statistically significant effect on the trait. That is why a condition like endometriosis, which is highly genetically determined but is obviously bad for fertility, can exist, because of an unfortunate combination of thousands of SNPs. So all that natural seldom can do is to remove the most profoundly deleterious mutations from the population.

Darwin’s Greatest Discovery: Design Without Designer
https://www.ncbi.nlm.nih.gov/books/NBK254313/
It was Darwin’s greatest accomplishment to show that the complex organization and functionality of living beings can be explained as the result of a natural process—natural selection—without any need to resort to a Creator or other external agent. The origin and adaptations of organisms in their profusion and wondrous variations were thus brought into the realm of science. Darwin seeks to explain the design of organisms, their complexity, diversity, and marvelous contrivances, as the result of natural processes. Darwin brings about the evidence for evolution because evolution is a necessary consequence of his theory of design.

What is natural selection? 
Variation. Organisms (within populations) exhibit individual variation in appearance and behavior.  These variations may involve body size, hair color, facial markings, voice properties, or number of offspring.  On the other hand, some traits show little to no variation among individuals—for example, number of eyes in vertebrates.
Variation can be due to many different mechanisms. 

Inheritance.  Some traits are consistently passed on from parent to offspring.  Such traits are heritable, whereas other traits are strongly influenced by environmental conditions and show weak heritability.
The change of the environment will obviously provoke organismal change. But that change can be due to various mechanisms. 

High rate of population growth. Most populations have more offspring each year than local resources can support leading to a struggle for resources.  Each generation experiences substantial mortality.
That does also not demonstrate that natural selection was in action. 

Differential survival and reproduction.  Individuals possessing traits well suited for the struggle for local resources will contribute more offspring to the next generation.
Neither is that fact necessarly explained through natural selection

Natural Selection, Genetic Drift, and Gene Flow Do Not Act in Isolation in Natural Populations
In natural populations, the mechanisms of evolution do not act in isolation. This is crucially important to conservation geneticists, who grapple with the implications of these evolutionary processes as they design reserves and model the population dynamics of threatened species in fragmented habitats.

Natural selection, genetic drift, and gene flow are the mechanisms that cause changes in allele frequencies over time. When one or more of these forces are acting in a population, the population violates the Hardy-Weinberg assumptions, and evolution occurs. The Hardy-Weinberg Theorem thus provides a null model for the study of evolution, and the focus of population genetics is to understand the consequences of violating these assumptions. Natural selection occurs when individuals with certain genotypes are more likely than individuals with other genotypes to survive and reproduce, and thus to pass on their alleles to the next generation. 

As Charles Darwin (1859) argued in On the Origin of Species, if the following conditions are met, natural selection must occur:

There is variation among individuals within a population in some trait.
This variation is heritable (i.e., there is a genetic basis to the variation, such that offspring tend to resemble their parents in this trait).
Variation in this trait is associated with variation in fitness (the average net reproduction of individuals with a given genotype relative to that of individuals with other genotypes).
Directional selection leads to increase over time in the frequency of a favored allele.

Consider three genotypes (AA, Aa and aa) that vary in fitness such that AA individuals produce, on average, more offspring than individuals of the other genotypes. 

The  genetic  modification based on evolution through mutations and natural selection based on  environmental pressures is supposed to be due to:

1. higher SURVIVAL rates upon specific gene-induced phenotype adaptation to the environment. 
2. higher reproduction rates upon specific genetic modifications through evolution

Maybe the reproduction rate is not influenced by the new mutation. In that case, the population with the new trait would have to have a higher reproductionrate by luck or chance...... 
In any case, that are TWO DIFFERENT things. Natural selection concerns the survival of an existing species through the fixation of a positive trait in the population that supposedly emerged and was passed forward accidentally through random mutations.  Reproduction is however about the production of a new individual.

One of the main tenets of the theory of evolution is:
Differential survival and reproduction.  Individuals possessing traits well suited for the struggle for local resources will contribute more offspring to the next generation.

Understanding Evolution
http://evolution.berkeley.edu/evolibrary/article/evo_32
It's more accurate to think of natural selection as a process rather than as a guiding hand. Natural selection is the simple result of variation, differential reproduction, and heredity — it is mindless and mechanistic. It has no goals; it's not striving to produce "progress" or a balanced ecosystem.

What is the definition of "differential reproduction"?
This means that individuals with a certain genotype for a given locus or gene have more reproductive success than individuals within the same population that have  other genotypes for for that same gene. This difference in reproductive success can be the result of longer survival that results in more reproductive events over a lifetime, more offspring per reproductive event, or more frequent successful reproductive events.
Differential reproduction is the idea that those organisms best adapted to a given environment will be most likely to survive to reproductive age and have offspring of their own. Organisms that are successful in their environments will be more likely to be successful in reproduction, and therefore the better-adapted organisms will reproduce at a greater rate than the less well-adapted organisms. 2
Differential reproduction is needed because for natural selection to occur, one group with a specific trait has to have more reproductive success than another group within the same population.

The Extended synthesis, Pigliucci , pg.13
A second restriction overcome by the new approach is externalism. The nearly exclusive concentration of the Modern Synthesis on natural selection gave priority to all external factors that realize adaptation through differential reproduction, a fundamental feature of Darwinism not rooted solely in scientific considerations (Hull 2005).

If a short definition that catches the core of the process is desired, we can say that natural selection is “the differential reproduction of hereditary variations,” which is how textbooks often define it. That is saying simply that useful variants multiply more effectively over the generations than less useful (or harmful) variants. Thus a cheetah able to run faster will catch more prey, and therefore live longer and leave more offspring than a slower cheetah. So, a hereditary variant that boosts fleetness will increase in frequency over the generations and eventually replace the slower variant.

Its evident that harmful variants, where the mutation influences negatively health, fitness, and reproduction hability of an organisms diminshes. These are sorted out, or die through desease. That says nothing however in regard of an organism gaining MORE fitness through evolution of new advantageous traits. 

How can we quantify and compare the reproductive frequency of social rank of alpha individuals to  the strength of selection of new traits through  mutations  of non-alphas?

DOMINANCE RANK, COPULATORY BEHAVIOR, AND DIFFERENTIAL REPRODUCTION
http://www.journals.uchicago.edu.sci-hub.cc/doi/abs/10.1086/412672
The view that high social rank is associated with high levels of both copulatory behavior and the production of offspring is widespread in the study of animal social behavior.

This fact alone would falsify the claim that positive mutations would result automatically in higher replication of the animals with the evolved variations. At least in species which have the social hiearchy where higher ranked animals have preference to mate with females.

In order to demonstrate the validity of this hypothesis it is necessary first to resolve ambiguities in the concept of dominance and to assign ranks by means of valid procedures. Second, copulatory behavior must be properly sampled, measured, and related to rank. Finally, it must be demonstrated that rank and increased copulatory behavior actually lead to increased reproduction.

And it must be demonstrated that advantageous evolutionary traits outcompete social behavior and rank in terms of reproduction success. 

Each step in this process entails conceptual and methodological difficulties. There have been many studies of rank and copulatory behavior, fewer of rank and differential reproduction, and very few of rank, copulatory behavior, and differential reproduction. The consistency of results obtained varies with taxon; results of particular consistency appear in studies of carnivores and ungulates. Both the concept of dominance and the validity of the hypothesis relating it to copulatory behavior and to differential reproduction appear viable for at least some species, although the body of data relating rank to both copulation and differential reproduction remains minimal.

This is highly telling, and of crucial importance. Think about it. The body of data in regard of elucidating one of the most important ingredients of the theory of evolution are minimal !! The author admits conceptual and methodological difficulties to study this issue.  There are no relevant studies that provide empirical data that differential reproduction can outcompete rank and copulatory behavior. 
This fact alone puts Darwins ToE into speculative territory at best. Fantasia land at worst !! 

Among the most prominent hypotheses in the study of animal social behavior is the view that dominant animals gain differential access to mating partners and consequently leave more offspring than do their subordinates. This view was promulgated by some of the earliest students of dominance (e.g., Zuckerman, 1932; Mas- low, 1936) and is often asserted in secondary references. For example, Barash (1977) has written that "There is abundant evidence that such dominant individuals engage in more matings and hence are more fit than are subordinates" (p. 237). This hypothesis linking dominance, copulatory behavior, and differential reproduction has elicited vigorous skepticism as well as advocacy (e.g., Bernstein, 1976; Gartlan, 1968; Kolata, 1976; Rowell, 1974).

The very validity of the concept of dominance has been questioned, and inconsistencies in the results of studies designed to link dominance, copulatory behavior, and differential reproduction have been noted. Relevant research has been conducted on a wide range of species from cockroaches to chimpanzees and has appeared in the literature of animal science, anthropology, comparative psychology, ethology, and a variety of other biological disciplines. Most of the relevant reviews (e.g., Bernstein, 1976; Kolata, 1976; Rowell, 1974) have focused on a limited range of taxa. The objective of this paper is to review the literature on dominance, copulatory behavior, and differential reproduction in a broad perspective, in an attempt to bring together both the results and difficulties of research on various species, conducted within different disciplines and utilizing different methods. Emphasis is placed upon the nature of the data required to support the hypothesis and the adequacy of the evidence available.

Summary by Taxon 
Non-Mammalian Species. Relatively few studies of invertebrates were located. This may be due in part to the necessity of individual recognition as a prerequisite for stable dominance hierarchies (Schjelderup-Ebbe, 1935). Nevertheless, dominance relationships have been reported in a variety of invertebrate species (see Gauthreaux, 1978), and research on copulatory behavior and reproduction ought to be feasible. There are few studies of birds, presumably because so many are territorial or maintain stable pair bonds, or both. Those studies of the male of non-mammalian species that have been reported have generally been consistent in yielding results indicative of an association between rank and copulatory behavior. Studies of hens, however, suggest the possibility of an inverse correlation (Guhl, 1950; Guhl et el., 1945). 
Primates. The literature on primates is most difficult to summarize, both because primate behavior is so easily influenced by relatively subtle variables and because so many studies have been conducted. Fortunately, several good reviews of this literature treat the interpretation of primate behavior in greater depth than is possible here (e.g., Bernstein, 1976; Deag, 1977;). Some species of primates do not form stable hierarchies, and there are others in which rank may be uncorrelated with copulation and differential reproduction. Nevertheless, a substantial body of evidence suggests that rank is sometimes associated with preferred access to females. It is unlikely that all of these effects can be explained by the difficulties discussed by various critics. Rank and copulatory behavior do appear to be associated in some primate species at least under some conditions. It is important, however, not to generalize from this conclusion to the order as a whole.

CONCLUSIONS 
The important place given the problem of rank, copulatory behavior, and reproduction in the study of animal social behavior is appropriate because an understanding of these relationships could greatly facilitate an understanding of the broader problem of the evolution of social behavior.

The real issue is if copulatory behavior outperforms differential reproduction. 

The importance of the problem should not be overstated, however; 

The contrary is the case. If copulatory behavior outperforms differential reproduction, Darwins theory is falsified, since its a essential mechanism to spread new traits in the population. 

DIFFERENTIAL REPRODUCTIVE SUCCESS AND HERITABILITY OF ALTERNATIVE REPRODUCTIVE TACTICS IN WILD ATLANTIC SALMON (SALMO SALAR L.) 

To conclude, although our results showed unequal reproductive success between salmon tactics, a clear demonstration of equality (or not) of lifetime fitness of alternative reproductive tactics would be very difficult to achieve under natural conditions. This is mainly because individuals originating from one tactic can potentially switch to the other tactic and also because heritability might be highly variable depending on different sets of environmental conditions. Also, the variation in heritability between habitats and tactics observed in this study shows that previous models aiming to explain the coexistence of alternative reproductive tactics in the context of the conditional strategy theory (Gross and Repka 1998a,b) based on a single heritability estimate for the entire population are likely inappropriate to capture the complexity of factors involved in the expression of alternative
life-history tactics.

Since this problem extends to almost all life, above makes the ToE basically a "theory" that CANNOT BE TESTED. 

What about fitness?
http://evolution.berkeley.edu/evolibrary/article/evo_27
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.

Variation in fitness of organisms.  Definitions of fitness:
www.agron.iastate.edu/~weeds/AG517/Content/WeedEvol/NaturalSelection/natselect.html" target="_blank" rel="nofollow">http://agron-www.agron.iastate.edu/~weeds/AG517/Content/WeedEvol/NaturalSelection/natselect.html
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  

Natural selection: On fitness
http://inspiringscience.net/2012/03/20/natural-selection-on-fitness/
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. There are several ways to measure fitness; for example, “absolute fitness” measures the ratio of a given genotype before and after selection while “relative fitness” measures differential reproductive success  — that is, the proportion of the next generation’s gene pool that is descended from a particular organism (or genotype) compared with competing organisms (or genotypes). 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”?  After all, if fitness just means “relative reproductive success”, then the phrase becomes “survival of the successful reproducers”; since evolutionary survival can also be understood as reproductive success, this simply becomes “reproductive success of the successful reproducers”, reducing the vaunted theory of evolution to a circular argument  — a tautology.  Of course, evolution doesn’t actually reduce to a simple bit of circular reasoning.  The flaw in this argument is the idea that “survival of the fittest” describes the mechanism of evolution.  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 just a metric to keep track of this process.  There is no circular argument because “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.

Evolution made simple: heritable variation and differential reproduction
http://biologos.org/blogs/dennis-venema-letters-to-the-duchess/evolution-basics-an-introduction-to-variation-artificial-selection-and-natural-selection
Within any population of organisms, whether domesticated or in the wild, heritable differences exist. We now understand that these heritable differences arise from differences in genetic information (i.e. variation in DNA sequences), but this insight was unknown in Darwin’s time. What Darwin did appreciate, without knowing its molecular basis, was that offspring on average tend to resemble their parents more so than other members of the population at large. From this he inferred, correctly, that much variation was heritable: it was passed down from parent to offspring. Darwin would also note that if variation is subjected to selection, that average character traits of a population could shift over time.

In an nutshell, this is the core of evolutionary theory: that changes in heritable variation over time can shift average characteristics of a population, and that differential reproductive success (selection) is a major mechanism for driving changes in heritable variation from one generation to another.

The author suggests that a) higher reproduction rates ( differential reproductive success ) is the result of natural selection. But  higher SURVIVAL rates upon better adaptation to the environment based on random mutations are BOTH supposed to be the outcome of natural selection. These are TWO SEPARATE things that NS is supposed to explain.

How can random mutations give rise to  higher fitness and higher reproduction of of the individuals with the new allele variation favoured by natural selection, and so spreading in the population ? 

This seems in fact to be a core issue which raises questions.
Random mutations are random
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 of a organism and a survival advantage over the other individuals without the mutation ?

Effects of new mutations on fitness: insights from models and data 
http://onlinelibrary.wiley.com/doi/10.1111/nyas.12460/pdf
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); however, there have been recent advances on both fronts. Future work should be aimed at identifying factors driving the observed variation in the the distribution of fitness effects.

Conclusions
What can we say about the distribution of fitness effects of new mutations? For the DFE of beneficial mutations, experimentally inferred distributions seem to support theory for the most part. When the wild-type genotype is close to a fitness optimum, experiments uncover distributions that fit with EVT predictions of the generalized Pareto distribution. DFE has largely been unexplored and there is a need to extend both theory and experiment in this area.


Evolving Thoughts
http://scienceblogs.com/evolvingthoughts/2007/01/22/fitness/
All real populations, if they are not artificially restricted to a lab bench, are of finite size, have patchy environments (consider this: there have to be some members of a population at the fringes, and that causes different selection pressures to apply)., and have variable population densities across the range of the population. Some live in suburbs, some live in urban townhouses, and some live in rural shacks, as it were.


So fitness is something of an abstraction. It’s what would have occurred if none of these other factors intervened. Fitness is in my view an abstract property of the models of population genetics. It basically means the “reproductive value” (Fisher’s preferred term, and metaphor being investment practices. Evolution is capitalism in his mind!) in progeny over many generations. Any organism that has many surviving descendants after at least three generations is fitter than one that doesn’t.

Thats why my observation is: Darwins Theory cannot 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. 

The Distribution of Beneficial and Fixed Mutation Fitness Effects Close to an Optimum
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2429884/
UNDERSTANDING the distribution of fitness effects of beneficial mutation  is necessary to predict the rate and genetic basis of adaptation.

The distribution of fitness effects of new mutations
Nature Reviews Genetics 8610-618 (August 2007) 
http://www.nature.com.sci-hub.cc/nrg/journal/v8/n8/full/nrg2146.html
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. 



If fitness is a relative thing, it cannot be detected and proven that natural selection is the mechanism to produce more offspring, and therefore the new trait spreads in the population. Therefore, evolution is a tautology. It cannot be proven right. 

What is the relation of  mutations  in the genome, and the number of offsprings ? What mutations are  responsible for the number of offsprings produced ? If the theory of evolution is true, there must be a dectectable mechanism, that determines or induces or regulates  the number of offspring based and 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 above  not amazingly various and differentiated, and each species has individual, species specific mechanisms  ? Some have a 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 induece to 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 survivol of the individual ? What kind of environmental  factors influece the survival of a species ? What kind of mutations must be selected to garantee a higher survival rate ? 

Were ancestors , that lived in a certain enviornmental habitat, not exposed to the same environmental pressures ? If so, how did the same pressures cause such big species and phenotype variations ? Many complementary and interdependent ? For example:

There is a very interesting relationship between the Brazil nut tree, the Coryanthes vasquezii orchid, the orchid bee and the agouti. Remove the orchid from the scene and the bees won’t mate and if they don’t mate, the flowers do not get pollinated and produce seed pods. Remove the agouti from the scene and the opened seed pods do not get buried and germinate into new trees, thus greatly reducing the number of new trees to replace the older ones.From an evolutionary stand point, there is no good explanation for this relationship between the tree, orchid, bee and rodent
http://creationrevolution.com/brazil%E2%80%99s-menage-a-quad/


Why did the same environmental pressures  select such various traits, as chameleons with chromophores in their skin for hiding from their prey, apes with fure on the whole body, and human skin with no fure at all ?  

The traits and mechanisms of the nonreproductive or somatic features of life, the products of natural selection, are the means whereby organisms survive, whereas reproductive traits and mechanisms are the means that allow for the production of new generations. Natural selection produces fitness through adaptation, whereas reproduction is about creating new life. Natural selection produces its results without intention, while by all accounts reproduction is a mechanism that garantees the perpetuation of life through offspring.

 Natural selection and reproduction are not only stunningly different; they are contradictory and in some respects opposites. Critically, whereas reproduction seems to have a goal, production of the next generation and the continuance of life, natural selection cares not a whit about the future or for that matter the survival of life, it merely reacts on what is before it. This lack of intention is not incidental but is central to the theory. It is the key element in the proposition that natural selection impels evolution.

