Fitness,inclusive fitness,and optimization

Individual-as-maximizing agent analogies result in a simple understanding of the functioning of the biological world. Identifying the conditions under which individuals can be regarded as fitness maximizing agents is thus of considerable interest to biologists. Here, we compare different concepts of fitness maximization, and discuss within a single framework the relationship between Hamilton’s (J Theor Biol 7:1–16, 1964) model of social interactions, Grafen’s (J Evol Biol 20:1243–1254, 2007a) formal Darwinism project, and the idea of evolutionary stable strategies. We distinguish cases where phenotypic effects are additive separable or not, the latter not being covered by Grafen’s analysis. In both cases it is possible to define a maximand, in the form of an objective function ?(z), whose argument is the phenotype of an individual and whose derivative is proportional to Hamilton’s inclusive fitness effect. However, this maximand can be identified with the expression for fecundity or fitness only in the case of additive separable phenotypic effects, making individual-as-maximizing agent analogies unattractive (although formally correct) under general situations of social interactions. We also feel that there is an inconsistency in Grafen’s characterization of the solution of his maximization program by use of inclusive fitness arguments. His results are in conflict with those on evolutionary stable strategies obtained by applying inclusive fitness theory, and can be repaired only by changing the definition of the problem.     

Offspring fitness and individual optimization of clutch size

Within-year variation in clutch size has been claimed to be an adaptation to variation in the individual capacity to raise offspring. We tested this hypothesis by manipulating brood size to one common size, and predicted that if clutch size is individually optimized, then birds with originally large clutches have a higher fitness than birds with originally small clutches. No evidence was found that fitness was related to the original clutch size, and in this population clutch size is thus not related to the parental capacity to raise offspring. However, offspring from larger original clutches recruited better than their nest mates that came from smaller original clutches. This suggests that early maternal or genetic variation in viability is related to clutch size.     

The simplest formal argument for fitness optimization

The Formal Darwinism Project aims to provide a formal argument linking population genetics to fitness optimization, which of necessity includes defining fitness. This bridges the gulf between those biologists who assume that natural selection leads to something close to fitness optimization and those biologists who believe on theoretical grounds that there is no sense of fitness that can usefully be said to be optimized. The current paper’s main objective is to provide a careful mathematical introduction to the project, and it also reflects on the project’s scope and limitations. The central argument is the proof of close ties between the mathematics of motion, as embodied in the Price equation, and the mathematics of optimization, as represented by optimization programmes. To make these links, a general and abstract model linking genotype, phenotype and number of successful gametes is assumed. The project has begun with simple dynamic models and simple linking models, and its progress will involve more realistic versions of them. The versions given here are fully mathematically rigorous, but elementary enough to serve as an introduction.     

Mitonuclear match: optimizing fitness and fertility over generations drives ageing within generations

Many conserved eukaryotic traits, including apoptosis, two sexes, speciation and ageing, can be causally linked to a bioenergetic requirement for mitochondrial genes. Mitochondrial genes encode proteins involved in cell respiration, which interact closely with proteins encoded by nuclear genes. Functional respiration requires the coadaptation of mitochondrial and nuclear genes, despite divergent tempi and modes of evolution. Free-radical signals emerge directly from the biophysics of mosaic respiratory chains encoded by two genomes prone to mismatch, with apoptosis being the default penalty for compromised respiration. Selection for genomic matching is facilitated by two sexes, and optimizes fitness, adaptability and fertility in youth. Mismatches cause infertility, low fitness, hybrid breakdown, and potentially speciation. The dynamics of selection for mitonuclear function optimize fitness over generations, but the same selective processes also operate within generations, driving ageing and age-related diseases. This coherent view of eukaryotic energetics offers striking insights into infertility and age-related diseases.     

Genetics of Darwinian fitness. II. Pleiotropic selection on fertility and survival

A non-overlapping generation model is proposed which links Wright's adaptive topography concept to the rather inexact notion of Darwinian fitness as survival and reproduction. In general, evolution is seen to weight proportionate increases in survival twice as greatly as proportionate increases in fertility. Certain special cases are also delineated in which measurements of survival and fertility receive equal weight in the fitness equations. In addition, some implications of the present study for Wright's shifting balance theory and models based on Fisher's reproductive value are discussed.     

Human fertility and land tenure in highland Bolivia

Abstract

Basic demographic data of landless and landed peasants from the highlands and valley of Northern Potosi, Bolivia, are compared. Household size and crude birth rates are larger in the highlands than in the valley. Within the highland population, no statistically significant difference was observed between the age‐specific fertility of landless and landed women, nor in the survivorship ratio of their offspring. The prevalence of exchange and reciprocity at the village level may be responsible for the absence of important differences in the fertility and mortality patterns of the landed and landless.     

