Samuel Pavard

The Size–Life Span Trade-Off Decomposed: Why Large Dogs Die Young

Large body size is one of the best predictors of long life span across species of mammals. In marked contrast, there is considerable evidence that, within species, larger individuals are actually shorter lived. This apparent cost of larger size is especially evident in the domestic dog, where artificial selection has led to breeds that vary in body size by almost two orders of magnitude and in average life expectancy by a factor of two. Survival costs of large size might be paid at different stages of the life cycle: a higher early mortality, an early onset of senescence, an elevated baseline mortality, or an increased rate of aging. After fitting different mortality hazard models to death data from 74 breeds of dogs, we describe the relationship between size and several mortality components. We did not find a clear correlation between body size and the onset of senescence. The baseline hazard is slightly higher in large dogs, but the driving force behind the trade-off between size and life span is apparently a strong positive relationship between size and aging rate. We conclude that large dogs die young mainly because they age quickly.

Sex-specific demographic behaviours that shape human genomic variation

In the human species, the two uniparental genetic systems (mitochondrial DNA and Y chromosome) exhibit contrasting diversity patterns. It has been proposed that sex‐specific behaviours, and in particular differences in migration rate between men and women, may explain these differences. The availability of high‐density genomic data and the comparison of genetic patterns on autosomal and sex chromosomes at global and local scales allow a reassessment of the extent to which sex‐specific behaviours shape our genome. In this article, we first review studies comparing the genetic patterns at uniparental and biparental genetic systems and assess the extent to which sex‐specific migration processes explain the differences between these genetic systems. We show that differences between male and female migration rates matter, but that they are certainly not the only contributing factor. In particular, differences in effective population size between men and women are also likely to account for these differences. Then, we present and discuss three anthropological processes that may explain sex‐specific differences in effective population size and thus human genomic variation: (i) variance in reproductive success arising from, for example, polygyny; (ii) descent rules; and (iii) transmission of reproductive success.

Mother's death and child survival: the case of early Quebec.

The aim of this paper is to account for the effect of mothers death on child survival in a historical population. Using comprehensive data on the early French Canadian population of Quebec, evidence is provided for a higher risk of dying for motherless children that remains significant over all childhood and long after the death of the mother. The specific effect of the loss of maternal care was estimated by comparing mortality before and after mothers death, furnishing a means to control for family heterogeneity. No differential in investment between genders was detected before age 3, but older girls suffered a three-fold higher susceptibility to mothers death than their male counterparts. This suggests that grown-up girls assuming the responsibilities of the missing mother had a lower chance of survival.

Can Life History Trade-Offs Explain the Evolution of Short Stature in Human Pygmies? A Response to Migliano et al. (2007)

Abstract Walker et al. [“Growth rates and life histories in twenty-two small-scale societies,” Am. J. Hum. Biol. 18:295–311 (2006)] used life history theory to develop an innovative explanation for human diversity in stature. Short stature could have been selected for in some human populations as a result of the advantage of an earlier growth cessation and earlier reproduction in a context of high mortality. Migliano et al. [“Life history trade-offs explain the evolution of human pygmies,” Proc. Natl. Acad. Sci. USA 104:20,216–20,219 (2007)] recently published an important article that tested this hypothesis to explain short stature in human pygmy populations. However innovative this work may be, we believe that some of the data and results presented are controversial if not questionable. As problematic points we note (1) the use of an arbitrary threshold of height (155 cm) to categorize populations into pygmies and nonpygmies; (2) the use of demographic data from Philippine pygmy groups that have experienced dramatic cultural and environmental changes in the last 20 years, and (3) the use of demographic data concerning African pygmy groups because good systematic data on these groups are not available. Finally, we report here mathematical errors and loopholes in the optimization model developed by Migliano and colleagues. In this paper we suggest alternative trade-offs that can be used to explain Miglianos results on more reliable bases.

The effect of maternal care on child survival: a demographic, genetic, and evolutionary perspective.

Abstract Models of population dynamics generally assume that child survival is independent of maternal survival. However, in humans, the death of a mother compromises her immature childrens survival because children require postnatal care. A childs survival therefore depends on her mothers survival in years following her birth. Here, we provide a model incorporating this relationship and providing the number of children surviving until maturity achieved by females at each age. Using estimates of the effect that a mothers death has on her childs survival until maturity, we explore the effect of the model on population dynamics. Compared to a model that includes a uniform child survival probability, our model slightly raises the finite rate of increase λ and modifies generation time and the stable age structure. We also provide estimates of selection on alleles that change the survival of females. Selection is higher at all adult ages in our model and remains significant after menopause (at ages for which the usual models predict neutrality of such alleles). Finally, the effect of secondary caregivers who compensate maternal care after the death of a mother is also emphasized. We show that allocare (as an alternative to maternal care) can have a major effect on population dynamics and is likely to have played an important role during human evolution.

THE INFLUENCE OF MATERNAL CARE IN SHAPING HUMAN SURVIVAL AND FERTILITY

Abstract The influence of maternal care on child survival has evolved throughout human history due to variation in altriciality, allocare, and maternal behaviors. Here, we study the impact of these factors on the force of selection acting on age-specific survival and fertility (measured with elasticity analysis) in a model that incorporates the dependence of child survival on maternal survival. Results reveal life-history changes that cannot be elucidated when considering childs survival independent of maternal survival: decrease of late fertility and increase of late survival, and concomitant decrease of early and late fertility. We also show that an increase of child altriciality in early humans might explain the main human life-history traits: a high life expectancy and postreproductive life; a long juvenile period and a higher, and narrowed, fertility at the peak of the reproductive period.

