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
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.
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
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.
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
Since this problem extends to almost all life, above makes the ToE basically a "theory" that CANNOT BE TESTED.
What about fitness?
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:
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:
2. Struggle for existence with competitors
3. Avoidance of predators
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
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
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.
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.
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
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 8, 610-618 (August 2007)
All organisms undergo mutation, the effects of which can be broadly divided into three categories. First, there are mutations that are harmful to the fitness of their host; these mutations generally either reduce survival or fertility. Second, there are ‘neutral’ mutations, which have little or no effect on fitness. Finally, there are advantageous mutations, which increase fitness by allowing organisms to adapt to their environment. Although we can divide mutations into these three categories, there is, in reality, a continuum of selective effects, stretching from those that are strongly deleterious, through weakly deleterious mutations, to neutral mutations and then on to mutations that are mildly or highly adaptive.
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 between mutations in the genome, and the number of offspring? What mutations are responsible for the number of offspring produced? If the theory of evolution is true, there must be a detectable mechanism, that determines or induces, or regulates the number of offspring based due to specific genetic mutations. Only a specific section in the genome is responsible for this regulation.
There are specific regions in the genome responsible for each mechanism of reproduction, being it sexual, or asexual reproduction, that is:
1. regulation and programming of sexual attraction ( hormones, pheromones, instinct, etc.)
2. frequency of sexual intercourse and reproduction
3. the regulation of the number of offspring produced
What influence do environmental pressures have on these 3 points? What pressures induced organisms to evolve sexual, and asexual reproduction? Are the tree mechanisms mentioned not amazingly various and differentiated, and each species have individual, species-specific mechanisms? Some have an enormous number of offspring that helps the survival of the species, while others have a very low reproduction rate ( whales ? ) How could environmental pressures have induced this amazing variation, and why? That means also on a molecular level, enormous differences from one species to the other exist. how could accidental mutations have been the basis for all this variation? Would there not have to be SPECIFIC environmental pressures resulting in the selection of SPECIFIC traits based on mutations of the organism to be selected that provide survival advantage and fitness? ( genome or epigenome, whatever ) AND higher reproduction rates of the organism at the same time?
What is the chance, that random mutations provoke positive phenotypic differences, that help the survival of the individual? What kind of environmental factors influence the survival of a species? What kind of mutations must be selected to guarantee a higher survival rate?
Were ancestors, that lived in a certain environmental 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 standpoint, there is no good explanation for this relationship between the tree, orchid, bee and rodent
Why did the same environmental pressures select such various traits, such as chameleons with chromophores in their skin for hiding from their prey, apes with fur on the whole body, and human skin with no fur 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 an organism to survive is, according to the theory, not an active selection. It's just the survival of the animals that best adapts to the environment.
The question is if there is a correlation between 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 a mechanism to permit an animal of the same species and population with a random mutation in its genome to survive better than an individual who 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.
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?
Experimental test and refutation of a classic case of molecular adaptation in Drosophila melanogaster
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.
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 lengths) independently 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.]
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.
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.
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.
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.
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 .
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.
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)
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.
Last edited by Otangelo on Sat Oct 22, 2022 5:24 am; edited 60 times in total