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The criteria used to evaluate each contrast

Demography is the quantitative study of population processes, while evolution is a population process that influences all aspects of biological organisms, including their demography. Demographic traits common to all human populations are the products of biological evolution or the interaction of biological and cultural evolution. Demographic variation within and among human populations is influenced by our biology, and therefore by natural selection and our evolutionary background. Demographic methods are necessary for studying populations of other species, and for quantifying evolutionary fitness. Comparisons among species allow for a greater understanding of how and why demographic patterns evolve.

The extensive literature on the costs and benefits of sexual reproduction often concludes that increased offspring viability is a benefit of sexual reproduction as compared to parthenogenesis. We show that all comparisons contributing to this conclusion involve cases of meiotic parthenogenesis, the most sex-like form of asex. Meiotic parthenogenesis does consistently achieve lower offspring viability than does sex. However when sexual reproduction is compared to forms of asex that don't involve meiosis, asex results in higher offspring viability. Combined with experimental and demographic data, this result demonstrates that failures associated with meiosis are a major cause of offspring inviability not only for meiotic parthenogenesis, but for sexual reproducers such as humans. Meiosis is necessary for genetic recombination in eukaryotes, but is vestigial, and costly, in parthenogens. The question of why meiosis persists in parthenogens despite its clear fitness costs and lack of benefits for them is addressed in terms of mechanistic constraints upon what selection can achieve. This provides a clear example of evolutionary inertia having a major and maladaptive effect on the demography of a wide range of organisms.

In this study, we tested the hypothesis that maternal effects on offspring production and quality are greater than paternal effects in both offspring number (fertility) and offspring viability (mortality). We used the model filamentous fungus Neurospora crassa. This fungus is anisogamous, obligately outcrossing with two mating types (mat-A and mat-a), and hermaphroditic. We designed a fully crossed mating scheme using 11 mat-A and 11 mat-a N. crassa strains chosen from a set of 24 mat-A and 24 mat-a strains from North America, the Caribbean, and Africa that were genotyped previously (Ellison, Hall, & Kowbel 2011). Precise genetic distances between mating pairs were calculated to control for the effects of crossing distance on offspring production. We performed reciprocal crosses of all 121 strain pairings and collected data on perithecial production, ascospore (sexual spore) production, and various ascospore characteristics. Mixed effects models of these data show that the female parent accounts for the majority of variation in perithecial production, number of spores produced, and spore germination. Surprisingly, both sexes equally influence the percentage of spores that are pigmented. In this fungus, pigmented spores are viable and unpigmented spores are inviable. These results show that while both parents influence all these traits, maternal influence is strongest on both fertility and mortality traits until the spores are physiologically independent of the maternal cytoplasm.

How many post-reproductive individuals are found in a population depends on how many individuals survive to reproductive cessation and how long they live thereafter. Post-reproductive Representation (PrR), a measure of post-reproductive lifespan intended for interspecific comparisons, allows a close examination, via decomposition, of the relative importance of survival to and life-expectancy after cessation. We show that the survival portion of PrR, rather than the life-expectancy portion, is the primary driver of variation in PrR. Variation in survival to reproductive cessation explains the majority of variation in PrR among a group of small cohorts of rotifers, and among several historical Swedish cohorts. We emphasize that women are distinct from other primates in the proportion reaching reproductive cessation, but not in the proportion of adult life-expectancy that is post-reproductive. Research on the evolution of post-reproductive lifespan should take into account the primary importance of survival to reproductive cessation, rather than focusing on the length of life thereafter.

Gerontology focuses on deterioration with increasing age, but in most populations most variables, including survival probability, improve at early ages (ontogenescence) before deteriorating at advanced ages (senescence). The extent to which gerontology needs to consider this U-shaped pattern of risk over age depends upon the mechanistic, demographic and evolutionary links and interactions between ontogenescence and senescence. In reading the literature on both senescence and ontogenescence, and in interacting with other biogerontologists, we have encountered a set of what we view as inaccurate or oversimplified claims about ontogenescence, its relationship to senescence and its importance to gerontology. Here, after briefly introducing ontogenescence, we address four of these claims. We demonstrate the counterfactual nature of Claim 1. Ontogenescence is an environmental effect largely absent in protected environments. We then briefly review the literature which leads to Claim 2. Senescence and ontogenescence are parts of the same phenomenon, and describe why we reject this view. We then explain why the rejection of Claim 2 does not necessarily support Claim 3, the idea that senescence and ontogenescence are easily separable. Finally, we examine Claim 4. Gerontologists don’t need to think about ontogenescence, and give some examples of why we consider this misguided.

Gerontology focuses on deterioration with increasing age, but in most populations most variables, including survival probability, improve at early ages (ontogenescence) before deteriorating at advanced ages (senescence). The extent to which gerontology needs to consider this U-shaped pattern of risk over age depends upon the mechanistic, demographic and evolutionary links and interactions between ontogenescence and senescence. In reading the literature on both senescence and ontogenescence, and in interacting with other biogerontologists, we have encountered a set of what we view as inaccurate or oversimplified claims about ontogenescence, its relationship to senescence and its importance to gerontology. Here, after briefly introducing ontogenescence, we address four of these claims. We demonstrate the counterfactual nature of Claim 1. Ontogenescence is an environmental effect largely absent in protected environments. We then briefly review the literature which leads to Claim 2. Senescence and ontogenescence are parts of the same phenomenon, and describe why we reject this view. We then explain why the rejection of Claim 2 does not necessarily support Claim 3, the idea that senescence and ontogenescence are easily separable. Finally, we examine Claim 4. Gerontologists don't need to think about ontogenescence, and give some examples of why we consider this misguided.

There persist two widely held but mutually inconsistent views on the evolution of post-fertile lifespan of human females. The first, prevalent within anthropology, sees post-fertile lifespan (PFLS) in the light of adaptive processes, focusing on the social and economic habits of humans that selected for a lengthy PFLS. This view rests on the assumption that human PFLS is distinct from that of other species, and focuses on quantifying the selective causes and consequences of that difference. The second view, prevalent within gerontology and comparative biology, emphasizes that PFLS is a phylogenetically widespread trait or that human PFLS is predictable based on life-history allometries. In this view, human PFLS is part of a broad cross-species pattern and its genesis cannot, therefore, rely on human-specific traits. Those who advocate the second view have questioned the "special pleading" for human specific explanations of PFLS, and have argued that human PFLS is quantitatively greater but not qualitatively different than PFLS in many other animals. Papers asking whether human PFLS is explained by the importance of mothers more than grandmothers, whether paternal or maternal grandparents have more of an effect on child survival, or who is providing the excess calories are associated with the first view that assumes the need to explain the existence of human PFLS on the basis of a uniquely human socioecology. Anthropologists largely see human PFLS as derived, while comparative gerontologists point to evidence that it is one instance of a ubiquitous cross-species pattern. The two groups generally occupy non-overlapping research circles, in terms of conferences and journals, and therefore interact little enough to largely avoid the need to reconcile their views, allowing the persistence of misconceptions in each field. Our goal is to identify and address the most important of these misconceptions and thereby make clear that both of these seemingly incongruent views contain valid points. We argue that two distinct but related traits have been lumped together under the same concept of "post-reproductive lifespan," one (post-fertile viability) that is tremendously widespread and another (a post-fertile life stage) that is derived to hominins, and that the differences and connections between these two traits are necessary for understanding human life-history evolution.