Selection suggests that something is actively selected. But that is not the case. If i go to a store, i choose if i want to buy water, or a beer. I select what i want. The selection of a trait that helps a organism to survive is, according to the theory,  not a active  selection. Its just a survivol of the animals that best adapts  to the environment. 

The question is if there is a correlation of random mutations, and if they are capable of providing a survival advantage upon randomness. Upon events, that are not controlled , or directed. The temperature, weather conditions etc. of the environment occur randomly without a defined course. Every day , the weather changes randomly.  The question is, does this environmental change suffice as mechanism to permit a animal of the same species and population with a random mutation in its genome to survive better than an individual which does not have that mutation ? 

If selection was goal driven, there would have to be a “setter of goals,” God or some godless designer. And without doubt the most important thing about Darwin's theory is its exclusion of design or purpose.
Evolution just occurs. Given that the two occurrences are so contradictory, it is appropriate to ask how natural selection can have produced the reproductive features of life.

Beneficial Mutation–Selection Balance and the Effect of Linkage on Positive Selection 1
 The amount of variation is determined by a balance between selection, which destroys variation, and beneficial mutations, which create more. The behavior depends in a subtle way on the population parameters: the population size, the beneficial mutation rate, and the distribution of the fitness increments of the potential beneficial mutations. The mutation–selection balance leads to a continually evolving population with a steady-state fitness variation. 

beneficial mutations, despite their rarity, are what cause long-term adaptation and can also dramatically alter the genetic diversity at linked sites. Unfortunately, our understanding of their dynamics remains poor by comparison. Some more complex forms of positive selection may also prove tractable within the framework we describe, while others will not; these leave open many avenues for future work.

In this case, assuming that the selective regime remains constant and that the action of selection is the only violation of Hardy-Weinberg assumptions, the A allele would become more common each generation and would eventually become fixed in the population. The rate at which an advantageous allele approaches fixation depends in part on the dominance relationships among alleles at the locus in question . The initial increase in frequency of a rare, advantageous, dominant allele is more rapid than that of a rare, advantageous, recessive allele because rare alleles are found mostly in heterozygotes. A new recessive mutation therefore can't be "seen" by natural selection until it reaches a high enough frequency (perhaps via the random effects of genetic drift — see below) to start appearing in homozygotes. A new dominant mutation, however, is immediately visible to natural selection because its effect on fitness is seen in heterozygotes. Once an advantageous allele has reached a high frequency, deleterious alleles are necessarily rare and thus mostly present in heterozygotes, such that the final approach to fixation is more rapid for an advantageous recessive than for an advantageous dominant allele. As a consequence, natural selection is not as effective as one might naively expect it to be at eliminating deleterious recessive alleles from populations.
http://www.nature.com/scitable/knowledge/library/natural-selection-genetic-drift-and-gene-flow-15186648

Pigliucci, the new synthesis:
The original Darwinism, as it was soon to be known, was based on two fundamental ideas: the common descent of all living organisms, and the claim that natural selection is the major agent of evolutionary change, as well as the only one that can bring about adaptation. Organismal shape and structure were interpreted as products uniquely of external selection regimes.

In the book  Divine Action and Natural Selection: Science, Faith, and Evolution, Joseph Seckbach - 2009, page 376 writes : 
The theory of Natural Selection states that all varieties reproduce more than is required to maintain the species in a world in which there is a cruel competitive struggle for survival, and most of those born are destroyed. There are small differences in the characteristics of individuals of each species which affect their ability to survive, so that the organisms which have characteristics most suitable to the environment have a greater chance of surviving long enough to pass on their characteristics to the next generation.

Natural Selection: According to the theory of natural selection, evolution, or the development of life, is neither totally random nor totally directed, but constitutes a combination of these two types of processes. Mutations are accidental, but adaptation to the environment is deliberate. The idea behind natural selection is rather simple, although its operation is most complex and delicate. In every population, some individuals have more offspring than others. Individuals whose hereditary changes are more positive will survive, while individuals with unsuccessful hereditary characteristics will die before giving birth to a continuing generation. Changes that are passed down result in phenomena of differential survival, which accumulate from generation to generation. In this way natural selection acts to constantly improve and preserve the adaptations of life forms and plants to their environment and way of life.

Darwin attached great importance to the principle of natural selection he discovered and considered it the foremost mechanism, the primary driving force behind the evolution of species in the animal world. (Darwin didn’t think it was the exclusive force behind the evolution. He did accept that other forces, such as randomness and sexual selection play an important role.‡‡). Darwin believed that, as this mechanism is so powerful, there is no need for any other element or force, thus there is no role for the Creator or other metaphysical force to play in this picture.§§ Based on this approach, Darwin created a biological base for a materialistic view of reality.

We have no alternative to natural selection for describing, explaining and understanding evolution  and many other biological phenomena. Anyone sees a gap ?

“No one has yet witnessed, in the fossil record, in real life, or in computer life, the exact transitional moments when natural selection pumps its complexity up to the next level” (Kelly, 1995, p. 475).

Scientists engineer animals with ancient genes to test causes of evolution
January 13, 2017
“For the first test case, we chose a classic example of adaptation-how fruit flies evolved the ability to survive the high alcohol concentrations found in rotting fruit. We found that the accepted wisdom about the molecular causes of the flies’ evolution is simply wrong.

Siddiq and Thornton realized that this hypothesis could be tested directly using the new technologies. Siddiq first inferred the sequences of ancient Adh genes from just before and just after D. melanogaster evolved its ethanol tolerance, some two to four million years ago. He synthesized these genes biochemically, expressed them, and used biochemical methods to measure their ability to break down alcohol in a test tube. The results were surprising: the genetic changes that occurred during the evolution of D. melanogaster had no detectable effect on the protein’s function.

What’s that you say? No detectable effect?

One supposes that the gene selected is one, among very many, that can be best ‘reverse-engineered’ to give a facsimile of the ‘ancient’ form. Yet, when tested in vivo, there is no difference found between the supposed ‘slow’ ancestral gene, and the ‘fast’ extant form. This is not how neo-Darwinism is supposed to work. Something is seriously wrong, no?

It might be that the techniques employed to identify the ‘ancestral’ form are bad. Maybe that’s it, and it alone. But, OTOH, maybe something is seriously wrong with current neo-Darwinian theory.


Some notions concerning adaptation will therefore remain difficult to study rigorously. Nevertheless, because of technical and conceptual advances, it should now be possible to experimentally assess the causal predictions of many previously untested or weakly tested hypotheses of historical molecular adaptation, allowing them to be corroborated or, like the classic hypothesis of ADH divergence in D.melanogaster, decisively refuted.


One wonders what’s really left of Darwinism. Between Behe’s Edge of Evolution, Shapiro’s “Natural Genetic Engineering,” the whole field of epigenetics, the disappearing of “Junk-DNA”, and now the disappearance of a ‘fitness’ change in a “classic case” of molecular adaptation, can anyone seriously believe that Darwinism has much to say about how life evolves?

https://m.phys.org/news/2017-01-scientists-animals-ancient-genes-evolution.html
http://www.uncommondescent.com/intelligent-design/refutation-of-a-classic-case-of-molecular-adaptation/

Experimental test and refutation of a classic case of molecular adaptation in Drosophila melanogaster
http://www.nature.com.sci-hub.cc/articles/s41559-016-0025


The frailty of adaptive hypotheses for the origins of organismal complexity
There is no evidence at any level of biological organization that natural selection is a directional force encouraging complexity.
http://www.pnas.org/content/104/suppl_1/8597.full

At PubMed, there are over 30,000 papers about natural selection as the mechanism of evolution. But none which provides empirical proof that the proposal is true. Science does not even know how to measure NS.
So that might be one of the biggest scientific scams and hoaxes, which are kept as "scientific facts", for over 150 years, up to the present day.  When will it be time to acknowledge that biodiversity does NOT rely on that mechanism ? And not even microadaptation/evolution ?  Let's not  equal natural selection to evolution. There are other mechanisms that provoke change over time and frequencies of alleles.

As Creation Safari puts it :

Natural selection has long been in the center of the  controversy of evolution.  Historians agree that Darwin succeeded best in making the general idea of evolution acceptable – but he failed to win the case for natural selection as the mechanism of evolution.  Natural-selection  became "ajour" by the neo-Darwinian synthesis in the 1940s, but that was more by peace treaty between disagreeing groups of scientists (fossil hunters, field naturalists and geneticists) than by demonstration – and the peace treaty signers knew nothing of the revolution in molecular biology just around the corner.

Constraint, natural selection, and the evolution of human body form
March 3, 2016
The authors point out that one cannot measure directional selection on one bone without taking into account how all the other bones are affected.

Human morphological variation is thought to have been partially shaped by natural selection associated with environmental factors like climate. Patterns of variation in body form correspond with latitude, but evolutionary processes that yielded this variation are not yet established. Examining the traits used in these studies (e.g., limb lengthsindependently ignores their genetic covariation, which affects their responses to evolutionary forces. To address this relationship, we estimated the directional selection necessary to evolve correlated traits reflecting body shape across latitudes and examined trait-specific responses. Although most traits appear to be under directional selection, their response is constrained by between-trait covariance. This finding suggests that trait differences among human groups may not directly reflect the forces of selection that shaped them. [Emphasis added.]
http://www.pnas.org/content/113/34/9492.full
see also:
https://www.evolutionnews.org/2016/08/natural_selecti_5/

Measuring Natural Selection on Genotypes and Phenotypes in the Wild
2010 Apr 22
Although estimates of genotypic and phenotypic selection are each informative in their own right, comparisons across both levels, when coupled with identification of the agent(s) of selection, allows us to link genotype, phenotype, and the environment. At present, such studies are rare, but we suspect that comparisons among selection estimates—measured with different data and using distinct approaches—will ultimately provide a more complete picture of the adaptive process.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3918505/

Darwinism for the Genomic Age: Connecting Mutation to Diversification
Front. Genet., 07 February 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.

Consideration of the forces shaping molecular evolution provides one piece of an intricate macroevolutionary puzzle. Molecular phylogenetic analysis has given us the ability to be able to consider both molecular processes and diversification rates simultaneously, giving us a new tool with which to explore the connections between the supply of variation and the production of biodiversity.
http://journal.frontiersin.org/article/10.3389/fgene.2017.00012/full

Differential Strengths of Positive Selection Revealed by Hitchhiking Effects at Small Physical Scales in Drosophila melanogaster
2014 Apr; 31
Despite the central importance of natural selection in evolution, important properties of the selection-driven dynamics of beneficial mutations through populations remain poorly understood. For example, the relative roles of beneficial mutations of small and large effect are still debated, and the extent to which adaptive evolution may be mutation limited is unclear. The intersection of these issues with the extent of variation in adaptive landscapes (e.g., the number of fitness optima and whether such optima are constant or moving over time due to changing environment) and the organization of particular biological functions are also important. Identifying adaptive substitutions is a natural step toward empirically addressing all of these questions. A population genetic approach is important because those beneficial mutations that can be directly genetically analyzed are of unusually large effect and constitute a relatively biased sample of all adaptive variants.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4043186/

Population genomics of rapid adaptation by soft selective sweeps
Trends Ecol Evol. 2013 Nov; 28
Experimental evidence suggests that adaptation via selective sweeps is often rapid, involving multiple adaptive mutations that rise in parallel at the same locus, yet population genetic models typically assume mutation-limited scenarios and hard selective sweeps. We argue that this discrepancy reflects the confusion of two different definitions of the effective population size and that adaptation is actually not limited by mutation in many species. Clearly, in order to arrive at a more comprehensive understanding of the adaptive process, we need to develop better methods for quantifying soft sweeps in population genomic data, determining their rate and strength, and ultimately identifying the causal adaptive mutations.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3834262/

Genetic evidence for natural selection in humans in the contemporary United States
Published online 2016 Jul 11
My results suggest that natural selection has been operating on the genetic variants associated with EA, and possibly with AAM. Although I find no evidence that natural selection has been operating on the genetic variants associated with the other phenotypes or that nonlinear selection has been operating, I emphasize that this could be because my polygenic scores are imperfect proxies for the true genetic scores, which limits the statistical power of my analyses.  In sum, and keeping those limitations in mind, my results strongly suggest that genetic variants associated with EA have slowly been selected against among both female and male Americans of European ancestry born between 1931 and 1953, and that natural selection has thus been occurring in that population—albeit at a rate that pales in comparison with the rapid changes that have occurred in recent generations.    So they claim to have EVIDENCE. But its not EMPIRICALLY , experimentally shown .
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4948342/

Genome-wide analysis of a long-term evolution experiment with Drosophila.
"Genomic changes caused by epigenetic mechanisms tend to fail to fixate in the population, which reverts back to its initial pattern." That's not all that doesn't fixate. Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles. This is notable because in wild populations we expect the strength of natural selection to be less intense and the environment unlikely to remain constant for ~600 generations. Consequently, the probability of fixation in wild populations should be even lower than its likelihood in these experiments.
https://www.ncbi.nlm.nih.gov/pubmed/20844486

Does Natural Selection Exist?
The main problem was, and still is, a paucity of evidence. While the idea of natural selection seems eminently sound, people want to see it actually changing species in nature. And since the process is usually very slow, that evidence is hard to get for living organisms and nearly impossible for fossils. (Coyne 2010)
https://answersingenesis.org/natural-selection/does-natural-selection-exist/

Natural selection is not random. Really ? 
Evolution by natural selection is not a random process. Selection is a function of particular environments.

This gives the impression that environments are goal oriented, and selection being a ACTIVE process. But that is not the case. Environmental conditions like the weather or food supply develop randomly. Events cannot be predicted.  Environments do not have a FUNCTION OF SELECTING, or providing to animals actively or purpose driven or guided  advantages of survival. 

Fitness" itself changes over time in ways that are sometimes hard to predict: the opening of a land bridge, changes in climate, the discovery of new territory, extreme weather.  Every so often, an asteroid drops onto the earth, wiping out pretty much everything, and surviving that is a combination of luck and having the right traits.
https://www.quora.com/Is-evolution-by-natural-selection-a-random-process

Individuals with certain characteristics in a particular environment will contribute more offspring to the next generation relative to other individuals with an alternative set of characteristics. The greater relative contribution of some individuals over others can be due to a survival advantage, an advantage in finding and securing mates or fertility, or all of the above, either way it doesn't matter, all that matters in terms of selection is that some individuals are contributing more to the next generation relative to others. Because there are certain characteristics that outperform other characteristics in the context of a particular environment then the process of selection is not random rather it is contingent on the environment.
https://www.quora.com/Is-evolution-by-natural-selection-a-random-process

Natural Selection Is Not 'Nature's Intelligence'
Research shows that environmental changes are just as random as mutations. Proponents of evolution claim reproductive abilities were not designed, but emerged by natural selection's powers to blindly see traits and lawfully save them with no final purpose to build complexity. Christians must categorically push back the invalid claim that environments select organisms or even traits. This fallacy is essential to perpetuating evolutionary theory. No natural explanation exists for how creatures originally reproduced varieties of traits. It is not survival of the fittest, it is really survival of the "fitted."
https://www.icr.org/article/5326/


1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1931526/

2. https://biology-forums.com/definitions/index.php/Differential_reproduction



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Interaction-based evolution: how natural selection and nonrandom mutation work together
The modern evolutionary synthesis leaves unresolved some of the most fundamental, long-standing questions in evolutionary biology: What is the role of sex in evolution? How does complex adaptation evolve? How can selection operate effectively on genetic interactions? More recently, themolecular biology and genomics revolutions have raised a host of critical new questions, through empirical findings that the modern synthesis fails to explain: for example, the discovery of de novo genes; the immense constructive role of transposable elements in evolution; genetic varianceand biochemical activity that go far beyond what traditional naturalselection can maintain; perplexing cases of molecular parallelism; andmore.
https://biologydirect.biomedcentral.com/articles/10.1186/1745-6150-8-24

Jonathon Wells, Ph.D.
I focused on the mechanism of evolution-specifically, the neo-Darwinian mechanism of natural selection acting on random genetic mutations. I found that evidence for selection, with a few highly questionable exceptions, was limited to minor changes within existing species. I learned that genetic mutations are almost always harmful… I found absolutely no evidence that genetic mutations can produce beneficial changes in anatomy, of the sort needed by evolutionary theory. Nor did I find evidence that mutations (any more than selection) could produce a new species.
William Dembski, Darwin’s Nemesis: Phillip Johnson and the Intelligent Design Movement (IVP Academic, 2006) 165.


THE LEVELS OF SELECTION DEBATE: TAKING INTO ACCOUNT EXISTING EMPIRICAL EVIDENCE
http://www.scielo.org.co/scielo.php?script=sci_arttext&pid=S0120-548X2016000300001
For over five decades the dominant neo-Darwinian view is that natural selection acts only at the genic and organismal levels, but the ignored empirical evidence of multilevel selection occurring in nature obtained over the last fifty years does not agree with it. A long exchange of mathematical and theoretical arguments about the levels at which natural selection acts constitutes what is known as the 'levels of selection debate'. The large amount of empirical evidence, studied by quantitative genetics means, specifically contextual analysis, indicates that natural selection acts on levels of the biological hierarchy above and below that of the gene and organism, from the molecular to the ecosystem level, thus supporting what is called the multilevel selection theory. Beyond theoretical arguments, if empirical evidence for multilevel selection and contextual analysis results are carefully examined, the debate on the levels of selection is easily resolved: natural selection occurs in nature at different levels of biological hierarchy. 

Does natural selection operate at different biological levels besides these of the organism and/or gene? Is group selection a significant evolutionary force? Are neo-Darwinian theories as kin selection and direct reciprocity the exclusive explanations of cooperation and social behavior? These questions have overwhelmed entire generations of evolutionary biologists, generating hundreds of mathematical and theoretical papers in what is called the "levels of selection debate". There is abundant empirical evidence of multilevel selection processes occurring in nature. Of course there are instances when the empirical evidence contradicts long-held theoretical arguments, but should this happen, the theory must be adjusted to the evidence rather than the evidence being adjusted to fit the theory.

Since 1960s, the controversy over the level at which selection occurs has been particularly strong. With the publication of Animal Dispersion in Relation to Social Behavior (Wynne-Edwards, 1962), a naïve vision of multilevel selection was developed. This early definition of multilevel selection suggested that natural selection acts by the good of the group, or in other words, natural selection only operates at levels higher than that of the individual. Multilevel selection, as the name implies, is now known to operate at a minimum of two levels of the biological hierarchy. Of course, the work of Wynne-Edwards (1962) was immediately and famously criticized (Hamilton, 1963; Hamilton, 1964a; Hamilton, 1964b; Maynard-Smith, 1964; Williams, 1966; Maynard-Smith, 1976). During the 1970's, several seminal works concerning cooperation and social behavior also appeared (Wilson, 1975a and Sociobiology by Wilson, 1975b). More recently, the controversy has revived. Nowak et al. (2010), Nowak et al. (2011) and Wilson and Nowak (2014) have made strong criticisms against the theory of inclusive fitness (Hamilton, 1964a; Hamilton, 1964b). These authors have shown mathematically that this theory applies to very limited cases. As such, they suggest choosing a social behavior model much closer to the concept of multilevel selection.

