Search bioRxiv⌕ Search

Biology subjects

Malani, A.

Publications and source records attributed to Malani, A..

4 recordsLinked to original sources

Accounting for the life history structure of fitness in tests for adaptive reproductive acceleration

A prominent developmental plasticity theory proposes that early life adversity accelerates life history trajectories so organisms can maximize fitness in challenging environments. Standard tests of this hypothesis rely on empirical predictions about observable life history variables (e.g., age at first birth), because the proposed internal processes cannot be directly measured. However, the observable proxies are themselves mechanically linked, and regressions that ignore this may conflate causal effects with mechanical relationships among proxies. Here, we develop theory that explicitly justifies some existing empirical tests but rejects others. We integrate an accounting model that incorporates age at first birth, interbirth intervals, and lifespan with an optimization model, to derive the mathematical form that tests of the hypothesis should take. We apply these tests to data from wild female baboons, using early life rainfall as an exogenous proxy for early adversity so that estimates can plausibly be interpreted causally. The accounting model explains >98% of the variation in lifetime reproductive success among females that reproduced. However, our theory-derived tests find no evidence for the reproductive acceleration hypothesis. Our study illustrates the value of formal theory for causal inference in developmental plasticity research, where intertwined measurable variables may be obscured by strictly verbal hypotheses.

evolutionary biology↗

Testing frameworks for early life effects: the developmental constraints and adaptive responsehypotheses do not explain key fertility outcomes in wild female baboons

In evolutionary ecology, two classes of explanations are frequently invoked to explain "early life effects" on adult outcomes. Developmental constraints (DC) explanations contend that costs of early adversity arise from limitations adversity places on optimal development. Adaptive response (AR) hypotheses propose that later life outcomes will be worse when early and adult environments are poorly "matched." Here, we use recently proposed mathematical definitions for these hypotheses and a quadratic-regression based approach to test the long-term consequences of variation in developmental environments on fertility in wild baboons. We evaluate whether low rainfall and/or dominance rank during development predict three female fertility measures in adulthood, and whether any observed relationships are consistent with DC and/or AR. Neither rainfall during development nor the difference between rainfall in development and adulthood predicted any fertility measures. Females who were low-ranking during development had an elevated risk of losing infants later in life, and greater change in rank between development and adulthood predicted greater risk of infant loss. However, both effects were statistically marginal and consistent with alternative explanations, including adult environmental quality effects. Consequently, our data do not provide compelling support for either of these common explanations for the evolution of early life effects.

evolutionary biology↗

Seeing the future: a better way to model and test for adaptive developmental plasticity

In many species, individuals who experience harsh conditions during development often have poor health and fitness outcomes in adulthood relative to peers who do not. There are two classes of evolutionary hypotheses for the origins of these early life contributors to inequality in adulthood: developmental constraints (DC) models, which focus on the deleterious effects of low-quality early-life environments, and predictive adaptive response (PAR) hypotheses, which emphasize the cost of mismatches between early and adult environments. Distinguishing DC and PAR models empirically is difficult for both conceptual and analytical reasons. Here, we resolve this difficulty by providing explicit mathematical definitions for DC, PARs, and related concepts, and propose a novel, quadratic regression-based statistical test derived from these definitions. Simulations show that this approach improves the ability to discriminate between DC and PAR hypotheses relative to a common alternative based on testing for interaction effects between developmental and adult environments. Simulated data indicate that the interaction effects approach often conflates PARs with DC, while the quadratic regression approach yields high sensitivity and specificity for detecting PARs. Our results highlight the value of linking verbal and visual models to a formal mathematical treatment for understanding the developmental origins of inequitable adult outcomes.

evolutionary biology↗

Vaccination and the evolution of seasonal influenza

1Although vaccines against seasonal influenza are designed to protect against circulating strains, by affecting the emergence and transmission of antigenically divergent strains, they might also change the rate of antigenic evolution. Vaccination might slow antigenic evolution by increasing immunity, reducing the chance that even antigenically diverged strains can survive. Vaccination also reduces prevalence, decreasing the supply of potentially beneficial mutations and increasing the probability of stochastic extinction. But vaccination might accelerate antigenic evolution by increasing the transmission advantage of more antigenically diverged strains relative to less diverged strains (i.e., by positive selection). Such evolutionary effects could affect vaccinations direct benefits to individuals and indirect benefits to the host population (i.e., the private and social benefits). To investigate these potential impacts, we simulated the dynamics of an influenza-like pathogen with seasonal vaccination. On average, more vaccination decreased the rate of viral antigenic evolution and the incidence of disease. Notably, this decrease was driven partly by a vaccine-induced decline in the rate of antigenic evolution. To understand how the evolutionary effects of vaccines might affect their social and private benefits, we fitted linear panel models to simulated data. By slowing evolution, vaccination increased the social benefit and decreased the private benefit. Thus, in the long term, vaccinations potential social and private benefits may differ from current theory, which omits evolutionary effects. These results suggest that conventional seasonal vaccines against influenza, if protective against transmission and given to the appropriate populations, could further reduce disease burden by slowing antigenic evolution.

evolutionary biology↗