From a new book Otangelo Grasso is working on – comments welcome:
I am looking for comments, if my conclusion is sound, that evolution cannot be a theory. It cannot be tested, on how natural selection influences differential reproduction and the fitness landscape.
Is there evidence for natural selection?
According to Darwin’s Theory, the main actors that drive evolution, is natural Selection, Genetic Drift, and Gene Flow. Natural selection depends on variation through random mutations. Inheritance, differential survival, and reproduction ( reproductive success which permits new traits to spread in the population). The genetic modification is supposed to be due to: Survival of the fittest, in other words, 1. higher survival rates upon specific gene-induced phenotype adaptations to the environment, and 2. higher reproduction rates upon specific evolutionary genetic modifications. Keep in mind that these are two different, distinct factors. It’s a fact that harmful variants, where a mutation influences negatively health, fitness, and reproduction ability of organisms diminish. These are sorted out, or die through disease. In that regard, natural selection is a fact. That says nothing however about an organism gaining more fitness ( reproductive success ) through the evolution of new advantageous traits.
Definitions of fitness:
J. Dekker (2007): 1. The average number of offspring produced by individuals with a certain genotype, relative to the numbers produced by individuals with other genotypes. 2: The relative competitive ability of a given genotype conferred by adaptive morphological, physiological, or behavioral characters, expressed and usually quantified as the average number of surviving progeny of one genotype compared with the average number of surviving progeny of competing genotypes; a measure of the contribution of a given genotype to the subsequent generation relative to that of other genotypes
A condition necessary for evolution to occur is variation in fitness of organisms according to the state they have for a heritable character. Individuals in the population with some characters must be more likely to reproduce, more fit. Organisms in a population vary in reproductive success. We will discuss fitness in Life History when we discuss competition, interference and the effects of neighbor plants.
Three Components of Fitness. These different components are in conflict with each other, and any estimate of fitness must consider all of them:
2. Struggle for existence with competitors
3. Avoidance of predators 2
S.El-Showk (2012): The common usage of the term “fitness” is connected with the idea of being in shape and associated physical attributes like strength, endurance or speed; this is quite different from its use in biology. To an evolutionary biologist, fitness simply means reproductive success and reflects how well an organism is adapted to its environment.The main point is that fitness is simply a measure of reproductive success and so won’t always depend on traits such as strength and speed; reproductive success can also be achieved by mimicry, colorful displays, sneak fertilization and a host of other strategies that don’t correspond to the common notion of “physical fitness”.
What then are we to make of the phrase “survival of the fittest”? Fitness is just book-keeping; survival and differential reproduction result from natural selection, which actually is a driving mechanism in evolution. Organisms which are better suited to their environment will reproduce more and so increase the proportion of the population with their traits. Fitness is simply a measurement of survival (which is defined as reproductive success); it’s not the mechanism driving survival. Organisms (or genes or replicators) don’t survive because they are fit; rather, they are considered fit because they survived. 3
The environment is not stable, but changes. Science would need to have the knowledge of what traits of each species are favored in a specific environment. Adaptation rates and mutational diversity and other spatiotemporal parameters, including population density, mutation rate, and the relative expansion speed and spatial dimensions. When the attempt is made to define with more precision what is meant by the degree of adaptation and fitness, we come across very thorny and seemingly intractable problems.
As Evolution. Berkley explains: Of course, fitness is a relative thing. A genotype’s fitness depends on the environment in which the organism lives. The fittest genotype during an ice age, for example, is probably not the fittest genotype once the ice age is over. Fitness is a handy concept because it lumps everything that matters to natural selection (survival, mate-finding, reproduction) into one idea. The fittest individual is not necessarily the strongest, fastest, or biggest. A genotype’s fitness includes its ability to survive, find a mate, produce offspring — and ultimately leave its genes in the next generation. 1
Claim: Adam Eyre-Walker (2007): All organisms undergo mutation, the effects of which can be broadly divided into three categories. First, there are mutations that are harmful to the fitness of their host; these mutations generally either reduce survival or fertility. Second, there are ‘neutral’ mutations, which have little or no effect on fitness. Finally, there are advantageous mutations, which increase fitness by allowing organisms to adapt to their environment. Although we can divide mutations into these three categories, there is, in reality, a continuum of selective effects, stretching from those that are strongly deleterious, through weakly deleterious mutations, to neutral mutations and then on to mutations that are mildly or highly adaptive. The relative frequencies of these types of mutation are called the distribution of fitness effects (DFE)5
R. G. Brajesh et.al., (2019): Mutations occur spontaneously during the course of reproduction of an organism. Mutations that impart a beneficial characteristic to the organism are selected and consequently, the frequency of the mutant allele increases in the population. Mutations can be single base changes called point mutations like substitutions, insertions, deletions, as well as gross changes like chromosome recombination, duplication, and translocation 7
Reply: How can random mutations give rise to higher fitness and higher reproduction of the individuals with the new allele variation favored by natural selection, and so spread in the population? This seems in fact to be a core issue that raises questions. The environmental conditions of a population, the weather, food resources, temperatures, etc. are random How do random events, like weather conditions, together with random mutations in the genome, provoke a fitness increase in an organism and a survival advantage over the other individuals without the mutation?