THE CONCEPT OF MULTILEVEL SELECTION
Multilevel selection occurs when natural selection acts simultaneously on two or more levels of the biological hierarchy. Thus, starting from the molecular level, to the genetic, cellular, organismal, family, deme, group, sub-population, population and even to the community or ecosystem level, it is possible for natural selection to occur given that the principles of evolution by natural selection are met: phenotypic variation, heritability and differential fitness. In addition, the strength and direction of natural selection acting on each hierarchical level may different. One of the main consequences of multilevel selection is that selfish individuals, meaning the lower level, outcompete altruistic individuals within the group, the higher level, however altruistic groups outcompete selfish groups. When the strength of selection at a higher level of the biological hierarchy is strong enough for individual selection to be suppressed, a major transition in evolution occurs. Famously, there are three common features to a major evolutionary transition: entities capable of independent replication before the transition can only replicate as parts of a larger unit after it, labour division and changes in information storage and transmission.

Here are the arguments that support the existence of multilevel selection in nature: i) the abstract nature of the concept of natural selection, derived from the concept of evolution by natural selection, which always occurs in entities which possess phenotypic variation, are heritable, and have differential levels of fitness, ii) the existence of a biological hierarchy, meaning that to achieve the complexity of a gene or a multicellular organism, natural selection must have occurred at lower levels of the biological hierarchy, i.e., a major transition in evolution, and iii) the abundant empirical evidence showing cases in which natural selection operates at different biological levels besides that of the gene or the multicellular organism. Having stated these three arguments, what is the strength of natural selection at higher biological levels, the group, compared to lower levels of the hierarchy, as the individual? Although in the 1960's it was argued that group selection was theoretically possible, it has also been argued that its strength would be irrelevant and ultimately suppressed by the strength of individual selection. However, the empirical evidence, derived from quantitative genetics, suggests that this is not always the case in nature. In many cases, the strength of natural selection at the group level is higher than at the individual level. Also, manipulative experiments that have artificially imposed group selection indicate that its strength is much higher than expected.

RESOLVING THE DEBATE: CONTEXTUAL ANALYSIS AND EMPIRICAL EVIDENCE
Rather than having long argumentative exchanges, a simple way to resolve this 50-year old debate is to simply look at the empirical evidence, which is strongly based in theoretical grounds and empirical methods from quantitative genetics.

Wiki: Quantitative genetics is a branch of population genetics that deals with phenotypes that vary continuously (in characters such as height or mass)—as opposed to discretely identifiable phenotypes and gene-products (such as eye-colour, or the presence of a particular biochemical).

So rather than deduce natural selection on EMPIRICAL OBSERVATION ON THE MOLECULAR LEVEL, natural selection is inferred based on theoretical grounds and change of phenotype. Wow !! If that is true, we can say there is no observational empirical evidence for NS !

One of the main sources of evidence supporting multilevel selection theory is derived from quantitative genetics, specifically from contextual analysis. Contextual analysis is a type of multiple regression whereby the effect of phenotypic traits on relative fitness is assessed. Contextual analysis takes into account individual traits, aggregate traits, which are the group means excluding the focal individual, and emergent traits, which can only be measured in the context of the group, such as density. This type of regression method is similar to that which has been widely used to measure natural selection in nature, but it is extended to aggregate and emergent traits. Through methods such as path analysis, contextual analysis has been used to correctly detect multilevel selection processes occurring in nature.

It seems, the focus is to confirm that evolution happens , and then siimply infer on theoretical grund that natural selection happened. Thats guesswork, not science ! 

Where the relative fitness (W) from the individual i belonging to the group j, depends on:

the individual regression coefficients (βI) of the individual traits (z1, z2, ..., zn),
the aggregate regression coefficients (βC) of the aggregate traits (the group average excluding the focal individual), and
the emergent regression coefficients (βCn+1, βCn+2, ..., βCn+m) of the emergent traits (y1, y2, ..., ym).

Goodnight (2015) indicates that caution should be placed on the distinction between aggregate and emergent traits as both aggregate and emergent traits are traits 'which are experienced by the individual'. Thus, for example, each focal individual experiences a unique average height, an aggregate trait, and a unique density, an emergent trait.

The value and sign of each selection coefficient indicate the strength and direction of natural selection in each trait. For a given trait, when the regression coefficients are compared at the individual level, by means of the individual coefficient, and group level, by means of the aggregate coefficient, the strength and direction of natural selection at two levels of the biological hierarchy are being compared. Goodnight (2013) has shown that although contextual analysis and inclusive fitness basically originate from the same equation, inclusive fitness measures evolutionary change using a fitness optimization and evolutionary rates at equilibrium, while contextual analysis measures evolutionary change when populations are far from optimal, i.e., the strength of selection in a population. Taking into account their different approaches and objectives, these two metrics for explaining social behavior and cooperation appear to be complementary.

For decades the main focus of research has been placed on demonstrating that group selection evolutionary modification occurs in nature ( nobody doubts that, we know it happens, so whats the deal, and why all the effort? ) , and traditionally 'groups' are thought of as groups of organisms, and no other entities in the biological hierarchy. Yet to date, most of the empirical evidence of multilevel selection acting in nature through contextual analysis, has been obtained for individual organisms and groups of organisms ranging from ants and plants to birds and humans. Two important exceptions of this include studies at the community level. Campbell et al. (1997) used contextual analysis to measure multilevel selection in pollinator visitation patterns in two species of Ipomopsis (Polemoniaceae), and recently, Campobello et al. (2015) also used contextual analysis to measure the strength of selection of individual and group activity in the nest and its effect on relative fitness in a community of two species of birds.  

Since the last major Darwin drum-beating celebrations in 1959 (the centennial of Darwin’s black book), natural selection has been treated like a truism, rarely questioned.  Some are still objecting to it, though.  One reason is that the phrase portrays nature operating with a purposeful hand, choosing traits it wants for a purpose.  As Darwin envisioned it (aware of the inherent personification in the phrase), it could only operate on small variations in the immediate present.  No foresight or planning was involved.  Another problem recognized later was that it conveys no information.  If fitness is measured by what survives, and survivors are assumed to be the fit ones, then it is a tautology: survivors survive.  Proponents of evolution have squirmed around this problem with lots of bellowing and bluff, but their answers merely shield the tautology with synonyms 

The most serious and enduring objection to natural selection theory has been its insistence on randomness.  Natural selection is supposed to produce endless forms most beautiful from selecting positive random mutations , which are a unguided, accidental  process.  But chance is not a process!  Oh, but the randomness in variation is selected by the environment, is said.  Well, guess what: the environment is random, too, so this reduces to chance acting on chance.  But chance is not a law of nature.  Chance is not a mechanism.  Chance is not an explanation.  Chance is nothing.  Darwin is celebrated because he liberated biology from theology and supposedly brought it under the reign of “laws of nature.”  Big deal.   Moreover, natural selection has never been shown to be creative.  One major impetus for the intelligent design movement has been the lack of evidence that natural selection is capable of originating the complex, interacting organs that permeate biology. Darwin wanted pure, natural mechanisms in his biology, not “God makes stuff happen.”  



A man cannot select from the shelves of a store what the store does not carry.  Before evolution can work, there must be varieties from which to select.  The variations, moreover, must offer improvements which involve surviving or producing offspring.  The improvements must also eventually lead to different kinds of animals or plants.  Otherwise there is no evolution.  But alas, there is difficulty finding a source for new material with such a capability. 1
   There are two prominent current ideas which attempt to provide for the desired variation.  They are: (1) mutations, and (2) modern “Lamarckism.”  Lamarck, a French scientist whose famous hypothesis began to be accepted around 1802, believed that animals can pass on to their descendants the characteristics they have acquired in adapting themselves to their surroundings.
   It was later proved to the satisfaction of nearly all scientists that such “acquired characteristics” are not inherited.  Similarly, skills developed by deliberate practice–golf, typing, playing a trombone–are not passed on to one’s children, at least not by heredity.
   There is a modern form of Lamarckism, however.  It holds that, as a result of an animal’s practice or habits, its hormones are changed.  This results in inheritance by the offspring of  the variations thus called forth by the parents’ adaptation to environment.  Imagine a bird which must walk in shallow water and must continually attempt to stretch its legs.  Its hormones, they say, will become modified by this practice.  Its eggs are then supposed to be influenced by this hormonal change.  The offspring will tend to have longer legs as a result, according to modern Lamarckism.
   Many scientists, if not most, consider this a mere reversion to a hypothesis disproved earlier.  They see no solid evidence that such a process exists.  Evolutionists, however, must have some plan for producing change.  As we will see, mutations are far from ideal as a solution.  Lamarckism is taken by some as an alternative.
   André de Cayeux, French paleontologist and geologist, wrote, “At the present time, most Anglo-Saxons believe in the idea of mutation.  The French tend toward Lamarckism.  The Russians, too, favor Lamarckism, which fits in well with the Marxist doctrine.  But there are exceptions.”4
   Even if hormonal changes were possible, this could not begin to explain the first formation of complex protein molecules.  The hormone system itself is complex, delicately regulated, and many hormones are proteins.  They would first have to exist, before they could help evolution.

Computers That Vetoed Natural Selection

   In an ingenious experiment at Stanford University, Michael Conrad and H. H. Pattee tried to get computers to perform natural selection.  The scientists programmed the computers to simulate “ecosystems”–imaginary environments with imaginary organisms of several types.  The organisms were put through various lifelike stresses.  They were given opportunities to “struggle for survival.”  Their food supply was slowly diminished so that some would not survive.  They were jumped into new environments, to bring out possible adaptations leading to evolution.  They were primed to seek symbionts, partner organisms which would help each other in the way that bees and flowers work together.  
   The carefully planned experiment turned out dismally discouraging for evolution.  Reporting in the Journal of Theoretical Biology, the scientists wrote concerning the “organisms” that survived:


The predominant types of organisms were definitely inefficient.  Many organisms carried phenome sequences of no apparent selective value. . . . Organisms with efficiently placed parametric symbols exhibited no clear advantage over those with inefficiently placed symbols 2

Make room:  Science Daily asked, “Natural Selection Not The Only Process That Drives Evolution?”  Scientists at Uppsala University are finding a bigger role for neutral genetic drift.  They examined “fast-evolving” human genes by comparing them with those of other primates, and claim that many did not show signals of natural selection.  “The research not only increases our understanding of human evolution, but also suggests that many techniques used by evolutionary biologists to detect selection may be flawed,” the article said.  They may have trouble selling this idea: “many of the genetic changes leading to human-specific characters may be the result of the fixation of harmful mutations.”  It’s not clear how a degrading process led to human language, civilization and fast-food restaurants, but “This contrasts the traditional Darwinistic view that they are the result of natural selection in favour of adaptive mutations.”
Tree pruning:  A “dramatic” rearrangement of Darwin’s tree of life reported by Science Daily claims that “evolutionary relationships among animals are not as simple as previously thought.”  The new tree developed by researchers at the American Museum of Natural History appears to have two trunks near the base.  All the sponges, comb jellies, jellyfish and placozoans are on one branch, and all other animals on another.  Placozoans look like slimy multicellular amoebas that glide along the surfaces of household aquariums.  Nature News titled this, “Humans and sponges may share a slimy ancestor.”
What are the implications of this approach?  For one, it means the “genetic tool kit” for complex organs appeared before the split, and for another, convergent evolution was widespread after the split.  “Some people might initially be shocked to see that nerve cells in cnidarians and higher animals (Bilateria), the group of animals that includes humans, evolved independently,” a researcher commented, claiming that the nervous systems are not that similar.  “It is the underlying genetic tool kit that is similar amongst these basal animals,” another said.  “Placozoa have all of the tools in their genome to make a nervous system, but they just don’t do it.”  On the face of it, this would seem to raise questions about natural selection.  Why would selection invent tools that are not used?
Nature News understood the difficulties the new tree presents.  One “difficult implication” means that nervous systems evolved independently in the two branches.  “This is hard to swallow,” one biologist remarked.  The supporters of the new tree just brushed it off.  “The placula already had all the genes necessary to make all the building blocks [of a nervous system], but it didn’t have to make it because ecology didn’t force it to do so,” said Bernd Schierwater [University of Veterinary Medicine Hannover in Germany].  For him, this problem is “not too complicated at all.”  His answer begs the question, though, of why natural selection would produce a genetic tool kit in the first place, if “ecology” did not “force” it to use it.
Nature News quoted others who remain wary of the way these trees are calculated.  “Small alterations in the settings of some of these analysis tools can make major differences to the outcomes,” one said.  Another worried about adequate taxon sampling.  “I am tired of these molecular papers that don’t make sufficient controls to check the reliability of the phylogenetic inferences.  The other critic remarked, “This certainly isn’t the last word on the scheme of animal evolution.”
White eyes:  If the environment forces evolutionary change, as Darwin insisted, why would some white-eyed birds diversify quickly across multiple habitats while others stay the same?  PhysOrg reported on this biological puzzle.  It claims that bird members of the family Zosteropidae are among the fastest diversifying species ever found, even faster than the cichlid fishes in African lakes.  What’s more, the diversification does not appear to be related to geographical features, because other species in those areas do not diversify so quickly.  “As we started to compile the data, we were shocked,” one researcher said about how similar the genetics of these diverse white-eyed birds were across a wide range.  To her, this represented “a recent origin and incredibly rapid diversification.”
The article claims this confirms a hypothesis by Ernst Mayr 80 years ago that certain species are intrinsically better at diversifying than others.  Mayr’s “Great Speciator” hypothesis proposed that internal factors like sociability, the ability to survive in a variety of habitats, and a short time between generations relative to other animals can be more important than geography in generating changes.  Although the article did not mention natural selection, it seems to relegate it to a lesser role.  Darwin had emphasized environmental factors as drivers for natural selection.  Researcher Christopher Filardi recognized the debate: “This leaves the question: are the white eyes really special, or have we simply caught them at a special time in their evolution?  That we don’t know, but our results indicate that high rates of diversification may have as much to do with a species’ ‘personality’ as they have to do with more classical geographic or geological drivers of speciation.”  Filardi did not characterize what “personality” might mean in biochemical or genetic terms, or why this bird family would have such a different “personality” than other families that would cause rapid diversification.  The word is foreign to evolutionary nomenclature.  He seemed to use it as a place-holder for ignorance of the cause of diversification.

http://creationsafaris.com/crev200901.htm
1. http://creationsafaris.com/epoi_c05.htm#ec05f03x
2. http://www.sciencedirect.com.sci-hub.cc/science/article/pii/0022519370900779



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Natural selection ≠ evolution 1

The all-wise Creator knew the different environments that His creatures would have to adapt to after the Fall and Curse, and particularly after the Flood of Noah, in order to survive. He included in the genetic information of each ‘kind’ of creature He created, a smorgasbord of variety in their makeup. This includes those features that would interact with the environment: the overall size of a plant, animal or person; the size of individual organs or limbs such as beaks and noses, leaf sizes, skin colours, hair and feather lengths, textures and colours. All of these and many more variations were programmed into the DNA of His creatures in order that as populations of the various kinds moved into new environments, expression of those variations enabled individuals to survive those environments. Individuals with those variations then passed them on to their young. When these variations and the habitat of the population expressing that variation are distinct enough, we might distinguish different ‘species’. In all of this selection process, new information is never added. It can be conserved or lost, but never gained.

WHY EVOLUTION IS TRUE Jerry Coyne

For the process of evolution—natural selection, the mechanism that drove the first naked, replicating molecule into the diversity of millions of fossil and living forms—is a mechanism of staggering simplicity and beauty. And only those who understand it can experience the awe that comes with realizing how such a straightforward process could yield features as diverse as the flower of the orchid, the wing of the bat, and the tail of the peacock.

Darwin’s theory that all of life was the product of evolution, and that the evolutionary process was driven largely by natural selection, has been called the greatest idea that anyone ever had. But it is more than just a good theory, or even a beautiful one. It also happens to be true. Although the idea of evolution itself was not original to Darwin, the copious evidence he mustered in its favor convinced most scientists and many educated readers that life had indeed changed over time.

Its remarkable how Coyne conflates NS with evolution. He is not alone. I see it being done all over science literature on evolution and NS. And doing that, it hides that evolution does not equal NS. They are two different things. Evolution is modification by descent. NS is part of the mechanism by which it supposedly happened. They are two different , distinct issues, and should be treated as such.

This took only about ten years after The Origin was published in 1859. But for many years thereafter, scientists remained skeptical about Darwin’s key innovation: the theory of natural selection. Indeed, if ever there was
a time when Darwinism was “just a theory,” or was “in crisis,” it was the latter half of the nineteenth century, when evidence for the mechanism of evolution was not clear, and the means by which it worked—genetics—
was still obscure. This was all sorted out in the first few decades of the twentieth century, and since then the evidence for both evolution and natural selection has continued to mount, crushing the scientific opposition
to Darwinism. While biologists have revealed many phenomena that Darwin never imagined—how to discern evolutionary relationships from DNA sequences, for one thing—the theory presented in The Origin of Species has, in the main, held up steadfastly. Today scientists have as much confidence in Darwinism as they do in the existence of atoms, or in microorganisms as the cause of infectious disease.

Wow. They have confidence. Do you need confidence, if a fact is reportedly true, a proven fact ?

Why then do we need a book that gives the evidence for a theory that long ago became part of mainstream science? After all, nobody writes books explaining the evidence for atoms, or for the germ theory of disease. What is so different about evolution? Nothing—and everything. True, evolution is as solidly established as any scientific fact (it is, as we will learn, more than “just a theory”), and scientists need no more convincing. But things are different outside scientific circles. To many, evolution gnaws at their sense of self. If evolution offers a lesson, it seems to be that we’re not only related to other creatures, but, like them, also the product of blind and impersonal evolutionary forces. If humans are just one of many outcomes of natural selection, maybe we aren’t so special after all. You can understand why this doesn’t sit well with many people who think that we came into being in a different way from other species, as the special goal of a divine intention.

In essence, the modern theory of evolution is easy to grasp. It can be summarized in a single (albeit slightly long) sentence:

Life on Earth evolved gradually beginning with one primitive species—perhaps a selfreplicating molecule—that lived more than 3.5 billion years ago; it then branched out over time, throwing off many new and diverse species; and the mechanism for most (but not all) of evolutionary change is natural selection. When you break that statement down, you find that it really consists of six components: 


1.evolution, 
2.gradualism, 
3.speciation, 
4.common ancestry, 
5.natural selection, and 
6.nonselective mechanisms of evolutionary change.