Human fertility and land tenure in highland Bolivia

Basic demographic data of landless and landed peasants from the highlands and valley of Northern Potosi, Bolivia, are compared. Household size and crude birth rates are larger in the highlands than in the valley. Within the highland population, no statistically significant difference was observed between the age-specific fertility of landless and landed women, nor in the survivorship ratio of their offspring. The prevalence of exchange and reciprocity at the village level may be responsible for the absence of important differences in the fertility and mortality patterns of the landed and the landless. Information was obtained from a total of 333 households, which included a population of about 1700 people or 20% of the Jukumani ayllu (ethnic group). No relationship between altitude and human reproduction was noted among Jukumanis. Highland Jukumani women begin reproducing in their late teens; by their mid-20s only about 30% of the 21-25 year old female cohort remains childless. 2 major tax categories of people emerge in the area under consideration: taseros, the landed peasantry who are obligated to pay taxes, and kantu runas, the landless laborers who do not pay taxes. Tasero women are most fertile from their mid-20s until their mid-30s whild kantu runa women are more fertile later in life. Within the highland territory there are no statistically significant differences in the infant and child mortality patterns of taseros and kantu runas. The higher household size and crude birth rates of highlanders suggests that hypoxic stress may not depress fertility. Taseros and kantu runas differ in fertility patterns in degree rather than in kind. It is concluded that although differential access to natural resources may translate into slightly higher crude birth rates and child/woman ratios, it does not have much bearing on the fertility of women, or the mortality or household size of taxpayers and kantu runas. A possible explanation for the Jukumani anomaly may be the prevalence of reciprocity and exchange between taseros and kantu runas, especially relating to land access and physical care.     

Human fertility,evolutionary biology,and the demographic transition

Though increased food supply and lowered mortality lead to population growth in most species, in our own these are often associated with a change in the rate of population increase known as the “demographic transition.” Evolutionary biology suggests that the transition might result from our maximizing fitness by increasing the quality of our offspring at the expense of their quantity, but this explanation has little predictive power. Another hypothesis holds that males in traditional societies increase their fitness at the expense of females by forcing the latter to bear more than their optimal number of children, and that the post-transition phase results from increased female autonomy associated with modernization. Analysis of the hypothesis indicates that a male tactic of forcing increased fertility is likely to occur only in a few special cases. An alternative hypothesis that human females would fail to bear their optimal number of children without the pressure of mates and kin does appear possible, given the unique selection pressures generated by the rise of intelligence. A brief look at the complex demographic transition literature reveals the limited usefulness of global hypotheses drawn from evolutionary biology.     

Human fertility studies under field conditions. Introduction.

Human fertility is part of biological anthropology embracing human population biology devoted to the analysis of the nature, caused, origin, and development of human variation at molecular, cellular, and whole body levels. The successful outcome of human fertility depends on the interactions of biochemical, physiological, and psychological processes whose disturbance results in slight variations in behavior and even total infertility. The Hutterites in the US have the highest average fertility with over 11 live births/women. Hunter-gatherer groups rarely have more than 4 children/woman. The case of a woman who gave birth to 67 children was recorded. Total infertility often occurs even in noncontracepting societies. The most important factor that determines the character of genetic variation within the human species seems to be comparative population growth, as this was the factor determining which populations spread and which became extinct. The study of the determinants of female fertility has attracted attention recently because pregnancy and motherhood affect daily life, and in turn, reproduction is also affected by daily life. Lactational amenorrhea plays a vital role in child spacing, but the mechanism of breast feeding is complex with factors of duration, frequency, milk production, and suckling frequency interwoven. Female reproduction comprises whole body function, nutrition, body composition (the recent debate on fat stores affecting the onset of fertility), physical work, and mental health all influencing the endocrinological state. Heavy physical labor and intensive training by sportswomen can result in amenorrhea. Beta-endorphins also play a role in lactational amenorrhea along with nutrition and body composition. Infectious and venereal diseases particularly affect fertility, yet genetics protect the placenta against falciparum malaria in sickle-cell trait women.     

Low fertility increases descendant socioeconomic position but reduces long-term fitness in a modern post-industrial society

Adaptive accounts of modern low human fertility argue that small family size maximizes the inheritance of socioeconomic resources across generations and may consequently increase long-term fitness. This study explores the long-term impacts of fertility and socioeconomic position (SEP) on multiple dimensions of descendant success in a unique Swedish cohort of 14 000 individuals born during 1915–1929. We show that low fertility and high SEP predict increased descendant socioeconomic success across four generations. Furthermore, these effects are multiplicative, with the greatest benefits of low fertility observed when SEP is high. Low fertility and high SEP do not, however, predict increased descendant reproductive success. Our results are therefore consistent with the idea that modern fertility limitation represents a strategic response to the local costs of rearing socioeconomically competitive offspring, but contradict adaptive models suggesting that it maximizes long-term fitness. This indicates a conflict in modern societies between behaviours promoting socioeconomic versus biological success. This study also makes a methodological contribution, demonstrating that the number of offspring strongly predicts long-term fitness and thereby validating use of fertility data to estimate current selective pressures in modern populations. Finally, our findings highlight that differences in fertility and SEP can have important long-term effects on the persistence of social inequalities across generations.     