Actuarial senescence can increase the risk of extinction of mammal populations

Despite recent acknowledgement that senescence can have negative impact on survival and fertility in natural environments across a wide range of animal species, we still do not know if it can reduce the viability of wild endangered populations. Focusing on actuarial senescence (i.e., the decline of survival probabilities at old ages), we use species-specific demographic information to project the extinction risk of wild populations of 58 species of mammals, accounting (or not) for senescence. Our projections reveal potential negative effects of aging on population viability, with an average decrease of 27% of the time to extinction and a potential deterioration of the population-level projected conservation status in 10% of the species. Senescence is associated with particularly strong increases of the extinction risk in species with low mortality rates and long intervals between litters, independently of their place in the phylogeny, indicating that the pace of life history can be used to forecast the detrimental effects of aging on the viability of species. The aim of the various existing systems of classification of threatened species is to set conservation priorities based on assessments of extinction risk. Our results indicate that the quantitative effects of senescence on extinction are highly heterogeneous, which can affect the ranking of species and populations when setting conservation, priorities. In mammals, based on life history traits of a few species, generic patterns of senescence can be incorporated into projection population models to minimize these biases in viability assessments.

Residence rule flexibility and descent groups dynamics shape uniparental genetic diversities in South East Asia

OBJECTIVES Social organization plays a major role in shaping human population genetic diversity. In particular, matrilocal populations tend to exhibit less mitochondrial diversity than patrilocal populations, and the other way around for Y chromosome diversity. However, several studies have not replicated such findings. The objective of this study is to understand the reasons for such inconsistencies and further evaluate the influence of social organization on genetic diversity. MATERIALS AND METHODS We explored uniparental diversity patterns using mitochondrial HV1 sequences and 17 Y-linked short tandem repeats (STRs) in 12 populations (n = 619) from mainland South-East Asia exhibiting a wide range of social organizations, along with quantitative ethno-demographic information sampled at the individual level. RESULTS MtDNA diversity was lower in matrilocal than in multilocal and patrilocal populations while Y chromosome diversity was similar among these social organizations. The reasons for such asymmetry at the genetic level were understood by quantifying sex-specific migration rates from our ethno-demographic data: while female migration rates varied between social organizations, male migration rates did not. This unexpected lack of difference in male migrations resulted from a higher flexibility in residence rule in patrilocal than in matrilocal populations. In addition, our data suggested an impact of clan fission process on uniparental genetic patterns. CONCLUSIONS The observed lack of signature of patrilocality on Y chromosome patterns might be attributed to the higher residence flexibility in the studied patrilocal populations, thus providing a potential explanation for the apparent discrepancies between social and genetic structures. Altogether, this study highlights the need to quantify the actual residence and descent patterns to fit social to genetic structures.

State transitions: a major mortality risk for seasonal species

Ageing results from the accumulation of multifactorial damage over time. However, the temporal distribution of this damage remains unknown. In seasonal species, transitions between seasons are critical periods of massive physiological remodelling. We hypothesised that these recurrent peaks of physiological remodelling are costly in terms of survival. We tested whether captive small primates exposed to an experimentally increased frequency of seasonal transitions die sooner than individuals living under natural seasonality. The results show that experiencing one additional season per year increases the mortality hazard by a factor of 3 to 4, whereas the expected number of seasons lived is only slightly impacted by the seasonal rhythm. These results demonstrate that physiological transitions between periods of high and low metabolic activity represent a major mortality risk for seasonal organisms, which has been ignored until now.

Trait level analysis of multitrait population projection matrices

In most matrix population projection models, individuals are characterized according to, usually, one or two traits such as age, stage, size or location. A broad theory of multitrait population projection matrices (MPPMs) incorporating larger number of traits was long held back by time and space computational complexity issues. As a consequence, no study has yet focused on the influence of the structure of traits describing a life-cycle on population dynamics and life-history evolution. We present here a novel vector-based MPPM building methodology that allows to computationally-efficiently model populations characterized by numerous traits with large distributions, and extend sensitivity analyses for these models. We then present a new method, the trait level analysis consisting in folding an MPPM on any of its traits to create a matrix with alternative trait structure (the number of traits and their characteristics) but similar asymptotic properties. Adding or removing one or several traits to/from the MPPM and analyzing the resulting changes in spectral properties, allows investigating the influence of the trait structure on the evolution of traits. We illustrate this by modeling a 3-trait (age, parity and fecundity) population designed to investigate the implications of parity-fertilitytrade-offs in a context of fecundity heterogeneity in humans. The trait level analysis, comparing models of the same population differing in trait structures, demonstrates that fertility selection gradients differ between cases with or without parity-fertility trade-offs. Moreover it shows that age-specific fertility has seemingly very different evolutionary significance depending on whether heterogeneity is accounted for. This is because trade-offs can vary strongly in strength and even direction depending on the trait structure used to model the population.