The fifth part of evolutionary theory is what Darwin clearly saw as his greatest intellectual achievement: the idea of natural selection. This idea was not in fact unique to Darwin—his contemporary, the naturalist Alfred Russel Wallace, came up with it at about the same time, leading to one of the most famous simultaneous discoveries in the history of science. Darwin, however, gets the lion’s share of credit because in The Origin he worked out the idea of selection in great detail, gave evidence for it, and explored its many consequences.

The idea of natural selection is not hard to grasp. If individuals within a species differ genetically from one another, and some of those differences affect an individual’s ability to survive and reproduce in its environment, then in the next generation the “good” genes that lead to higher survival and reproduction will have relatively more copies than the “not so good” genes. Over time, the population will gradually become more and more suited to its environment as helpful mutations arise and spread through the population, while deleterious ones are weeded out. Ultimately, this process produces organisms that are well adapted to their habitats and way of life.

There are a lot of assertions here.

1. http://creation.com/natural-selection-evolution



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Darwins evolutionary mechanism of natural selection is a unsubstantiated claim

The philosopher Daniel Dennett once called the theory of evolution by natural selection "the single best idea anyone has ever had." 3

In order to claim natural selection as scientific, it should and would have to be  possible to make scientific predictions of what genetic change given specific environmental forces acting upon organisms would provoke through natural selection. There are other mechanisms, like genetic drift, gene flow, and sexual selection. But natural selection is by far the most predominantexplanation as evolutionary mechanism.

Lenski's long-term E. Coli evolution experiment and intelligent design 4
In June 2008 the popular science magazine New Scientist printed a story about Professor Richard Lenski's twenty-year project examining the evolution of E. coli.[2] They reported that, as a result of several beneficial mutations, his organisms had acquired the ability to metabolize citrate — or more correctly an ability to transport it through the cell wall prior to metabolizing it. This was an entirely new ability for this species — an increase in complexity provided by a beneficial mutation. This beneficial trait was then fixed in the population by natural selection. How do they know ? 

Lenski affair 5

We make no claim to having identified the genetic basis of the mutations observed in this study. However, we have found a number of mutant clones that have heritable differences in behavior (growth on citrate), and which confer a clear advantage in the environment where they evolved, which contains citrate. Our future work will seek to identify the responsible mutations."In addition, there is skepticism that 3 new and useful proteins appeared in the colony around generation 20,000." We make no such claim anywhere in our paper, nor do I think it is correct. Proteins do not "appear out of the blue", in any case. We do show that what we call a "potentiated" genotype had evolved by generation 20,000 that had a greater propensity to produce Cit+ mutants.

So all Lenskis experiments do, show what happened, but not HOW.

In the book Evolution, Carl Bergstrom writes :  

Natural Selection in the Laboratory, page 78  

Watch as tens of thousands of generations of evolution take place before your eyes.

• Manipulate the physical environment to control nutrient availability, temperature, spatial structure, and other features, and manipulate the biotic environment, adding or removing competitors, predators, and parasites.
• Create multiple parallel universes with the same starting conditions in which to watch evolution unfold in replicate worlds.
• Move organisms around in a “time machine” so that they can interact with—and compete against—their ancestors or their descendants.
• Go back in time to rerun evolution from any point, under the same or different environmental conditions.
• Easily measure both allele frequencies and fitnesses to accuracies of 0.1% or smaller.

If you could do all of these things, how would you study the process and consequences of evolution? What questions would you ask, and what experiments would you do?

Lenski’s Long-Term Evolution Experiment

As far-fetched a fantasy as this may seem, researchers indeed can do all of this and more when they study bacterial evolution in the laboratory. One of the most striking examples has been provided by Richard Lenski and his colleagues, who have been tracking evolutionary change for over 50,000 generations in the bacterium Escherichia coli. Let us examine Lenski’s experimental system in some detail and see how it allows him to perform the seemingly superhuman manipulations enumerated earlier and to test fundamental ideas in evolutionary science. Lenski’s study species, E. coli, reproduces rapidly, dividing at rates upward of once per hour under favorable environmental conditions. As a result, Lenski and his colleagues have been able to observe evolution occurring in real time, and they have been able to monitor over 50,000 generations of bacterial evolution. To put this number into perspective, Lenski’s bacterial evolution experiment now encompasses more generations than there have been in the entire history of our species, Homo sapiens.

Starting with a genetically homogeneous strain of E. coli bacteria, Lenski created 12 parallel experimental lines—the original colonists of 12 parallel “universes”— differing only by an unselected marker gene that allowed researchers to keep track of which experimental line was which. All 12 lines were kept in identical experimental conditions, but the 12 lines were never mixed with one another (Figure 3.16).



Instead, every day, Lenski and his students transferred cells from each of the 12 lines into fresh growth medium. Overnight these cells went through 6 to 7 generations of replication, and the next day the process started
anew. Periodically, Lenski froze a sample of the cells from each line in a -80°C freezer. This freezer served as his “time machine”: Researchers could thaw those cells at any point and could let them compete with their descendants. They could even use them to “start over” and could thus replicate the experiment from any point in time.

So Lenski was unable to observe under the microscope what actually happened, and provoked the evolutionary change ! 

Evolutionary Change: Predictability and Quirks

So what can you do with an experimental system like this? We only know about one history of life: the one that actually took place on Earth and of which we are a living part. One question that has always fascinated evolutionary biologists is, what if you could “run evolution over again”? Would the same phenotypes evolve the second time around? Or would we see something completely different? And if the same phenotypes did evolve, would the same underlying genetic changes be responsible, or would natural selection find a different genetic path to a similar phenotypic outcome? Lenski and his colleague Michael Travisano set out to address this question
by comparing what happened in the 12 replicate lines—the 12 parallel runs of evolutionary history—in their experiment (Lenski and Travisano 1994). To do so, they looked at a trait that evolved rapidly early in their experiment: the physical size of the individual E. coli cells. These cells could be thawed at any time and allowed to compete against their descendants in order to see whether the descendants had increased in fitness or whether they had merely changed in phenotype (Box 3.1).



As Figure 3.17A illustrates, the average cell volume increased substantially over the first 2000 to 3000 generations of the experiment.



In the course of their experiment, the researchers removed a sample of E. coli cells after every 500 generations and then stored them in a freezer. Figure 3.17B reveals that the fitness of E. coli cells did indeed increase over the course of the experiment. Only 500 generations into the experiment, natural selection had already increased the fitness of the evolved strains relative to their ancestors, and this fitness difference continued to accumulate as the experiment progressed and more generations elapsed.



Figure 3.17 shows just 1 of the 12 lines, and in this line, cell size increased and fitness increased with it. Was this outcome a quirk of fate? What would happen if we were to replay the tape? Would cell size increase again? Lenski and Travisano were able to test this question directly, by looking at the other 11 lines, each of which was an independent evolutionary run (Lenski and Travisano 1994). They found that in these lines, as in the first, cell size invariably increased, and fitness of the cells increased relative to ancestral cells (Figure 3.18) Phenotypically, the populations evolved in a similar fashion. Cell size always increased. But notice that despite starting with genetically identical cells and subjecting them to identical environments, cell size increased more in some lineages than in others. Natural selection operated in a similar direction in each case, but it appears not to have taken an identical path. Likewise, fitness increased in every one of the 12 lines, but some of the lines seem to have found better paths than others and there was considerable variation in fitness between the lines after 10,000 generations. Lenski and Travisano’s results highlight the fact that evolution by natural selection is in some aspects a predictable, repeatable process—and yet it is also one in which random events, such as which mutations occur, or the order in which they occur, can play a significant role in shaping the course of history.

Once again: they observe evolution in action, but take mutations and natural selection as the driving mechanism as a fact. Why ? 

Over the past two decades, Lenski and his colleagues have studied numerous additional traits in these 12 bacterial lines, and in doing so, they have tested a number of evolutionary hypotheses. In the next section, we will look at a thermal adaptation experiment that Lenski and colleagues used to test another important question in evolutionary biology: What are the constraints on what natural selection can achieve? Why are organisms not perfectly adapted to all environmental conditions?



What, if we invert and call it  the theory of evolution by natural selection as  "the single worst and most deceptive idea anyone has ever had." ?

The theory of natural selection is essentially about the properties of individuals and their survival to reproduce.* 1

1. The fittest are, by definition, those which survive.
2. Natural selection is, by definition, the survival of the fittest. Therefore, by substitution of definitions.
3. Natural selection is the survival of those which survive.

By definition ? If so, the relevant question is : what selects, how, when, what exactly is that mechanism ?!! Through  what exactly is the organism becoming fitter ?

Darwin’s process of natural selection has four components. 2

Variation. Organisms (within populations) exhibit individual variation in appearance and behavior.  These variations may involve body size, hair color, facial markings, voice properties, or number of offspring.  On the other hand, some traits show little to no variation among individuals—for example, number of eyes in vertebrates.
Variation can be due to many different mechanisms.

Inheritance.  Some traits are consistently passed on from parent to offspring.  Such traits are heritable, whereas other traits are strongly influenced by environmental conditions and show weak heritability.
The change of the environment will obviously provoke organismal change. But that change can be due to various mechanisms.

High rate of population growth. Most populations have more offspring each year than local resources can support leading to a struggle for resources.  Each generation experiences substantial mortality.
That does also not demonstrate that natural selection was in action.

Differential survival and reproduction.  Individuals possessing traits well suited for the struggle for local resources will contribute more offspring to the next generation.
Neither is that fact necessarly explained through natural selection

From one generation to the next, the struggle for resources (what Darwin called the “struggle for existence”) will favor individuals with some variations over others and thereby change the frequency of traits within the population.  This process is natural selection.

Question : what mechanism "selects" ? The environment through environmental pressures ?  What is the agency doing the job of selection ? Why can the selection not be a planned , or pre-programmed process ? How do we know its not ?   why has the selection rate never been measured,  observed, and registrated , and described scientifically ? why is it rather  a naturally occuring mechanism that selects,  instead a  intelligently installed  program, which triggers, turnes  on, switches  on, provokes , begins  to act,  changes, , modifies and  helps the organism to adapt to new environmental conditions, and that does  not  necessarly provoke genetic, but epigenetic changes in various organismal levels, that is molecular, and changing phenotypes but on species level ? or in other words, there might be  mechanisms in place that are acting on genetic and epigenetic level , and help the organism to adapt, change, and speciate ?  What is the reason to infer that this mechanism is a natural biological arrangement  that only selects variations on a genetic level ? why not a pre-programmed one or various  , installed by a intelligent designer ?

Why is natural selection on species level, acting on microevolution, not a  claim put into question  even by creationists / proponents of intelligent design ?

Evidence of Natural Selection

During the Industrial Revolution, soot and other industrial wastes darkened tree trunks and killed off lichens. The light-colored morph of the moth became rare and the dark morph became abundant. In 1819, the first melanic morph was seen; by 1886, it was far more common -- illustrating rapid evolutionary change. Eventually light morphs were common in only a few locales, far from industrial areas. The cause of this change was thought to be selective predation by birds, which favored camouflage coloration in the moth. In the 1950's, the biologist Kettlewell did release-recapture experiments using both morphs. A brief summary of his results are shown below. By observing bird predation from blinds, he could confirm that conspicuousness of moth greatly influenced the chance it would be eaten.

Thats all observed and proven evolutionary change. No dispute here. But no word in the text that NATURAL SELECTION was observed to provoke the change. The focus of the reader is directed to the fact of evolutionary change, which does not mean however that the mechanism is explained and understood as well. 

Can natural selection be falsified ?

Its remarkable that if we google that question, of the first ten links, only the tenth will respond the question with a philosophical essay. All previous nine ask if evolution can be falsified. But thats a different question.



1. Evolution by natural Selection     Confidence, Evidence and the Gap
2. http://www.globalchange.umich.edu/globalchange1/current/lectures/selection/selection.html
3. https://blogs.scientificamerican.com/cross-check/dubitable-darwin-why-some-smart-nonreligious-people-doubt-the-theory-of-evolution/
4. http://rationalwiki.org/wiki/Richard_Lenski
5. http://rationalwiki.org/wiki/The_Lenski_Affair



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Todays news: Darwins Theory of  Natural selection has been falsified and is dead.  R.I.P.

http://reasonandscience.heavenforum.org/t2458-is-there-evidence-for-natural-selection#5338



Thanks Jorge Rodriguez

In the last few days, i was actively searching, and  expecting to find  science papers providing empirical evidence,  demonstrating how natural selection would lead  to increase over time in the frequency of a favored allele,  producing more offspring than individuals of the other genotypes. The favoured allele would become more common at each generation and would eventually become fixed in the population. That was the long standing claim.

What Jorge linked to at uncommon descent, is  demonstrable evidence that the theory of NS  is wrong. It was demonstrably falsified and refuted.  

There are other grounds to refute Darwins claims through the Theory of evolution , regarding other aspects:

http://reasonandscience.heavenforum.org/t1666-failed-and-falsified-evolutionary-predictions

but i am referring specifically to NS.

thats BIG ! And put BIG on that !! Wow....

It was reported in January 2017 by PHY.ORG, and Nature, but surprisingly, did not cause much buzz, and i didn't take note  either.

Scientists engineer animals with ancient genes to test causes of evolution
January 13, 2017
“For the first test case, we chose a classic example of adaptation-how fruit flies evolved the ability to survive the high alcohol concentrations found in rotting fruit. We found that the accepted wisdom about the molecular causes of the flies’ evolution is simply wrong.

Siddiq and Thornton realized that this hypothesis could be tested directly using the new technologies. Siddiq first inferred the sequences of ancient Adh genes from just before and just after D. melanogaster evolved its ethanol tolerance, some two to four million years ago. He synthesized these genes biochemically, expressed them, and used biochemical methods to measure their ability to break down alcohol in a test tube. The results were surprising: the genetic changes that occurred during the evolution of D. melanogaster had no detectable effect on the protein’s function.

What’s that you say? No detectable effect?

One supposes that the gene selected is one, among very many, that can be best ‘reverse-engineered’ to give a facsimile of the ‘ancient’ form. Yet, when tested in vivo, there is no difference found between the supposed ‘slow’ ancestral gene, and the ‘fast’ extant form. This is not how neo-Darwinism is supposed to work. Something is seriously wrong, no?

It might be that the techniques employed to identify the ‘ancestral’ form are bad. Maybe that’s it, and it alone. But, OTOH, maybe something is seriously wrong with current neo-Darwinian theory.

Some notions concerning adaptation will therefore remain difficult to study rigorously. Nevertheless, because of technical and conceptual advances, it should now be possible to experimentally assess the causal predictions of many previously untested or weakly tested hypotheses of historical molecular adaptation, allowing them to be corroborated or, like the classic hypothesis of ADH divergence in D.melanogaster, decisively refuted.

One wonders what’s really left of Darwinism. Between Behe’s Edge of Evolution, Shapiro’s “Natural Genetic Engineering,” the whole field of epigenetics, the disappearing of “Junk-DNA”, and now the disappearance of a ‘fitness’ change in a “classic case” of molecular adaptation, can anyone seriously believe that Darwinism has much to say about how life evolves?

Remarkably, already in 2010, following paper reported that the claim of NS was not observed in Drosophila.

Genome-wide analysis of a long-term evolution experiment with Drosophila.
2010 Sep 15
"Genomic changes caused by epigenetic mechanisms tend to fail to fixate in the population, which reverts back to its initial pattern." That's not all that doesn't fixate. Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles. This is notable because in wild populations we expect the strength of natural selection to be less intense and the environment unlikely to remain constant for ~600 generations. Consequently, the probability of fixation in wild populations should be even lower than its likelihood in these experiments.
https://www.ncbi.nlm.nih.gov/pubmed/20844486

A more accurate appraisal is the following, from an article by George F. Howe and P. William Davis: “Under close scrutiny, however, natural selection is seen predominantly as a ‘weeding out’ operation in which harmful mutations are slowly reduced in future populations.”

https://m.phys.org/news/2017-01-scientists-animals-ancient-genes-evolution.html
http://www.uncommondescent.com/intelligent-design/refutation-of-a-classic-case-of-molecular-adaptation/

Principal Meanings of Evolution in Biology Textbooks
http://reasonandscience.heavenforum.org/t2358-principal-meanings-of-evolution-in-biology-textbooks

Primary, and secondary speciation
http://reasonandscience.heavenforum.org/t2360-primary-and-secondary-speciation

Is there evidence for natural selection ?
http://reasonandscience.heavenforum.org/t2458-is-there-evidence-for-natural-selection

Eukaryotes evolved from Prokaryotes. Really ?
http://reasonandscience.heavenforum.org/t1568-eukaryotes-evolved-from-prokaryotes-really

On the Origin of Mitochondria: Reasons for Skepticism on the Endosymbiotic Story
http://reasonandscience.heavenforum.org/t1303-challenges-to-endosymbiotic-theory

Unicellular and multicellular Organisms are best explained through design
http://reasonandscience.heavenforum.org/t2010-unicellular-and-multicellular-organisms-are-best-explained-through-design

"Tetrapods evolved" . Really ?  
http://reasonandscience.heavenforum.org/t2219-the-evolution-of-tetrapods

Is there evidence for natural selection ?
http://reasonandscience.heavenforum.org/t2458-is-there-evidence-for-natural-selection

What are the mechanisms that drive adaptation to the environment, microevolution, and secondary speciation ?
http://reasonandscience.heavenforum.org/t2460-what-are-the-mechanisms-that-drive-adaptation-to-the-environment-microevolution-and-secondary-speciation

Macroevolution. Fact, or fantasy ?
http://reasonandscience.heavenforum.org/t1390-macroevolution#1982

Where Do Complex Organisms Come From?
http://reasonandscience.heavenforum.org/t2316-where-do-complex-organisms-come-from

The tree of life, common descent, common ancestry, a failed hypothesis
http://reasonandscience.heavenforum.org/t2239-the-tree-of-life-common-descent-common-ancestry-a-failed-hypothesis



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6 Andrew Catherall on Mon Apr 10, 2017 5:03 am

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Andrew Catherall 

Just a few as I'm going out in 5 mins, as I said there are literally hundreds, just a very quick google required.