T.Bataillon (2014): The rates and properties of new mutations affecting fitness have implications for a number of outstanding questions in evolutionary biology. Obtaining estimates of mutation rates and effects has historically been challenging, and little theory has been available for predicting the distribution of fitness effects (DFE); Future work should be aimed at identifying factors driving the observed variation in the distribution of fitness effects. What can we say about the distribution of fitness effects of new mutations? For the distribution of fitness effects DFE of beneficial mutations, experimentally inferred distributions seem to support theory for the most part. Distribution of fitness effects DFE has largely been unexplored and there is a need to extend both theory and experiment in this area. 4
The above confession demonstrates that a key question, namely how mutations in fact affect fitness has not been answered. I go further and say: Darwin’s Theory can in reality not be tested, nor quantified. The unknown factors in each case are too many, and the variations in the environment, and population and species behavior vary too. It cannot be defined what influence the given environment exercises in regard to specific animals and traits in that environment, nor how the environmental influence would change the fitness and reproduction success of each distinct animal species. Nor how reproduction success given new traits would change upon environmental changes. What determines whether a gene variant spreads or not would depend theoretically on an incredibly complex web of factors – the species’ ecology, its physical and social environment, and sexual behavior. A further factor adding complexity is the fact that high social rank is associated with high levels of both copulatory behavior and the production of offspring which is widespread in the study of animal social behavior.
As alpha males have on average higher reproductive success than other males, since they outcompete weaker individuals, and get preference to copulate if other (weaker) males gain beneficial mutations (or the alphas’ negative mutations) as the alphas can outperform and win the battle for reproduction, thus selection has an additional hurdle to overcome and spread the new variant in the population. This does not say anything about the fact that it would have to be determined what gene loci are responsible for sexual selection and behavior, and only mutations that influence sexual behavior would have an influence on fitness and the struggle to contribute more offspring to the next generation. It is in praxis impossible to isolate these factors and see which is of selective importance, quantify them, plug them in (usually in this context) to a mixed multivariate computational model, see what’s statistically significant, and get meaningful, real-life results. The varying factors are too many and nonpredictive. Darwin’s idea, therefore, depends on variable, unquantifiable multitude of factors that cannot be known, and cannot be tested, which turns the theory at best into a non-testable hypothesis, which then remains just that: a hypothesis. Since Darwin’s idea cannot be tested, it’s by definition, unscientific.
If fitness is a relative thing, it cannot be detected and proven that natural selection is the mechanism that generates variations that produce more offspring, and therefore the new trait spreads in the population. Therefore, mutations and natural selection cannot be demonstrated to have the claimed effects. What is the relation between mutations in the genome, and the number of offspring? What mutations are responsible for the number of offspring produced? If the theory of evolution is true, there must be a detectable mechanism, that determines or induces, or regulates the number of offspring based due to specific genetic mutations. Only a specific section in the genome is responsible for this regulation.