Absolute fitness, relative fitness, and utility

It is well known that (1) natural selection typically favors an allele with both a large mean fitness and a small variance in fitness; and (2) investors typically prefer a portfolio with both a large mean return and a small variance in returns. In the case of investors, this mean-variance trade-off reflects risk aversion; in the case of evolution, the mathematics is straightforward but the result is harder to intuit. In particular, it is harder to understand where, in the mathematics of natural selection, risk aversion arises. Here I present a result that suggests a simple answer to this question. Although my answer is essentially identical to one offered previously, my path to it differs somewhat from previous approaches. Some may find this new approach easier to intuit.     

Human fertility variation, size-related obstetrical performance and the evolution of sexual stature dimorphism

In several animal species, change in sexual size dimorphism is a correlated response to selection on fecundity. In humans, different hypotheses have been proposed to explain the variation of sexual dimorphism in stature, but no consensus has yet emerged. In this paper, we evaluate from a theoretical and an empirical point of view the hypothesis that the extent of sexual dimorphism in human populations results from the interaction between fertility and size-related obstetric complications. We first developed an optimal evolutionary model based on extensive simulations and then we performed a comparative analysis for a total set of 38 countries worldwide. Our optimization modelling shows that size-related mortality factors do indeed have the potential to affect the extent of sexual stature dimorphism. Comparative analysis using generalized linear modelling supports the idea that maternal death caused by deliveries and complications of pregnancy (a variable known to be size related) could be a key determinant explaining variation in sexual stature dimorphism across populations. We discuss our results in relation to other hypotheses on the evolution of sexual stature dimorphism in humans.     

Human immunodeficiency virus evolution towards reduced replicative fitness in vivo and the development of AIDS

Human immunodeficiency virus (HIV) infection progresses to AIDS following an asymptomatic period during which the virus is thought to evolve towards increased fitness and pathogenicity. We show mathematically that progression to the strongest HIV-induced pathology requires evolution of the virus towards reduced replicative fitness in vivo. This counter-intuitive outcome can happen if multiple viruses co-infect the same cell frequently, which has been shown to occur in recent experiments. According to our model, in the absence of frequent co-infection, the less fit AIDS-inducing strains might never emerge. The frequency of co-infection can correlate with virus load, which in turn is determined by immune responses. Thus, at the beginning of infection when immunity is strong and virus load is low, co-infection is rare and pathogenic virus variants with reduced replicative fitness go extinct. At later stages of infection when immunity is less efficient and virus load is higher, co-infection occurs more frequently and pathogenic virus variants with reduced replicative fitness can emerge, resulting in T-cell depletion. In support of these notions, recent data indicate that pathogenic simian immunodeficiency virus (SIV) strains occurring late in the infection are less fit in specific in vitro experiments than those isolated at earlier stages. If co-infection is blocked, the model predicts the absence of any disease even if virus loads are high. We hypothesize that non-pathogenic SIV infection within its natural hosts, which is characterized by the absence of disease even in the presence of high virus loads, could be explained by a reduced occurrence of co-infection in this system.     

On the problems of the evolutionary optimization of life history. I. Markov model of Leslie life cycle and optimization of fertility

The paper considers the properties of individual life history corresponding to the Leslie model of age-structured population. The life history is modelled as a finite Markov chain with absorption at a death state of individual. In this model, individual longevity, average number of offspring R _L (produced by an individual over the entire life), and some other known characteristics of the life history have been derived using simple probability methods that do not involve matrix calculus and their individual components have been interpreted. In the linear Leslie population model (derived by simple modification of a Markov chain), R _L determines the growth or decline of a population. Individuals with higher R _L values have evolutionary advantages in the population due to accelerated growth in their number. The selection of fertility as a factor of the increase in R _L is considered. In the Leslie model, fertility is a set of correlated quantitative traits, where the age-specific fertility components are determined both by multiple loci and the environment. According to the genetic theory of quantitative trait selection, they evolve towards an increase in R _L . Taking into account the limited resources for reproduction, selection optimizes the fertility distribution according to age. Optimal distribution corresponds to the attainment of the maximum R _L . This complies with the maximization of the rate of population growth (r-selection), which is characteristic of linear population models. The search for the R _L maximum and optimal distribution of fertility belongs to the field of linear programming.     

Thyroid and fertility

The aim of this work is to specify the relationship between the thyroid function and the hypothalamo-hypophyso-gonadal axis. Qualitative and quantitative repercussions of a thyroid pathology on human or animal fertility, male or female are very variable. A review of mechanisms of action is presented, illustrating: the complexity of the phenomena in cause; the necessity not to dissociate thyroid and reproductive function either clinically or biologically; the serious consequences of either undetected or untreated neo-natal thyroid pathology.     

Hypervirulence and pathogen fitness

Historically, pathogenesis research has focused on the identification and characterization of virulence factors. More recently, 'anti-virulence' genes have been discovered. Mutations in these loci result in a hypervirulent phenotype, as measured by a lower lethal dose, a colonization advantage, reduced clearance or decreased survival time of the host. If these genes function to reduce pathogen virulence, why have they been retained? Multiple hypotheses have been offered to explain this phenomenon.