1) On the Hawaiian Island of Kauai an acoustically-orienting tachinid fly parasitoid invaded targeting oceanic field crickets. More than 90% of male field crickets (Teleogryllus oceanicus) shifted in less than 20 generations from a normal-wing morphology to an altered wing structure that renders males unable to call (flatwing). Flatwing morphology protects male crickets from the parasitoid - this has been tracked at the genomic level and selection created differences in ~2000 transcripts in a few generations 
http://onlinelibrary.wiley.com/doi/10.1111/jeb.12865/abstract

2) Transposons regularly arize in crops lwhich confer maladaptive cytoplasmic male sterility (i.e. failed pollen production in hermaphroditic plants leading to a mixture of male-sterile and hermaphroditic individuals) - we have many example sof autosomal supressor genes arising e.g. Texas cytoplasm in maize to supress this 

3) With Geospiz (Darwin's finches) on the Galapagos, Peter and Rosemary Grant have gone to Daphne Major every summer for 6 months since 1972 and recorded the traits of medium-beaked ground finch there, and have tracked the evolution of beak size and how it follows variation in rainfall/seed size availabilty. They then saw a new species, the large ground finch colonize and saw character displacement and natural selection acting on beak sizes with a very strong selection coefficent, this again has been tracked genomically (e.g. http://www.genengnews.com/.../genetic-study-of.../81252647 for lay summary, https://www.ncbi.nlm.nih.gov/pubmed/27102486 for recent paper)

4) Peter Berthold's work has tracked the evolution of a new migratory route in blackcaps within a few generations. German populations usually go to Africa but recently due to climate change and increased food provisioning have begun to head north to Britain, with a narrow-sense hertiability of ~ 0.45, which is very high. This macroevolutionary change has been tracked to variation in allele length at 3' UTR of ADCYAP1, some very cool work here (://rspb.royalsocietypublishing.org/.../278/1719/2848.full.pd)

5) Experimental evolution, where selective pressures are applied in the lab - e.g. Ratcliff's work on multicellularity: "We observed the rapid evolution of clustering genotypes that display a novel multicellular life history characterized by reproduction via multicellular propagules, a juvenile phase, and determinate growth. The multicellular clusters are uniclonal, minimizing within-cluster genetic conflicts of interest. Simple among-cell division of labor rapidly evolved. Early multicellular strains were composed of physiologically similar cells, but these subsequently evolved higher rates of programmed cell death (apoptosis), an adaptation that increases propagule production. These results show that key aspects of multicellular complexity, a subject of central importance to biology, can readily evolve from unicellular eukaryotes. "

Selection of lactose metabolism in bacteria.
Selection acting on chromosomal inversions in Drosophila.
Selection on life history traits in Tribolium beetles.
Sexual selection on male secondary sexual characters in guppies, widowbirds and peacocks.

Evolution of Character Displacement in Darwin’s Finches
http://www.d.umn.edu/~jetterso/IBS8012/documents/EvolCharacterdisplacementDarwinfinchGandG2007.pdf

A beak size locus in Darwin’s finches facilitated character displacement during a drought
https://www.researchgate.net/publication/301552707_A_beak_size_locus_in_Darwin%27s_finches_facilitated_character_displacement_during_a_drought

Is information a selectable trait?
While information content (as a phenotypic trait) has a number of appealing characteristics, we hasten to add that there are numerous caveats associated with it, which (at least today) give fitness measurements the edge. For estimating information content, we cannot rely on the substitution patterns obtained from small populations, as the shared descent of molecules creates a spurious signature of information (Huang et al., 2004). To remedy this, we must generate artificial ensembles by creating all point-wise single mutants, double mutants, and so on, of a sequence. Neglecting the high-order correlations between sites is the only feasible computational shortcut, but this can lead to important biases (mostly under-estimating the information content, see Gupta and Adami 2014). However, we believe that thinking in terms of information rather than in terms of fitness can help us navigate the sometimes bewildering jungle of evolutionary genetics, and put evolutionary theory on an even more solid quantitative footing. 

https://arxiv.org/pdf/1408.3651.pdf

The application of statistical physics to evolutionary biology
a precise mathematical analogy can be drawn between certain evolutionary and thermodynamic systems, allowing application of the powerful machinery of statistical physics to analysis of a family of evolutionary models. 

http://www.pnas.org/content/102/27/9541.abstract



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The paradox of natural selection, the strange relationship between natural selection and reproduction

“In natural selection some organisms, particular variants, are favored over others in a struggle to survive all sorts of challenging environmental (natural) circumstances".

QUESTIONS ABOUT NATURAL SELECTION
Yet curiously the theory's initial acceptance was not due to recognition of its central premise—that natural selection is the mechanism of evolution—but to the simple realization that biological evolution occurred and did so over extremely long periods of time, millions, or as we now know, billions of years, not the six days allotted by Genesis.

In fact, though the occurrence of biological evolution is no longer questioned other than by the most obscurantist critics and the most severe and insistent skeptics, natural selection's role and character, its agency, was and continues to be hotly debated. To this day it is the subject of intense and impassioned argument and analysis both within and outside the academy. Many questions have been raised over the years. Some of the more durable are the following:

Are there causes of evolution other than natural selection?
Are adaptations its sole products?
How does it produce speciation?
Does it act in a gradual and relatively continuous fashion, or in fits and starts, or both?
Can natural selection account for gaps in the historical record?
Can the many seemingly haphazard events of natural selection account for systems of the exceptional organization, complexity, and even perfection found in biology?
Can natural selection explain altruism, behavior that expresses “unselfish concern for the welfare of others”?
Does natural selection act on parts or, conversely, groups of organisms, in addition to individuals?

Finally, and perhaps most pointedly,

Is natural selection merely a metaphor without substance in the material world or, worse yet, a tautology?
Many of these questions were posed by Darwin and Wallace themselves and have shaped debate about the theory since. whatever the answer to a particular question, whether we think it affirms the theory or proves it false, these questions as well as others that I might have included are about the theory's goodness of fit to the observable or external world. None concern its internal consistency. This is, as said, because supporters and critics
alike have believed the theory to be internally consistent.

A CURIOUS DISSONANCE
Yet there is a curious and rather obvious dissonance. Though both natural selection and reproduction are needed for evolution to take place, strikingly and self-evidently they are events of very different kinds:

First and foremost, natural selection concerns the survival of an existing organism, whereas reproduction is about the production of a new one. Likewise, the mechanisms wrought by natural selection seek to ensure survival of an existing individual, whereas those of reproduction concern the production of new ones. Natural selection acts on individuals, even as it affects groups, while reproduction, though carried out by individuals, is about groups, family lines, and species. Natural selection acts in the moment, whereas reproduction secures the future. The object of natural selection exists when it acts, whereas reproduction is about objects prior
to their realization. Indeed, in sexual attraction, it is about the yet to be conceived, the nonexistent, the only imagined, even the unimagined. The traits and mechanisms of the nonreproductive or somatic features of life, the products of natural selection, are the means whereby organisms survive, whereas reproductive traits and mechanisms are the means that allow for the production of new generations. Natural selection produces progress in a negative and harsh fashion, eventually destroying all living creatures in the process, whereas reproduction is resolutely positive because, whatever its other flaws, it creates life.

Finally, and most importantly, Natural selection produces its results without intention, while by all accounts reproduction intends to produce offspring. Natural selection and reproduction are not only stunningly different; they are contradictory and in some respects opposites. Critically, whereas reproduction seems to have a goal, production of the next generation and the continuance of life, natural selection cares not a whit about the future or for that matter the survival of life, it merely acts on what is before it. This lack of intention is not incidental but is central to the theory. It is the key element in the proposition that natural selection impels evolution.

If selection was goal driven, there would have to be a “setter of goals,” God or some godless designer. And without doubt the most important thing about Darwin's theory is its exclusion of design or purpose.

Evolution just occurs. Given that the two occurrences are so contradictory, it is appropriate to ask how natural selection can have produced the reproductive features of life.

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Survival of the fittest theory: Darwinism’s limits

In effect, the mechanism of trait transmission it postulates consists of a random generator of genotypic variants that produce the corresponding random phenotypic variations, and an environmental filter that selects among the latter according to their relative fitness. And that’s all. Remarkable if true.

Compelling evidence
But we don’t think it is true. A variety of different considerations suggesting that it is not are mounting up. We feel it is high time that Darwinists take this evidence seriously, or offer some reason why it should be discounted. Our book about what Darwin got wrong reviews in detail some of these objections to natural selection and the evidence for them; this article is a brief summary.

Here’s how natural selection is supposed to work. Each generation contributes an imperfect copy of its genotype – and thereby of its phenotype – to its successor. Neo-Darwinism suggests that such imperfections arise primarily from mutations in the genomes of members of the species in question.

What matters is that the alterations of phenotypes that the mechanisms of trait transmission produce are random. Suppose, for example, that a characteristic coloration is part of the phenotype of a particular species, and that the modal members of the ith generation of that species are reddish brown. Suppose, also, that the mechanisms that copy phenotypes from each generation to the next are “imperfect” in the sense given above. Then, all else being equal, the coloration of the i + 1th generation will form a random distribution around the mean coloration of the parent generation; most of the offspring will match their parents more or less, but some will be more red than brown, and some will be more brown than red.

This assumption explains the random variation of phenotypic traits over time, but it doesn’t explain why phenotypic traits evolve. So let’s further assume that, in the environment that the species inhabits, the members with brownish coloration are more “fit” than the ones with reddish coloration, all else being equal. It doesn’t much matter exactly how fitness is defined; for convenience, we’ll follow the current consensus according to which an individual’s relative fitness co-varies with the probability that it will contribute its phenotypic traits to its offspring.

Given a certain amount of conceptual and mathematical tinkering, it follows that, all else again being equal, the fitness of the species’s phenotype will generally increase over time, and that the phenotypes of each generation will resemble the phenotype of its recent ancestors more than they resemble the phenotypes of its remote ancestors.

That, to a first approximation, is the neo-Darwinian account of how phenotypes evolve. To be sure, some caveats are required. For example, even orthodox Darwinists have always recognised that there are plenty of cases where fitness doesn’t increase over time. So, for example, fitness may decrease when a population becomes unduly numerous (that’s density-dependent selection at work), or when a species having once attained a “fitness plateau” then gets stuck there, or, of course, when the species becomes extinct.

Such cases do not show that neo-Darwinism is false; they only show that the “all else being equal” clauses must be taken seriously. Change the climate enough and the next generation of dinosaurs won’t be more fit than its parents. Hit enough dinosaurs with meteors, and there won’t be a next generation. But that does not argue against Darwinian selection, as this claims only to say what happens when the ecology doesn’t change, or only changes very gradually, which manifestly does not apply in the case of the dinosaurs and the meteorite strikes.

So much for the theory, now for the objections. Natural selection is a radically environmentalist theory. There are, therefore, analogies between what Darwin said about the process of evolution of phenotypes and what the psychologist B. F. Skinner said about the learning of what he called “operant behaviour” – the whole network of events and factors involved in the behaviour of humans and non-human animals.

Driven from within
These analogies are telling. Skinner’s theory, though once fashionable, is now widely agreed to be unsustainable, largely because Skinner very much overestimated the contribution that the structure of a creature’s environment plays in determining what it learns, and correspondingly very much underestimated the contribution of the internal or “endogenous” variables – including, in particular, innate cognitive structure.

In our book, we argue in some detail that much the same is true of Darwin’s treatment of evolution; it overestimates the contribution the environment makes in shaping the phenotype of a species and correspondingly underestimates the effects of endogenous variables. For Darwin, the only thing that organisms contribute to determining how next-generation phenotypes differ from parent-generation phenotypes is random variation. All the non-random variables come from the environment.

Suppose, however, that Darwin got this wrong and various internal factors account for the data. If that is so, there is inevitably less for environmental filtering to do.

The consensus view among neo-Darwinians continues to be that evolution is random variation plus structured environmental filtering, but it seems the consensus may be shifting. In our book we review a large and varied selection of non-environmental constraints on trait transmission. They include constraints imposed “from below” by physics and chemistry, that is, from molecular interactions upwards, through genes, chromosomes, cells, tissues and organisms. And constraints imposed “from above” by universal principles of phenotypic form and self-organisation – that is, through the minimum energy expenditure, shortest paths, optimal packing and so on, down to the morphology and structure of organisms.

Over the aeons of evolutionary time, the interaction of these multiple constraints has produced many viable phenotypes, all compatible with survival and reproduction. Crucially, however, the evolutionary process in such cases is not driven by a struggle for survival and/or for reproduction. Pigs don’t have wings, but that’s not because winged pigs once lost out to wingless ones. And it’s not because the pigs that lacked wings were more fertile than the pigs that had them. There never were any winged pigs because there’s no place on pigs for the wings to go. This isn’t environmental filtering, it’s just physiological and developmental mechanics.

So, how many constraints on the evolution of phenotypes are there other than those that environmental filtering imposes? Nobody knows, but the picture now emerging is of many, many of them operating in many, many different ways and at many, many different levels. That’s what the evolutionary developmental school of biology and the theory that gene regulatory networks control our underlying development both suggest. And it strikes us as entirely plausible.

It seems to us to be no coincidence that neo-Darwinian rhetoric in the literature of experimental biology has cooled detectably in recent years. In its place, we find 

evolutionary biologist Leonid Kruglyak being quoted in Nature in November 2008 (vol 456, p 18) ; 
“It’s a possibility that there’s something [about the contributions of genomic structure to the evolution of complex phenotypes] we just don’t fundamentally understand… That it’s so different from what we’re thinking about that we’re not thinking about it yet.”

And then there is this in March 2009 from molecular biologist Eugene Koonin, writing in Nucleic Acids Research (vol 37, p 1011);
“Evolutionary-genomic studies show that natural selection is only one of the forces that shape genome evolution and is not quantitatively dominant, whereas non-adaptive processes are much more prominent than previously suspected.” There’s quite a lot of this sort of thing around these days, and we confidently predict a lot more in the near future.

Darwinists say that evolution is explained by the selection of phenotypic traits by environmental filters. But the effects of endogenous structure can wreak havoc with this theory. Consider the following case; traits t1 and t2 are endogenously linked in such a way that if a creature has one, it has both. Now the core of natural selection is the claim that phenotypic traits are selected for their adaptivity, that is, for their effect on fitness. But it is perfectly possible that one of two linked traits is adaptive but the other isn’t; having one of them affects fitness but having the other one doesn’t. So one is selected for and the other “free-rides” on it.

We should stress that every such case (and we argue in our book that free-riding is ubiquitous) is a counter-example to natural selection. Free-riding shows that the general claim that phenotypic traits are selected for their effects on fitness isn’t true. The most that natural selection can actually claim is that some phenotypic traits are selected for their effects on fitness; the rest are selected for… well, some other reason entirely, or perhaps for no reason at all.

When phenotypic traits are endogenously linked, there is no way that selection can distinguish among them; selection for one selects the others, regardless of their effects on fitness. That is a great deal less than the general theory of the mechanics of evolution that the Darwinists suppose that natural selection provides. Worse still, there isn’t the slightest reason to suppose that free-riding exhausts the kinds of exceptions to natural selection that endogenous structures can produce.

“All right,” you may say, “but why should anybody care?” Nobody sensible doubts that evolution occurs – we certainly don’t. Isn’t this a parochial issue for professional biologists, with nothing cosmic turning on it? Here’s why we think that is not so.

Natural selection has shown insidious imperialistic tendencies. The offering of post-hoc explanations of phenotypic traits by reference to their hypothetical effects on fitness in their hypothetical environments of selection has spread from evolutionary theory to a host of other traditional disciplines; philosophy, psychology, anthropology, sociology, and even to aesthetics and theology. Some people really do seem to think that natural selection is a universal acid, and that nothing can resist its powers of dissolution.

However, the internal evidence to back this imperialistic selectionism strikes us as very thin. Its credibility depends largely on the reflected glamour of natural selection which biology proper is said to legitimise. Accordingly, if natural selection disappears from biology, its offshoots in other fields seem likely to disappear as well. This is an outcome much to be desired since, more often than not, these offshoots have proved to be not just post hoc but ad hoc, crude, reductionist, scientistic rather than scientific, shamelessly self-congratulatory, and so wanting in detail that they are bound to accommodate the data, however that data may turn out. So it really does matter whether natural selection is true.

1.http://www.newscientist.com.secure.sci-hub.cc/article/mg20527466.100-survival-of-the-fittest-theory-darwinisms-limits/?full=true

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9 Gene regulatory networks on Tue Apr 11, 2017 3:33 pm

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Evolution Impossible Dr. John F. Ashton, PhD Adjunct Professor of Biomedical Sciences

Since “natural selection” comprises the essential core of Darwin’s theory, Fodor’s paper presented a serious challenge to the scientific integrity of evolution. As a result, in July 2008, 16 of the world’s leading evolutionary scientists met in a castle in Altenberg, Austria, to discuss these serious threats to evolutionary science. Details of the conference were written up by science journalist Suzan Mazur. She reports interviews and comments from attendees and other thought leaders in the area of evolution. They highlight the growing realization by these scientists that if natural selection is now rejected or marginalized as the underpinning evolutionary process, then Darwin’s theory is dead. Dr. Jerry Fodor is quoted as saying, “Basically I don’t think anybody knows how evolution works.” This statement is a far cry from the confident assertions found in biology textbooks and museum displays. Furthermore, nobody knows how evolution works because nobody has ever observed evolution — it has never been observed in the past and it has not been observed in the laboratory. No one has been able to set up an experiment and make one type of organism evolve into a new type of organism (unless we deliberately remove genetic information or insert genetic information from another organism, neither of which is true evolution). To have no mechanism for how evolution can occur, as well as no experimental evidence, leaves evolution   natural selection  far from being a fact of science. ( micro-evolution is a observed fact ) 

From the book

WHAT DARWIN GOT WRONG

JERRY FODOR and MASSIMO PIATTELLI-PALMARINI

Gene regulatory networks
Extremely complex gene regulatory networks are at work in the developing organism and they offer important new keys to the origins of animal body plans and evolution .1 Davidson and Erwin (2006) argued that known microevolutionary processes cannot explain the evolution of large differences in development that characterize entire classes of animals.  Instead, they proposed that the large distinct categories called phyla arise from novel evolutionary processes involving large-effect mutations acting on conserved core pathways of development. Gene regulatory networks are also modular in organization.  This means, in essence, that they form compact units of interaction relatively separate from other similar, but distinct, units. The consequence is that these processes make the connection between specific biological traits, specific evolutionary dynamics and natural selection very complicated at best, impossible at worst. In the words of a leading expert of gene regulatory networks:

Developmental gene regulatory networks are inhomogeneous in structure and discontinuous and modular in organization, and so changes in them will have inhomogeneous and discontinuous effects in evolutionary terms ... These kinds of changes imperfectly reflect the Class, Order and Family level of diversification of animals. The basic stability of phylum-level morphological characters since the advent of bilaterian assemblages may be due to the extreme conservation of network kernels. The most important consequence is that contrary to classical evolution theory, the processes that drive the small changes observed as species diverge cannot be taken as models {or the evolution of the body plans of animals. These are as apples and oranges, so to speak, and that is why it is necessary to apply new principles that derive from the structure/function relations of gene regulatory networks to
approach the mechanisms of body plan evolution. 

