A meta-analysis of published studies with adult human participants was conducted to evaluate whether physical fitness attenuates cardiovascular reactivity and improves recovery from acute psychological stressors. Thirty-three studies met selection criteria; 18 were included in recovery analyses. Effect sizes and moderator influences were calculated by using meta-analysis software. A fixed effects model was fit initially; however, between-studies heterogeneity could not be explained even after inclusion of moderators. Therefore, to account for residual heterogeneity, a random effects model was estimated. Under this model, fit individuals showed significantly attenuated heart rate and systolic blood pressure reactivity and a trend toward attenuated diastolic blood pressure reactivity. Fit individuals also showed faster heart rate recovery, but there were no significant differences in systolic blood pressure or diastolic blood pressure recovery. No significant moderators emerged. Results have important implications for elucidating mechanisms underlying effects of fitness on cardiovascular disease and suggest that fitness may be an important confound in studies of stress reactivity.

This paper presents the first longitudinal study of sex disparities in COVID-19 cases and mortalities across U.S. states, derived from the unique 13-month dataset of the U.S. Gender/Sex COVID-19 Data Tracker. To analyze sex disparities, weekly case and mortality rates by sex and mortality rate ratios and rate differences were computed for each U.S. state, and a multilevel crossed-effects conditional logistic binomial regression model was fitted to estimate the variation of the sex disparity in mortality over time and across states. Results demonstrate considerable variation in the sex disparity in COVID-19 cases and mortalities over time and between states. These data suggest that the sex disparity, when present, is modest, and likely varies in relation to context-sensitive variables, which may include health behaviors, preexisting health status, occupation, race/ethnicity, and other markers of social experience.

Last spring, the US National Institutes of Health (NIH) announced a new policy calling for the use of both male and female materials-animals, tissues, cells, and cell lines-in preclinical research (1). Canada and the European Union have recently instituted similar policies. Advocates argue that requiring analysis of sex in preclinical research will advance scientific understanding of sex differences in human health outcomes, such as higher rates of adverse drug events (ADE) in women compared with men (2). We disagree.To be useful in addressing health disparities, sex-linked variables in preclinical materials must effectively model differences between human men and women. In the absence of evidence that this is so, the addition of sex as a variable in all preclinical studies is likely to introduce conceptual and empirical errors into research. Biomedical research institutions and funders can better remedy sex differences in health outcomes by focusing on the scientific study of the interaction of sex and gender variables in health outcomes in human populations.Sex differences in rates of ADE may be a result of biological factors, gender-related social factors, or a combination of sex-and gender-related variables. "Sex" refers to chromosomal complement, reproductive organs, or specific hormones related to sexual reproduction. "Gender" refers to sociocultural norms, expectations, and practices ascribed to males and females (3). Gendered factors, such as women's propensity to take multiple pharmaceuticals simultaneously (polypharmacy) compared with men, and their greater likelihood to see medical doctors than men, play a well-documented role in sex differences in health outcomes (4-6).Take the case of zolpidem (Ambien). In 2013, the Food and Drug Administration issued an unprecedented advisory reducing the recommended zolpidem dosage for women, following reports of higher numbers of ADE in women compared to men (7). Since then, researchers have sought the biological basis for this sex difference in reports of zolpidem-related ADE. Surprisingly, experimental studies of sex differences in the pharmacokinetics and pharmacodynamics of zolpidem in human men and women found that body weight, not sex, is the culprit. Women clear zolpidem from their system more slowly than men, but body weight eliminates the statistical significance of sex as a variable in clearance of zolpidem (8). Because body weight, not sex, is the independent biological variable, sex-based preclinical research protocols would likely not have predicted sex differences in rates of ADE with zolpidem.The zolpidem case provides an example of the need for studies aimed at uncovering the embodied interaction of human sex-and gender-related variables in sex differences in ADE. Weight is distributed differentially across male and female bodies. In presentday American populations, weight may interact with gender-related variables. For example, higher rates of zolpidem use and polypharmacy in women compared to men, as well as biopsychosocial factors, such as wome...

Human life history contains a series of paradoxes not easily explained by classical life history theory. While overall reproductive output is higher than in related primates, juvenile growth is slower and age-specific reproductive rates decline faster with age. A simple energetic model would predict that growth and reproductive rates should be positively correlated and that reproductive effort should not decelerate with age. The pattern of negative correlations in humans suggests the presence of trade-offs among peak reproductive rate, childhood growth, and reproductive rate at older ages. To address this puzzle, we propose a synthesis of reproductive ecology and behavioral ecology focused on intra-and inter-somatic energy transfers. This integration includes three concepts: the mother as final common pathway through which energy must pass to result in offspring; a distinction between direct and indirect reproductive effort, proposing the latter as a novel net energy allocation category relative to growth and direct reproductive effort; and a pooled energy budget representing the energetic contributions and withdrawals of all members of a breeding community. Individuals at all reproductive life stages are considered in light of their contributions to the pooled energy budget.

This review connects Tanner's contributions to contemporary understanding of puberty as a process fundamentally driven by neuroendocrine maturation. It introduces the concepts of the 'hour-glass of puberty' and 'somatic strategy' as heuristic constructs. The 'hour-glass of puberty' describes the converging pathways of information flow influencing the timing of the neuroendocrine events of puberty and its ramifying consequences throughout the body. Somatic strategy refers to the pattern of sex-specific, adult body morphology that develops at puberty as the individual undergoes a life history transition from juvenile to adult.