There are specific regions in the genome responsible for each mechanism of reproduction, being it sexual, or asexual reproduction, that is:
1. Regulation and programming of sexual attraction ( hormones, pheromones, instinct, etc.)
2. Frequency of sexual intercourse and reproduction
3. The regulation of the number of offspring produced
What influence do environmental pressures have on these 3 points? What pressures induced organisms to evolve sexual, and asexual reproduction? Are the tree mechanisms mentioned not amazingly various and differentiated, and each species have individual, species-specific mechanisms? Some have an enormous number of offspring that helps the survival of the species, while others have a very low reproduction rate ( whales ? ) How could environmental pressures have induced this amazing variation, and why? That means also on a molecular level, enormous differences from one species to the other exist. how could accidental mutations have been the basis for all this variation? Would there not have to be SPECIFIC environmental pressures resulting in the selection of SPECIFIC traits based on mutations of the organism to be selected that provide survival advantage and fitness? ( genome or epigenome, whatever ) AND higher reproduction rates of the organism at the same time?
What is the chance, that random mutations provoke positive phenotypic differences, that help the survival of the individual? What kind of environmental factors influence the survival of a species? What kind of mutations must be selected to guarantee a higher survival rate?
The lack of predictive power of natural selection is due to different environmental conditions that turn it impossible to quantify the effects and measure their outcome.
Ivana Cvijović (2015):Temporal fluctuations in environmental conditions can have dramatic effects on the fate of each new mutation, reducing the efficiency of natural selection and increasing the fixation probability of all mutations, including those that are strongly deleterious on average. This makes it difficult for a population to maintain specialist adaptations, even if their benefits outweigh their costs. Temporally varying selection pressures are neglected throughout much of population genetics, despite the fact that truly constant environments are rare. The fate of each mutation depends critically on its fitness in each environment, the dynamics of environmental changes, and the population size. We still lack both a quantitative and conceptual understanding of more significant fluctuations, where selection in each environment can lead to measurable changes in allele frequency. 6
More problems: R. G. Brajesh (2019): The genotypic mutational space of an organism is so vast, even for the tiniest of organisms like viruses or even one gene, that it becomes experimentally intractable. Hence, studies have limited to studying only small parts of the genome. For example, experiments have attempted to map the functional effect of mutations at important active site residues in proteins, like Lunzer et al. engineered the IDMH enzyme to use NADP as cofactor instead of NAD, and obtain the fitness landscape in terms of the mutational steps. Other experiments have attempted to ascertain how virulence is affected by mutations at certain important loci in viruses. However, due to the scale of the genotypic mutational space, it has been extremely difficult to experimentally obtain fitness landscapes of larger multicomponent systems, and study the statistical properties of these landscapes like the Distribution of Fitness Effects (DFE). Attempts have also been made to back-calculate the underlying DFE by experimentally observing how frequently new beneficial mutations emerge and of what strength, but the final results were inconclusive. As a result, how the beneficial, neutral, and deleterious mutations and their effects are distributed, when the organism genotype is at different locations on the fitness landscape, has remained largely intractable.7
And more problems: Adam Eyre-Walker (2007): The distribution of fitness effects DFE of deleterious mutations, in particular the proportion of weakly deleterious mutations, determine a population’s expected drift load—the reduction in fitness due to multiple small-effect deleterious mutations that individually are close enough to neutral to occasionally escape selection, but can collectively have important impacts on fitness. The DFE of new mutations influences many evolutionary patterns, such as the expected degree of parallel evolution, the evolutionary potential and capacity of populations to respond to novel environments, the evolutionary advantage of sex, and the maintenance of variation on quantitative traits, to name a few. Thus, an understanding of the DFE of mutations is a pivotal part of our understanding of the process of evolution. Furthermore, the available data suggest that some aspects of the DFE of advantageous mutations are likely to differ between species. 5
Conclusion: The effects of natural selection on differential reproduction cannot be tested, since too many unknown variables have to be included, and that cannot lead to meaningful, quantifiable results that permit a clear picture.
1. Evolution.Berkley: Evolutionary fitness
2. J.Dekker: www.agron.iastate.edu/~weeds/AG517/Content/WeedEvol/NaturalSelection/natselect.html” target=”_blank” rel=”nofollow”>Natural Selection and its Four Conditions 2007
3. S.El-Showk: Natural selection: On fitness (2012)
4. Thomas Bataillon: Effects of new mutations on fitness: insights from models and data 2014 Jul
5. Adam Eyre-Walker: The distribution of fitness effects of new mutations August 2007
6. Ivana Cvijović: Fate of a mutation in a fluctuating environment August 24, 2015
7. R. G. Brajesh: Distribution of fitness effects of mutations obtained from a simple genetic regulatory network model 08 July 2019