Davidson, 2.006, p. 195, emphasis added

Additional phenomena, such as developmental modules, entrenchment and robustness, further separate random mutations at the DNA level from expressed phenotypes at the level of organisms.

Entrenchment
The different components of a genome and/or of a developmental structure usually have different effects 'downstream', that is, on the characteristics of the fully developed adult, through the entire lifetime. The magnitude of these effects is measured by the 'entrenchment' of that structure. The entrenchment of a gene or a gene complex changes by degrees - it's not an all-or-none property. From an evolutionary point of view, the entrenchment of a unit has multiple and deep consequences for its role in different groups of organisms and different species, notably affecting other units that depend on its functioning. Generative entrenchment  is seen both as an 'engine' of development and evolutionary change, and as a constraint. This amounts to saying that crucial developmental factors ('pivots' in Wimsatt's terms) may be highly conserved and be buffered against change, or may undergo minor heritable changes with major evolutionary consequences. Generative entrenchment, as the expression aptly suggests, is very probably linked to spontaneous and quite general collective form-generating processes, but it is (of course) also under the control of genes, gene complexes and developmental pathways. How these different sources of order and change (some generically physico-chemical and some specifically genetic) interact is still largely unknown.

Robustness
A trait is said to be robust with respect to a genetic or environmental variable if variation of the one is only weakly correlated with variations in the other. In other words, robustness is the persistence of a trait of an organism under perturbations, be they random developmental noise, environmental change or genetic change. Many different features of an organism, both microscopic and macroscopic, could qualify as traits in this definition of robustness. A trait could be the proper fold or activity of a protein, a gene expression pattern produced by a regulatory gene network, the regular progression of a cell division cycle, the communication of a molecular signal from cell surface to nucleus or a cell interaction necessary for embryogenesis or the proper formation of a viable organism or organ, for example. Robustness is important in ensuring the stability of phenotypic traits that are constantly exposed to genetic and non-genetic variation. In recent years, robustness has been shown to be of paramount importance in understanding evolution, because robustness permits hidden genetic variation to accumulate. Such hidden variation may serve as a source of new adaptations and evolutionary innovations. The source of robustness lies in the fact that the developmental processes that give rise to complex traits are nonlinear (Nijhout, 2002). In a recent paper, two leading experts say:

A consequence of this nonlinearity is that not all genes are equally correlated with the trait whose ontogeny they control. Because robustness is not controlled independently from the core components of a system, it is not straightforward to disentangle buffering mechanisms that have been subject to natural selection from those that have not. This is a major challenge for future work.
Felix and Wagner, 2008, emphasis added


Robustness must involve non-additive genetic interactions, but quantitative geneticists have for the better part of a century generally accepted that it is only the additive component of genetic variation that responds to selection. Consequently, we are faced with the observation that biological systems are pervasively robust but find it hard to explain exactly how they evolve to be that way.
Gibson, 2005, p. 237


These multiple levels of internal constraints on possible phenotypes make the notion of evolution as the product of external selection operating on phenotypic variations generated at random radically untenable.  Darwin argued that (to borrow Dennett's phrase) phenotypes 'carry information about' the ecologies in which they evolved. The brown colour of the butterfly tells us that it evolved in a smoky atmosphere.  But it now seems undeniable that evolved phenotypes also carry information about the internal organization of the creatures that have them (about their genotypic and ontogenetic structures, for example.) It is an open, empirical and highly substantive
question how narrowly such endogenous effects constrain the phenotypic variations on which external selection operates.
It will take a while to find out. But, until that question gets answered, it is unadvisable to take a neo-Darwinist account of evolution for granted.

Master genes are 'masters'
Many different traits are indissociably genetically controlled by the same 'master gene' (this is technically called pleiotropism - from the ancient Greek, meaning 'motion in many directions'). Any mutation affecting one master gene, if viable, has an impact on many traits at once. Moreover, new variants of a trait may interact differently with variants of other traits. The timing and intensity of expression of genes are, as we saw, controlled through complex gene regulatory networks. An important consequence of genetic pleiotropism is that, when a gene affects several traits at once, any change in that gene that is not catastrophic (any viable mutation) will affect all or most of these traits. Supposing that one such change in one such trait is adaptive, then natural selection will eventually fixate that mutation. But then all the other changes in all the other traits will also be stabilized, possibly opening up wholly different selective processes, eventually dwarfing the effects of the initial selection driven by the initially adaptive trait. There is an interesting example that we choose here, tentative as it may be, because it concerns the evolution of brain and therefore of cognition. It has been suggested that there are regulatory genes that affect many different organs, including the development of the cerebral cortex (Simeone, 1998; Simeone et al., 1992, 1993). A wellstudied gene family, called Otx, masterminds the development of kidneys, cranio-facial structures (Suda et al., 2009), guts, gonads and the cerebral cortex (segmentation and cortical organization). 

Several mutants are known, including severe pathological cases in humans (at one extreme lissencephaly - an abnormally smooth brain surface - at the other schizoencephaly - an exaggeratedly deep inter-hemispheric cleft). Mutants are usually short lived and leave no progeny. Italian geneticist Edoardo Boncinelli has offered an interesting and relatively tentative hypothesis which, if even roughly correct, implies that there are significant aspects of our brain structure that are not consequences of selection for their fitness but rather side effects of selection for quite other phenotypic traits; in particular, since the OtXI 'master' gene controls the development of the larynx, inner ear, kidneys and external genitalia and the thickness of the cerebral cortex, selective pressures sensitive to changes in the functions of the kidneys (due to the bipedal station, or different liquid intake and excretion resulting from floods or droughts), or the fixation of different sexual patterns, may have had in turn secondary effects on the expansion of the cerebral cortex and the structure and function of the larynx. The peculiarity of the overall picture of the evolution of language and cognition in humans, should this reconstruction prove to be correct, has been stressed to us. Neither we nor Boncinelli are claiming that this actually is the right evolutionary story about the emergence of the enlarged cortex in the human brain, only that some such story might be correct and that it is, as far as we know, consonant with the facts currently available. A dogmatic adherence to adaptationism blinds one to such interesting possibilities.

Developmental modules
Let's start with a definition. A module is a unit that is highly integrated internally and relatively insensitive to context externally. Developmental modules exist at different levels of organization, from gene regulation to networks of interacting genes to organ primordia. They are relatively insensitive to the surrounding context and can thus behave invariantly, even when they are multiply realized in different tissues and in different developmental phases. Different combinations of developmental  modules in each context, however, produce a difference in their functions in development. There is evidence of the integration of several interacting elements into a module when perturbation of one element results in perturbations of the other elements in that module, or in gene-gene interaction (epistasis) within the module, in such a way that the overall developmental input-output relation is altered. This is another signal case in which the conservation of genetic and developmental building blocks, together with their multiple recombinations in different tissues and organisms, explains the diversity of life forms as well as the invariance of basic body plans. The doubleedged (so to speak) character of developmental modules consists in their relative context insensitivity to external factors and their relative context sensitivity to some internal substitutions of subcomponents.  This is presently a very active and very complex domain of inquiry. In evolution, developmental modules may preserve their integrity in spite of being embedded into different heritable variations of their context and also, in several cases, in spite of the replacement of some of their sub-modules by others. Gerhard Schlosser writes: '[Developmental modules 1 may form coherent and quasi-autonomous units in evolution (modules of evolution) that are repeatedly recombinable with other such units'.

In essence, the 'logical' role of a module is one of presenting cascades of interacting elements, where the output of one provides some of the input to the others. Developmental modules are triggered in a switch-like fashion by a variety of inputs, to which they are only weakly linked. This weak linkage admits variations and allows relatively novel inputs. These inputs are 'triggers' (sic, in this literature) not templates of shapes. The way in which modules affect different downstream processes depends on the overall genetic context. It's worth stressing that the internal machinery is predisposed to react in complex ways to a class of switches. All this makes the development of organisms an intricate network of context-independent processes (the modules) and of internally context-dependent ones (interactions between modules and interactions of the modules with other structures). The reverberation of the effects of gene mutations is usually multiple and only the viable overall result is then accessible to selection. There are different classes of modules. The most basic and earliest operating class affects the regulation of gene transcription at distinct but interacting levels. As a consequence, DNA sequences that act as promoters and enhancers can be swapped between genes. It is also the case that multiple enhancers exist for a single gene, each controlling a particular expression domain of the gene. These can be multiply recombined. The basic transcriptional apparatus (BT A) is itself modular, and its specificity can be changed by swapping different transcription factors.

An especially interesting class of modules are the signalling pathways, families (or classes) of proteins acting in concert in cascades that constitute whole cycles or networks, and representing biochemical 'signals' that have specific types of cells as their targets in different issues, such target cells often lying side by side with unresponsive (nontarget) cells. Only five major families appear to be important during early embryonic development (because of their [separate] initial discoveries, they bear names that sound bizarre to the uninitiated: hedgehog, TGF, Wnt, receptor tyrosine kinases [RTKs] and Notch). Each family is relatively autonomous with respect to the others; each class has its own primary role, but many can also play multiple roles in the development of very different tissues. For example, the Notch system also acts as a positive feedback loop between neighbouring cells, amplifying initial differences (determining different fates of neighbouring cells). This complex system of master signals regulates tissues as different as the central nervous system, pharynx, hair cells, odontoblasts, kidney, feathers, gut, lung, pancreas, hair and ciliated epidermal cells across many different vertebrate and invertebrate species. Every mutation in anyone of the genes involved will alter many organs and their functions - a far cry from 'beanbag genetics'. Organ primordia such as limb buds and mandible and teeth primordia act like mod ules (Zelditch et al., 2008) and can be transplanted to develop ectopically - that is, in different, non-canonical parts of the embryoY This can happen partially, to a certain extent, or even completely, in diverse parts of the embryo, with different results in different species. As a rule of thumb, the transplantation and activation of genes across species, or out of place (ectopically) in the same species, is more successful for genes that are normally expressed sooner in the life of the embryo than for genes that are expressed later. This, as Stephen Jay Gould and Brian Goodwin have argued, gives some, only some, substance to the old idea (originally due to K. E. von Baer and Ernst Haeckel) that ontogenesis recapitulates phylogenesis (the successive forms of the developing embryo are reminiscent of the ascent of forms in evolutionary time).

Some modules are systemic modules, distributed throughout the organism. The best examples are hormonally mediated processes, in which only a subset of cells in various tissues is responsive to a particular hormone, intermingled with unresponsive cells. Nonetheless, the response is substantially the same everywhere, with many orchestrated changes: new metabolic enzyme expressions are switched on; likewise extensive programmed cell death (or its inhibition), and the differentiation of new cell types (gut, epidermis); likewise the remodelling of muscles, and of parts of the nervous system. The thyroidhormone- dependent metamorphosis in amphibians is modulable at will by mere administration of various doses of the hormone. The lesson here is that modularity gives a new complex picture of evolution, one in which internal constraints and internal dynamics filter what selection can act upon, and to what extent it can do so. Precisely because so much cannot change, other things can change at the (so to speak) genetic periphery of organisms. It is often (although not always) the case that when we witness gene duplications, a ubiquitous kind of genetic modification, the 'original' gene continues acting as it did in earlier forms of life, while the 'copy' can 'explore' new functions over evolutionary time (these metaphors are commonplace in the professional literature) .



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Coordination
We saw earlier how badly misguided the additive, 'beanbag' conception of genes is. There is more to be said about this. The Russian zoologist and evolutionist Ivan Ivanovich Schmalhausen (1884-1963) had rightly stressed that living organisms are not the mere atomic 'adposition' of separate parts, but rather highly 'coordinated' systems (for a historical and critical review, see Levit et al., 2006). Today justice is done to Schmalhausen by experimental evidence that some mutations in genes specifically affecting one part of the body carry with them suitable modifications in other related parts. When limbs are induced ectopically (that is, where they don't belong), often sensory neurons, receptor organs, cartilage and blood vessels also develop as a consequence around them (see Kirschner and Gerhart, 2005 for stunning examples). A laboratory-induced and quantitatively controllable modification in two key proteinsll in chick and finch embryos early in development produces as the main result variable elongation and thinning of the upper part of the beak (Abzhanov et al., 2006). However, the lower beak and the neck muscles also 'follow'. The lesson here is, once again, that natural selection cannot select isolated traits, but rather coordinated complexes of traits, coming all together in virtue of pleiotropism, developmental solidarity (Schmalhausen's
coordination) and epigenetic modifications.

Morphogenetic explosions
It stands to reason that, in consequence of the many internal constraints on possible new life forms, when one or more of these constraints are internally, genetically, relaxed or withheld, new possibilities open up, sometimes in an explosive way. Over periods that are relatively short in geological terms, a great variety of new life forms appears suddenly and (as palaeontologists say) 'explosively'. This seems to have happened at least twice in the remote past, and at least once more recently. The Ediacara fossils (from 575 to 542 million years ago) represent Earth's oldest known complex macroscopic life forms. A comprehensive quantitative analysis of these fossils indicates that the oldest Ediacara assemblage, the Avalon assemblage, already encompassed the full range of the possible forms of the Ediacara (what is technically called their 'morphospace', the repertoire of accessible forms). A comparable morphospace range was occupied by the subsequent White Sea assemblage (560 to 550 million years ago) and Nama assemblage (550 to 542 million years ago), although it was populated differently (taxonomic richness increased in the White Sea assemblage but declined in the Nama assemblage).

These changes in diversity, occurring while the range of forms (the morpho space) remained relatively constant, led to inverse shifts in morphological variance. The Avalon morphospace expansion may well mirror the Cambrian explosion (about 545 million years ago) when in the relatively short period of 5 to 10 million years most of the complex life forms we see today appeared on Earth, and both events may reflect similar underlying mechanisms. The palaeontologist Douglas H. Erwin summarizes these findings, saying that they amount to the recognition that these ancestral forms of life apparently contained already a suite of developmental tools for differentiating their body plans, although not yet the sophisticated developmental tools capable of building the regional body patterning of higher animals. For that, we will have to wait until the momentous Cambrian explosion. Another example of morphological explosion and of its importance in the unravelling of poorly understood macroevolutionary processes is analysed in Moyle et al.. The relatively recent (between two million and a million and a half years ago) explosive Pleistocene diversification and hemispheric expansion of 'white-eye' passerine birds (Zosteropidae, a family containing among the most species-rich bird genera) represents a per-lineage diversification rate among the highest reported for vertebrates (estimated to be between 1.9 and 2.6 species per million years).

However, these authors stress that, unlike the much earlier explosions seen above, this rapid rich diversification was not limited in geographic scope, but instead spanned the entire Old World tropics, parts of temperate Asia and numerous Atlantic, Pacific and Indian Ocean archipelagos. Interestingly, this paper reports that the tempo and geographic breadth of this rapid radiation 'defy any single diversification paradigm, but implicate a prominent role for lineage-specific life-history traits (such as rapid evolutionary shifts in dispersal ability) that enabled white-eyes to respond rapidly and persistently to the geographic drivers of diversification'. By means of a comparative analysis of sequences of nuclear and mitochondrial DNA, a small group of ancestors characterized as 'great speciators'  has been extrapolated. This 'hyperdiversification' can only be explained via a complex interaction between intrinsic and extrinsic drivers of rapid speciation, combining with processes of reproductive isolation and migration. These authors conclude that 'the pattern and tempo of diversification recovered for the white-eyes do not fit comfortably within any single diversification paradigm (e.g., dispersal, vicariance, equilibrium island biogeography, etc.) and underscore the importance of casting a broad net, in terms of taxonomy, geography, and theory, in modern diversification studies. We can summarize by saying that morphological explosions may well reflect major changes in internal constraints as crucial components in speciation. If so, then the effects of natural selection may well consist largely of post-hoc fine-tuning in the distribution of subspecies and variants : quite a different kind of account!  from the one of gradual selection of randomly differing small variations.



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11 Does evolutionary theory need a rethink? on Fri Apr 14, 2017 8:53 pm

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Does evolutionary theory need a rethink? 1

Researchers are divided over what processes should be considered fundamental.
08 October 2014
Although genetic changes are required for adaptation, non-genetic processes can sometimes play a part in how organisms evolve. Laland and colleagues are correct that phenotypic plasticity, for instance, may contribute to the adaptedness of an individual. A seedling might bend towards brighter light, growing into a tree with a different shape from its siblings’. Many studies have shown that this kind of plasticity is beneficial, and that it can readily evolve if there is genetic variation in the response14. This role for plasticity in evolutionary change is so well documented that there is no need for special advocacy. Much less clear is whether plasticity can ‘lead’ genetic variation during adaptation.

Much less clear as well what processes are responsible for the plasticity of the organism, and what mechanism explains the hability of adaptation and speciation of the organism. That are the KEY questions.

More than half a century ago, developmental biologist Conrad Waddington described a process that he called genetic assimilation. Here, new mutations can sometimes convert a plastic trait into one that develops even without the specific environmental condition that originally induced it. Few cases have been documented outside of the laboratory, however. Whether this is owing to a lack of serious attention or whether it reflects a genuine rarity in nature can be answered only by further study.

Lack of evidence also makes it difficult to evaluate the role that developmental bias may have in the evolution (or lack of evolution) of adaptive traits. Developmental processes, based on features of the genome that may be specific to a particular group of organisms, certainly can influence the range of traits that natural selection can act on.

Maybe these development processes are pre-programmed in the organism, and respond to environmental change and causa it to adapt to the new conditions. If that is the case , natural selection plays no role. 

However, what matters ultimately is not the extent of trait variation, nor even its precise mechanistic causes. What matters is the heritable differences in traits, especially those that bestow some selective advantage. 

Again : Can these variations not be already extant but dormant in the genome, and only be activated when required ? 

Likewise, there is little evidence for the role of inherited epigenetic modification (part of what was termed ‘inclusive inheritance’) in adaptation: we know of no case in which a new trait has been shown to have a strictly epigenetic basis divorced from gene sequence. On both topics, further research will be valuable.

Probably the gene regulatory network, and the genetic information play a role together for adaptation ?

All four phenomena that Laland and colleagues promote are ‘add-ons’ to the basic processes that produce evolutionary change: natural selection, drift, mutation, recombination and gene flow.

How does the author know these phenomenas are not the ONLY causes , and NS, drift and gene flow, can be entirely dismissed ? 

None of these additions is essential for evolution, but they can alter the process under certain circumstances. For this reason they are eminently worthy of study.

Or maybe they are the sole mechanisms explaining evolutionary change, and therefore THEY are essential, while the classical just so explanations, aka NS, drift, and gene flow are made up stories that were never confirmed in the first place ? 

We invite Laland and colleagues to join us in a more expansive extension, rather than imagining divisions that do not exist. We appreciate their ideas as an important part of what evolutionary theory might become in the future. We, too, want an extended evolutionary synthesis, but for us, these words are lowercase because this is how our field has always advanced. The best way to elevate the prominence of genuinely interesting phenomena such as phenotypic plasticity, inclusive inheritance, niche construction and developmental bias (and many, many others) is to strengthen the evidence for their importance.

Predictable evolution trumps randomness of mutations 2

The DNA showed that in some cases identical mutations appeared independently in all three test tubes: despite the random nature of mutations, the same changes in the environment favoured the same genetic solutions.

That demonstrates that these mutations were not random, but a direct result of environment change, and pre-programmed adaptation. 

Neo-Darwinism, the Modern Synthesis and selfish genes: are they of use in physiology? 3

The weight of evidence in the physiological sciences is now much more favourable to the metaphor of ‘co-operation’ than of ‘selfishness’. Gene products all co-operate in robust networks one of whose functions is precisely to insulate the organism from many of the vagaries of gene mutation, and stochasticity at lower levels. Investigating these networks and their mechanisms is the way forward.

It is therefore time to move on and remove the conceptual barriers to integrating modern physiological science with evolutionary and developmental theory. The integrative approach can achieve this since it avoids the simplistic fallacies of the gene-centred differential approach and it is essentially what successful systems physiology has employed for many years.

1. http://www.nature.com/news/does-evolutionary-theory-need-a-rethink-1.16080
2. http://www.nature.com/news/predictable-evolution-trumps-randomness-of-mutations-1.12459
3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3060581/



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The true mechanisms that permit organisms to adapt to the environment - no, its not natural selection



Frank Stearns It doesn't. Selection can happen without genetics or epigenetics. I'll get the lande and Arnold paper for you.

But as a cartoon, if you have 100 beads 50 red and 50 blue and you remove 30 blue that's selection. It's observable and testable and actually that simple. If you want evolution by natural selection then that variation needs a heritable component.

I think you're confusing terms. Natural selection is not synonymous with evolution. Yes, selection only removes. But by doing so in conjunction with heritability and a creative force it enriches for variants as variant frequencies always sum to 1. That's a whole way down the line from this though. If you want to talk about selection you need to focus.

http://people.oregonstate.edu/~arnoldst/pdf_files/Lande%20&%20Arnold%201983.pdf

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3084352/


Andrew Catherall
So just before I respond, let me check I've got this right, you're saying that as alpha males have on average a higher lifetime reproducitve success than other males, it doesn't matter if the other males gain beneficial mutations (or the alphas negative mutations) as the alphas will win the battle for reproduction anyway, and thus selection can't operate?

So you are asking a methodological question, how can we quantify the reproductive benefit of social rank and the strength of selection on non-alphas?

So conceptually I don't see the issue in separating those two forces: the reproductive benefit of social rank can be quanitifed just by paternity analysis, something that was more difficult when Dewsbury wrote the paper you are quoting in 1982 but is now very easy with genomic tests.  The strength of selection operating on non-alphas can then be derived simply by seeing what % of remaining paternity they are competing for factoring any kin-selected benefits

Yeah, for example consider lion prides. Males go round in a group, and researchers were interested why this is the case if their behaviour is selfish. Craig Parker (1991) investigated this as part of his 30 yr lion study: He found that larger coalitions of males were better able to takeover prides and also gained a larger tenure. He found that the AVERAGE lifetime reproductive success was higher in each group - but in this case the average lifetime success is misleading

Its misleading as the lions have a dominance heiracy, with alpha, beta, gamma and delta males, with very high reproductive skew:
If 2 males are in a coalition, then alphas get 63% of the paternity and betas only 37%
if 3 males in a coalition, alphas get 60%, betas get 40% and gammas get 0%
if 4 males in a colaition, alphas get 50%, betas get 45%, gamma gets 5% and delta gets 0%
Why do delta and gamma males bother to join the coalitions at all?

Under the selection hypothesis, we'd need to find some genetic benefit to the gamma/delta males. Well here male teams often consist of relatives (brothers, half-brothers) - so we will get kin selection for cooperaton. In line with this hypothesis, unrelated males only ever join small coalitions in which they will get direct fitness benefits through high paternity,, but they never join the larger coalitions (as they will get no indirect benefits from kin-selection if they are not related to the others)

I have more examples of the evolutionary games played by organisms with alternate reproductive tactics in long-tailed tits, burying beetles, common lizards and side-blotched lizards if you are interested some time

Well the dominance of successful traits does not depend on random muations. Mutations are (as far as we know) undirected, and are responsible for generating mostly unsuccseful or neutral, but sometimes successful traits. 



An essential ingredient of Darwins theory is that " Individuals possessing traits well suited for the struggle for local resources will contribute more offspring to the next generation ". This means that individuals with a certain genotype for a given locus or gene have more reproductive success than individuals within the same population that have  other genotypes for for that same gene.   What determines whether a gene variant spreads or not depends  on an incredibly complex web of factors - the species' ecology, its physical and social environment and sexual behavior. A further factor adding complexity is  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 reproducitve 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 influence in fitness and the struggle to contribute more offspring to the next generation.   Science would need furthermore to have the knowledge what traits are favoured in which environment. adaptation rates and mutational diversity and other spatiotemporal parameters, including population density, mutation rate, and the relative expansion speed and spatial dimensions. 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 model, and see whats statistically significant, and get meaninful, real life results. The varying factors are too many, and non predictive. 

What we observe is  gene entropy. 

1. Random mutations deteriorate the genome.
http://reasonandscience.heavenforum.org/t2201-genetic-entropy
 In a new paper in Science,3Khan et al, working with Richard Lenski [Michigan State], leader of the longest-running experiment on evolution of E. coli, found a law of diminishing returns with beneficial mutations due to negative epistasis.  The abstract said:
Epistatic interactions between mutations play a prominent role in evolutionary theories. Many studies have found that epistasis is widespread, but they have rarely considered beneficial mutations. We analyzed theeffects of epistasis on fitness for the first five mutations to fix in an experimental population of Escherichia coli. Epistasis depended on the effects of the combined mutations—the larger the expected benefit, the more negative the epistatic effect. Epistasis thus tended to produce diminishing returnswith genotype fitness, although interactions involving one particular mutation had the opposite effect. These data support models in which negative epistasis contributes to declining rates of adaptation over time.

2. Adaptation of organisms to the environment happens.
WHAT DARWIN GOT WRONG JERRY FODOR and MASSIMO PIATTELLI-PALMARINI

Additional phenomena, such as developmental modules, entrenchment and robustness, further separate random mutations at the DNA level from expressed phenotypes at the level of organisms.
Entrenchment
The different components of a genome and/or of a developmental structure usually have different effects 'downstream', that is, on the characteristics of the fully developed adult, through the entire lifetime. The magnitude of these effects is measured by the 'entrenchment' of that structure. The entrenchment of a gene or a gene complex changes by degrees - it's not an all-or-none property. From an evolutionary point of view, the entrenchment of a unit has multiple and deep consequences for its role in different groups of organisms and different species, notably affecting other units that depend on its functioning. Generative entrenchment  is seen both as an 'engine' of development and evolutionary change, and as a constraint. This amounts to saying that crucial developmental factors ('pivots' in Wimsatt's terms) may be highly conserved and be buffered against change, or may undergo minor heritable changes with major evolutionary consequences. Generative entrenchment, as the expression aptly suggests, is very probably linked to spontaneous and quite general collective form-generating processes, but it is (of course) also under the control of genes, gene complexes and developmental pathways. How these different sources of order and change (some generically physico-chemical and some specifically genetic) interact is still largely unknown.

Robustness
A trait is said to be robust with respect to a genetic or environmental variable if variation of the one is only weakly correlated with variations in the other. In other words, robustness is the persistence of a trait of an organism under perturbations, be they random developmental noise, environmental change or genetic change. In recent years, robustness has been shown to be of paramount importance in understanding evolution, because robustness permits hidden genetic variation to accumulate. Such hidden variation may serve as a source of new adaptations and evolutionary innovations.  It is an open, empirical and highly substantive question how narrowly such endogenous effects constrain the phenotypic variations on which external selection operates. It will take a while to find out. But, until that question gets answered, it is unadvisable to take a neo-Darwinist account of evolution for granted.

Master genes are 'masters'
Many different traits are indissociably genetically controlled by the same 'master gene'. Any mutation affecting one master gene, if viable, has an impact on many traits at once.  A wellstudied gene family, called Otx, masterminds the development of kidneys, cranio-facial structures (Suda et al., 2009), gutsgonads and the cerebral cortex (segmentation and cortical organization). 

Developmental modules
Let's start with a definition. A module is a unit that is highly integrated internally and relatively insensitive to context externally. Developmental modules exist at different levels of organization, from gene regulation to networks of interacting genes to organ primordia. They are relatively insensitive to the surrounding context and can thus behave invariantly, even when they are multiply realized in different tissues and in different developmental phases. Different combinations of developmental  modules in each context, however, produce a difference in their functions in development. There is evidence of the integration of several interacting elements into a module when perturbation of one element results in perturbations of the other elements in that module, or in gene-gene interaction (epistasis) within the module, in such a way that the overall developmental input-output relation is altered. This is another signal case in which the conservation of genetic and developmental building blocks, together with their multiple recombinations in different tissues and organisms, explains the diversity of life forms as well as the invariance of basic body plans.  The reverberation of the effects of gene mutations is usually multiple and only the viable overall result is then accessible to selection. This complex system of master signals regulates tissues as different as the central nervous system, pharynx, hair cells, odontoblasts, kidney, feathers, gut, lung, pancreas, hair and ciliated epidermal cells across many different vertebrate and invertebrate species. Every mutation in anyone of the genes involved will alter many organs and their functions - a far cry from 'beanbag genetics'. The lesson here is that modularity gives a new complex picture of evolution, one in which internal constraints and internal dynamics filter what selection can act upon, and to what extent it can do so. Precisely because so much cannot change, other things can change at the (so to speak) genetic periphery of organisms. It is often (although not always) the case that when we witness gene duplications, a ubiquitous kind of genetic modification, the 'original' gene continues acting as it did in earlier forms of life, while the 'copy' can 'explore' new functions over evolutionary time (these metaphors are commonplace in the professional literature) .

Coordination
The Russian zoologist and evolutionist Ivan Ivanovich Schmalhausen (1884-1963) had rightly stressed that living organisms are not the mere atomic 'adposition' of separate parts, but rather highly 'coordinated' systems (for a historical and critical review, see Levit et al., 2006). Today justice is done to Schmalhausen by experimental evidence that some mutations in genes specifically affecting one part of the body carry with them suitable modifications in other related parts. When limbs are induced ectopically (that is, where they don't belong), often sensory neurons, receptor organs, cartilage and blood vessels also develop as a consequence around them (see Kirschner and Gerhart, 2005 for stunning examples). A laboratory-induced and quantitatively controllable modification in two key proteinsll in chick and finch embryos early in development produces as the main result variable elongation






 What we cannot know : that random mutations are selected and give more reproductive success than individuals within the same population that have other genotypes for for that same gene.

You have to be careful in saying 'environmental conditions' are random'. They do fluctuate, but usually around a mean value within a predictable standard deviation. For example wherever you live, there will be at a large-scale a predictable range of clmiatic variables (e.g. desert, temperate, forest, tropical, montane), predictable diurnal cues (length of days, seasons), predictable presence of organisms, predictable presence of the other sex etc.

You are right in saying that if an organism for one generation lived in a desert, then the next year the desert became a rainforest, then the next outer space, then selection could not act

"predictable at most part. But not always." Exactly, that's why organisms tend to have physiological tolerance across a range of conditions - for example species at higher latitudes have a higher range of thermal tolerances than species at lower latitudes in the tropics, so even though global warming is likely to be of a lesser magnitude at the tropics they are actually more at risk. This is because the climate in higher latitudes is more variable, so they have been selected to cope with a broader range of climatic conditions

"if the conditions suddenly change, what yesterday was a positive trait, might suddenly become a negative one." - indeed! That's like what happened with the acoustically orienting paraistioid fly that invaded Hawaii, which led to a previously positive trait (sexual singing) becmoing a trait with negative fitness consequences, so it was rapidly selected against and new reproductive behavioural tacitcs evolved.

But if you actually wrote down a list of all environmental parameters and then quantified their change from generation to generation, you'd find most were stable and that only a few showed a large deviation (that's what you'd expect mathematically from the summation of many quasindependent random variables).

"You would have to take 1. the environmental variations into consideratons. Undertstand how they influece the survival of the different species that live in that specific habitat and know their individual sexual and social behavior." you have just literally described my field, behavioural ecology

Highly reccomend a book by Davies, Krebs and West "An Introduction to Behavioural Ecology". Its very readable and provides a good into to this stuff (which is very different from the molecular biology I know you are more familiar with). I need to do some work now but was nice talking to you




What determines whether new allele variations  spread or not in the population depends on an incredibly complex web of factors - the species' ecology, its physical and social environment and mating behavior, reproduction rates etc. To isolate these factors and see which is of selective importance, and quantify them, plug them into a mixed multivariate model, and see whats statistically significant, will never provide accurate outcomes. There are too many variables to take into consideration.

The crux or relevant question is not if evolution happens  or not. Evidently it does ( at least, in a limited degree ). The question is, what is the mechanism that drives adaptation and variation by descent, and what are the relevant factors that determine and drive body form , phenotype, and first degree speciation in macro scale.

As i am pointing out, the variables , if it Darwins theory had to be put to test, are too many. That is

1. Random mutations and which mutations would be beneficial in each specific species, in regard of survival through natural selection, AND reproduction fitness ( that are two separate things )
2. Ecology and evironment conditions which behave in a non predictable way , and the influece of given new traits in the genome.
3. Competition of mating behavior of each species varies. In order to gain accurate data, it would have to be possible to quantify the rate upon which alpha males of each species outcompete their concurrent non-alpha males, and compare this data with reproduction success of other non alpha-males that gained the new positive mutation trait and so higher fitness, and measure if the alphas will win the battle for reproduction or not, and thus selection can either win the competition or not.

These are unquantifiable variables. They would have to be gained in a large number of different species to get a average number or close estimates, and in a number of different environments and conditions. Thats a far fetch and impossible challenge even for the most advanced scientific methods of today.

For example :

DIFFERENTIAL REPRODUCTIVE SUCCESS AND HERITABILITY OF ALTERNATIVE REPRODUCTIVE TACTICS IN WILD ATLANTIC SALMON (SALMO SALAR L.)

To conclude, although our results showed unequal reproductive success between salmon tactics, a clear demonstration of equality (or not) of lifetime fitness of alternative reproductive tactics would be very difficult to achieve under natural conditions. This is mainly because individuals originating from one tactic can potentially switch to the other tactic and also because heritability might be highly variable depending on different sets of environmental conditions. Also, the variation in heritability between habitats and tactics observed in this study shows that previous models aiming to explain the coexistence of alternative reproductive tactics in the context of the conditional strategy theory (Gross and Repka 1998a,b) based on a single heritability estimate for the entire population are likely inappropriate to capture the complexity of factors involved in the expression of alternative
life-history tactics.

Since this problem extends to almost all life, above makes the ToE basically a "theory" that CANNOT BE TESTED.



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13 Testing Natural Selection on Sat Apr 15, 2017 6:08 pm

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Testing Natural Selection 1
January 2009
Adaptive evolution is therefore a two-step process, with a strict division of labor between mutation and selection. In each generation, mutation brings new genetic variants into populations. Natural selection then screens them: the rigors of the environment reduce the frequency of “bad” (relatively unfit) variants and increase the frequency of “good” (relatively fit) ones.

That does not say anything about random mutations producing fitter variations then the extant ones. 

(It is worth noting that a population can store many genetic variants at once, and those variants can help it to meet changing conditions as they arise. The gene that protected the type 1 bacteria from the antibiotic may have been useless or even slightly harmful in the earlier, antibiotic-free environment, but its presence enabled the type 1s to survive when conditions changed.)

To what degree is it responsible for changes in the overall genetic makeup of a population? No one seriously doubts that natural selection drives the evolution of most physical traits in living creatures—there is no other plausible way to explain such large-scale features as beaks, biceps and brains.

Wow. Did you read that ? Thats a classical gap argument :  " we don't know , therefore natural selection"  

Until the 1960s biologists had assumed that the answer was “almost all,” but a group of population geneticists led by Japanese investigator Motoo Kimura sharply challenged that view. Kimura argued that molecular evolution is not usually driven by “positive” natural selection—in which the environment increases the frequency of a beneficial type that is initially rare. Rather, he said, nearly all the genetic mutations that persist or reach high frequencies in populations are selectively neutral—they have no appreciable effect on fitness one way or the other. (Of course, harmful mutations continue to appear at a high rate, but they can never reach high frequencies in a population and thus are evolutionary dead ends.) 

Since neutral mutations are essentially invisible in the present environment, such changes can slip silently through a population, substantially altering its genetic composition over time. The process is called random genetic drift; it is the heart of the neutral theory of molecular evolution.

By the 1980s many evolutionary geneticists had accepted the neutral theory. But the data bearing on it were mostly indirect; more direct, critical tests were lacking. Two developments have helped fix that problem. First, population geneticists have devised simple statistical tests for distinguishing neutral changes in the genome from adaptive ones. Second, new technology has enabled entire genomes from many species to be sequenced, providing voluminous data on which these statistical tests can be applied. The new data suggest that the neutral theory underestimated the importance of natural selection.
In one study a team led by David J. Begun and Charles H. Langley, both at the University of California, Davis, compared the DNA sequences of two species of fruit fly in the genus Drosophila. They analyzed roughly 6,000 genes in each species, noting which genes had diverged since the two species had split off from a common ancestor. By applying a statistical test, they estimated that they could rule out neutral evolution in at least 19 percent of the 6,000 genes; in other words, natural selection drove the evolutionary divergence of a fifth of all genes studied. (Because the statistical test they employed was conservative, the actual proportion could be much larger.) The result does not suggest that neutral evolution is unimportant—after all, some of the remaining 81 percent of genes may have diverged by genetic drift. But it does prove that natural selection plays a bigger role in the divergence of species than most neutral theorists would have guessed. Similar studies have led most evolutionary geneticists to conclude that natural selection is a common driver of evolutionary change even in the sequences of nucleotides in DNA.

The Genetics of Natural Selection
Even when biologists turn to ordinary physical traits (“beaks, biceps and brains”) and are confident that natural selection drove evolutionary change, they are often in the dark about just how it happened. Until recently, for instance, little was known about the genetic changes that derlie adaptive evolution. But with the new developments in genetics, biologists have been able to attack this problem head-on, and they are now attempting to answer several fundamental questions about selection. When organisms adapt by natural selection to a new environment, do they do so because of changes in a few genes or many? Can those genes be identified? And are the same genes involved in independent cases of adaptation to the same environment? Answering those questions is not easy. The main difficulty is that the increase in fitness arising from a beneficial mutation can be very small, making evolutionary change quite slow. One way evolutionary biologists have coped with this problem is to place populations of rapidly reproducing organisms in artificial environments where fitness differences are larger and evolution is, therefore, faster. It also helps if the populations of the organisms are large enough to provide a steady stream of mutations. In microbial experimental evolution, a population of genetically identical microorganisms is typically placed in a novel environment to which they must adapt. Since all the individuals begin by sharing the same DNA sequence, natural selection must operate only on new mutations that arise during the experiment. The experimenter can then plot how the fitness of the population changes with time by measuring the rate of reproduction in the new environment.

Some of the most intriguing research in experimental evolution has been performed with bacteriophages, viruses so small that they infect bacteria. Bacteriophages have commensurately tiny genomes, and so it is practical for biologists to sequence their entire genomes at the beginning and end of experiments as well as at any time in between. That makes it possible to track every genetic change that natural selection “grabs” and then perpetuates over time. K. Kichler Holder and James J. Bull, both at the University of Texas at Austin, performed such an experiment with two closely related species of bacteriophages: ΦX174 and G4. Both viruses infect the common gut bacterium Escherichia coli. The experimenters subjected the bacteriophages to an unusually high temperature and allowed them to adapt to the new, warm environment. In both species, fitness in the new environment increased dramatically during the experiment. Moreover, in both cases the experimenters saw the same pattern: fitness improved rapidly near the start of the experiment and then leveled off with time. Remarkably, Holder and Bull were able to identify the exact DNA mutations underlying the increased fitness.

That says nothing about the mechanism that permitted the phages to adapt. 

The studies of the monkeyflower and of hybrid sterility in fruit flies only begin to scratch the surface of a large and growing literature that reveals the hand of natural selection in speciation. Indeed, most biologists now agree that natural selection is the key evolutionary force that drives not only evolutionary change within species but also the origin of new species. Although some laypeople continue to question the cogency or adequacy of natural selection, its status among evolutionary biologists in the past few decades has, perhaps ironically, only grown more secure

Thats a explicit and blatant admittance that there is no hard empirical data which confirms without any doubt that natural selection is the mechanism upon which evolution happens. 

1. http://ogoapes.weebly.com/uploads/3/2/3/9/3239894/testing_natural_selection.pdf

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4573302/
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.

Can Purifying Natural Selection Preserve Biological Information? – May 2013 –
http://www.worldscientific.com/doi/pdf/10.1142/9789814508728_0010
Paul Gibson, John R. Baumgardner, Wesley H. Brewer, John C. Sanford
In conclusion, numerical simulation shows that realistic levels of biological noise result in a high selection threshold. This results in the ongoing accumulation of low-impact deleterious mutations, with deleterious mutation count per individual increasing linearly over time. Even in very long experiments (more than 100,000 generations), slightly deleterious alleles accumulate steadily, causing eventual extinction. These findings provide independent validation of previous analytical and simulation studies [2–13]. Previous concerns about the problem of accumulation of nearly neutral mutations are strongly supported by our analysis. Indeed, when numerical simulations incorporate realistic levels of biological noise, our analyses indicate that the problem is much more severe than has been acknowledged, and that the large majority of deleterious mutations become invisible to the selection process.,,,

Perhaps you can find something here:
http://www.geneticentropy.org/properties
Genetic Entropy – references to several peer reviewed numerical simulations analyzing and falsifying all flavors of Darwinian evolution,, (via Dr. John Sanford and company)

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One more important reason to be skeptic about Darwins Theory

http://reasonandscience.heavenforum.org/t2458-is-there-evidence-for-natural-selection#5372

I don't know if this has been apprechiated before, but in my view, following below  is a MAJOR DIFFICULTY in the construct and concept of Darwins Theory, which justifies major skepticism and concern. What i post in sequence, puts the Theory of Evolution  into speculation territory at best, fantasia-land at worst !!

http://reasonandscience.heavenforum.org/t2458-is-there-evidence-for-natural-selection

One of the main tenets of the theory of evolution is:
Differential survival and reproduction.  Individuals possessing traits well suited for the struggle for local resources will contribute more offspring to the next generation.

Understanding Evolution
http://evolution.berkeley.edu/evolibrary/article/evo_32
It's more accurate to think of natural selection as a process rather than as a guiding hand. Natural selection is the simple result of variation, differential reproduction, and heredity — it is mindless and mechanistic. It has no goals; it's not striving to produce "progress" or a balanced ecosystem.

What is the definition of "differential reproduction"?
This means that individuals with a certain genotype for a given locus or gene have more reproductive success than individuals within the same population that have  other genotypes for for that same gene. This difference in reproductive success can be the result of longer survival that results in more reproductive events over a lifetime, more offspring per reproductive event, or more frequent successful reproductive events.
Differential reproduction is the idea that those organisms best adapted to a given environment will be most likely to survive to reproductive age and have offspring of their own. Organisms that are successful in their environments will be more likely to be successful in reproduction, and therefore the better-adapted organisms will reproduce at a greater rate than the less well-adapted organisms. 2
Differential reproduction is needed because for natural selection to occur, one group with a specific trait has to have more reproductive success than another group within the same population.

The Extended synthesis, Pigliucci , pg.13
A second restriction overcome by the new approach is externalism. The nearly exclusive concentration of the Modern Synthesis on natural selection gave priority to all external factors that realize adaptation through differential reproduction, a fundamental feature of Darwinism not rooted solely in scientific considerations (Hull 2005).

If a short definition that catches the core of the process is desired, we can say that natural selection is “the differential reproduction of hereditary variations,” which is how textbooks often define it. That is saying simply that useful variants multiply more effectively over the generations than less useful (or harmful) variants. Thus a cheetah able to run faster will catch more prey, and therefore live longer and leave more offspring than a slower cheetah. So, a hereditary variant that boosts fleetness will increase in frequency over the generations and eventually replace the slower variant.

Its evident that harmful variants, where the mutation influences negatively health, fitness, and reproduction hability of an organisms diminshes. These are sorted out, or die through desease. That says nothing however in regard of an organism gaining MORE fitness through evolution of new advantageous traits, and spreading these in the population, resulting in evolutionary advancement.

DOMINANCE RANK, COPULATORY BEHAVIOR, AND DIFFERENTIAL REPRODUCTION
http://www.journals.uchicago.edu.sci-hub.cc/doi/abs/10.1086/412672
The view that high social rank is associated with high levels of both copulatory behavior and the production of offspring is widespread in the study of animal social behavior.

This fact alone would falsify the claim that positive mutations would result automatically in higher replication of the animals with the evolved variations. At least in species which have the social hiearchy where higher ranked animals have preference to mate with females.

In order to demonstrate the validity of this hypothesis it is necessary first to resolve ambiguities in the concept of dominance and to assign ranks by means of valid procedures. Second, copulatory behavior must be properly sampled, measured, and related to rank. Finally, it must be demonstrated that rank and increased copulatory behavior actually lead to increased reproduction.

And it must be demonstrated that advantageous evolutionary traits outcompete social behavior and rank in terms of reproduction success.

Each step in this process entails conceptual and methodological difficulties. There have been many studies of rank and copulatory behavior, fewer of rank and differential reproduction, and very few of rank, copulatory behavior, and differential reproduction. The consistency of results obtained varies with taxon; results of particular consistency appear in studies of carnivores and ungulates. Both the concept of dominance and the validity of the hypothesis relating it to copulatory behavior and to differential reproduction appear viable for at least some species, although the body of data relating rank to both copulation and differential reproduction remains minimal.

This is highly telling, and of crucial importance. Think about it. The body of data and evidence in regard of elucidating one of the most important ingredients of the theory of evolution are minimal !! The author admits conceptual and methodological difficulties to study this issue.  There are no relevant studies that provide empirical data that differential reproduction can outcompete rank and copulatory behavior.
This fact alone puts Darwins ToE into speculative territory at best. Fantasia land at worst !!

Among the most prominent hypotheses in the study of animal social behavior is the view that dominant animals gain differential access to mating partners and consequently leave more offspring than do their subordinates. This view was promulgated by some of the earliest students of dominance (e.g., Zuckerman, 1932; Mas- low, 1936) and is often asserted in secondary references. For example, Barash (1977) has written that "There is abundant evidence that such dominant individuals engage in more matings and hence are more fit than are subordinates" (p. 237). This hypothesis linking dominance, copulatory behavior, and differential reproduction has elicited vigorous skepticism as well as advocacy (e.g., Bernstein, 1976; Gartlan, 1968; Kolata, 1976; Rowell, 1974).

The important place given the problem of rank, copulatory behavior, and reproduction in the study of animal social behavior is appropriate because an understanding of these relationships could greatly facilitate an understanding of the broader problem of the evolution of social behavior.

The real issue is if copulatory behavior outperforms differential reproduction.

The importance of the problem should not be overstated, however;

The contrary is the case. If copulatory behavior outperforms differential reproduction, Darwins theory is falsified, since its a essential mechanism to spread new traits in the population.

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16 Re: Is there evidence for natural selection ? on Mon Apr 17, 2017 10:43 pm

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Why Darwins theory cannot be tested, and basically is a tautology

Jerry Coyne:
The idea of natural selection is not hard to grasp. If individuals within a species differ genetically from one another, and some of those differences affect an individual’s ability to survive and reproduce in its environment, then in the next generation the “good” genes that lead to higher survival and reproduction will have relatively more copies than the “not so good” genes. Over time, the population will gradually become more and more suited to its environment as helpful mutations arise and spread through the population, while deleterious ones are weeded out. Ultimately, this process produces organisms that are well adapted to their habitats and way of life.

http://reasonandscience.heavenforum.org/t2458-is-there-evidence-for-natural-selection

The genetic modification based on evolution through mutations and natural selection based on environmental pressures is supposed to be due to:

1. higher SURVIVAL rates upon specific gene-induced phenotype adaptation to the environment.
2. higher reproduction rates upon specific genetic modifications through evolution

Maybe the reproduction rate is not influenced by the new mutation. In that case, the population with the new trait would have to have a higher reproductionrate by luck or chance...... or genetic drift.
In any case, that are TWO DIFFERENT things. Natural selection concerns the survival of an existing species through the fixation of a positive trait in the population that supposedly emerged and was passed forward accidentally through random mutations. Reproduction is however about the production of a new individual.

Differential survival and reproduction. Individuals possessing traits well suited for the struggle for local resources will contribute more offspring to the next generation.

What determines whether new allele variations spread or not in the population depends on an incredibly complex web of factors - the species' ecology, its physical and social environment and mating behavior, reproduction rates etc. To isolate these factors and see which is of selective importance, and quantify them, plug them into a mixed multivariate model, and see whats statistically significant, will never provide accurate outcomes. There are too many variables to take into consideration.

The crux or relevant question is not if evolution happens or not. Evidently it does ( at least, in a limited degree ). The question is, what is the mechanism that drives adaptation and variation by descent, and what are the relevant factors that determine and drive body form , phenotype, and first degree speciation in macro scale.

As i am pointing out, the variables , if it Darwins theory had to be put to test, are too many. That is

1. Random mutations and which mutations would be beneficial in each specific species, in regard of survival through natural selection, AND reproduction fitness ( that are two separate things )
2. Ecology and evironment conditions which behave in a non predictable way , and the influece of given new traits in the genome.
3. Competition of mating behavior of each species varies. In order to gain accurate data, it would have to be possible to quantify the rate upon which alpha males of each species outcompete their concurrent non-alpha males, and compare this data with reproduction success of other non alpha-males that gained the new positive mutation trait and so higher fitness, and measure if the alphas will win the battle for reproduction or not, and thus selection can either win the competition or not.

These are unquantifiable variables. They would have to be gained in a large number of different species to get a average number or close estimates, and in a number of different environments and conditions. Thats a far fetch and impossible challenge even for the most advanced scientific methods of today.

For example :

DIFFERENTIAL REPRODUCTIVE SUCCESS AND HERITABILITY OF ALTERNATIVE REPRODUCTIVE TACTICS IN WILD ATLANTIC SALMON (SALMO SALAR L.)

To conclude, although our results showed unequal reproductive success between salmon tactics, a clear demonstration of equality (or not) of lifetime fitness of alternative reproductive tactics would be very difficult to achieve under natural conditions. This is mainly because individuals originating from one tactic can potentially switch to the other tactic and also because heritability might be highly variable depending on different sets of environmental conditions. Also, the variation in heritability between habitats and tactics observed in this study shows that previous models aiming to explain the coexistence of alternative reproductive tactics in the context of the conditional strategy theory (Gross and Repka 1998a,b) based on a single heritability estimate for the entire population are likely inappropriate to capture the complexity of factors involved in the expression of alternative
life-history tactics.

DOMINANCE RANK, COPULATORY BEHAVIOR, AND DIFFERENTIAL REPRODUCTION
http://www.journals.uchicago.edu.sci-hub.cc/doi/abs/10.1086/412672
The view that high social rank is associated with high levels of both copulatory behavior and the production of offspring is widespread in the study of animal social behavior.

This fact alone would falsify the claim that positive mutations would result automatically in higher replication of the animals with the evolved variations. At least in species which have the social hiearchy where higher ranked animals have preference to mate with females.

In order to demonstrate the validity of this hypothesis it is necessary first to resolve ambiguities in the concept of dominance and to assign ranks by means of valid procedures. Second, copulatory behavior must be properly sampled, measured, and related to rank. Finally, it must be demonstrated that rank and increased copulatory behavior actually lead to increased reproduction.

And it must be demonstrated that advantageous evolutionary traits outcompete social behavior and rank in terms of reproduction success.

Each step in this process entails conceptual and methodological difficulties. There have been many studies of rank and copulatory behavior, fewer of rank and differential reproduction, and very few of rank, copulatory behavior, and differential reproduction. The consistency of results obtained varies with taxon; results of particular consistency appear in studies of carnivores and ungulates. Both the concept of dominance and the validity of the hypothesis relating it to copulatory behavior and to differential reproduction appear viable for at least some species, although the body of data relating rank to both copulation and differential reproduction remains minimal.

This is highly telling, and of crucial importance. Think about it. The body of data in regard of elucidating one of the most important ingredients of the theory of evolution are minimal !! The author admits conceptual and methodological difficulties to study this issue. There are no relevant studies that provide empirical data that differential reproduction can outcompete rank and copulatory behavior.
This fact alone puts Darwins ToE into speculative territory at best. Fantasia land at worst !!

Since this problem extends to almost all life, above makes the ToE basically a "theory" that CANNOT BE TESTED.

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Spatiotemporal microbial evolution on antibiotic landscapes

http://science.sciencemag.org.sci-hub.cc/content/353/6304/1147

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Evolution by natural Selection Confidence, Evidence, and the Gap

FITNESS AND ADAPTATION: THE KEY CONCEPTS
Fitness and degree of adaptation are relativized to the environment. An ocean going pelagic fish such as a bluefin tuna is not well adapted to life in shallow, murky reed beds, let alone life on land. Albatrosses are well adapted to a life soaring on the oceans and not well adapted to tropical forests. This is agreed on all hands, even if it is far from clear what is going to count as the environment. At least a part of the problem is the extent of the environment. For example, the environment contains spasmodic random and catastrophic events such as earthquakes, meteor showers, severe fires, and the like. These events are part of the environment when they occur, but should they be regarded as exercising selective pressure on organisms or as mere stochastic effects? On the other hand, change inevitably occurs. Is change a part of the environment, or is it the supplanting of one environment with another? The answer to these questions is far from clear, but what is clear is that the answers will not be general. In some circumstances, a very infrequent catastrophic event such as severe wildfire can lead to changes in the fauna and, in particular, the flora in a region. This is certainly the case with many Acacia species in Eastern Australia, the seeds of many of which require exposure to fire before they germinate. For this reason, there is often a strong sense of the ad hoc in the characterization of the environment relative to which fitness is defined. This has led some to doubt whether comparisons across species or varieties with respect to fitness or adaptation even makes sense (Lewontin, 1978, 1985).

I disagree. Leaving aside empirical questions of measurement and so on, one of the two key phenomena the theory of evolution by natural selection is required to explain is the manifest adaptation of organisms to their environment. It is just because it is so obvious that organisms are so overwhelmingly well adapted that an explanation is required, whatever form such an explanation is to take. To be clear, adaptation is something that can be observed. Organisms and their environments are not randomly sorted. Organisms tend to occur in environments for which their features provide help. Darwin’s theory was, as we have already seen, aimed at explaining that manifest fact. It is important to realize that it is conceivable that the biological world was not organized like that. On the one hand, we can imagine that the very same organisms occur across a wide range of environments. On the other hand, we can conceive of situations in which organisms occur in environments to which they are not suited. This is conceivable but not what we observe.

When we try to become more precise about what we mean by the degree of adaptation, we come across very thorny and seemingly intractable problems. How, for example, should we begin to define what we mean by the environment to which the organism is adapted? There is a risk that in letting the organism define its environmental niche, we will be forced into conceding the absurd consequence that all organisms are equally well adapted to their own environment because, by definition, they fit it perfectly (Peters, 1976). The theory of natural selection requires that there be variation in fitness among varieties. If this is a conceptual impossibility, then the theory will founder.

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19 Re: Is there evidence for natural selection ? on Tue May 02, 2017 11:52 am

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How Evolution Became a Fact

An intelligent discussion of any issue involves knowing the definition of the words under consideration. This is particularly important with respect to the word science and the word evolution.
Evolution has recently been defined formally as a change in allele frequency over time. (Alleles are alternate forms of the same gene, i.e. blue eyes brown eyes) If more Mexicans than Germans die on a given day the frequency of blue eye alleles has increased and evolution has been proven to be true.
With this definition, we have something repeatably observable, repeatable testable, falsifiable, and subject to the scientific method.
But suppose we broaden this definition a little. Suppose we broaden it to include the idea that invertebrates turned into vertebrates in the late Cambrian.
NO ONE EVER OBSERVED THAT, since no human was there.
But evolution is a fact, ACCORDING TO OUR DEFINITION, and so this MUST be true also since the FACT of evolution is established by science.
This is a tactic called bait and switch, or more formally equivocation. You change the meaning of a word in mid-argument and reach an untenable conclusion:
The only man is rational
No woman is man
Therefore no woman is rational.
We have changed the definition of man from human being in the first premise to male in the second.

This is the way evolution became a fact. We define it as something observable and testable and then expand our definition to include the unobserved and unobservable, unrepeatable, untestable, and unfalsifiable, and PRETEND we have proven that.

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