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The classic anthropological hypothesis known as the “obstetrical dilemma” is a well-known explanation for human altriciality, a condition that has significant implications for human social and behavioral evolution. The hypothesis holds that antagonistic selection for a large neonatal brain and a narrow, bipedal-adapted birth canal poses a problem for childbirth; the hominin “solution” is to truncate gestation, resulting in an altricial neonate. This explanation for human altriciality based on pelvic constraints persists despite data linking human life history to that of other species. Here, we present evidence that challenges the importance of pelvic morphology and mechanics in the evolution of human gestation and altriciality. Instead, our analyses suggest that limits to maternal metabolism are the primary constraints on human gestation length and fetal growth. Although pelvic remodeling and encephalization during hominin evolution contributed to the present parturitional difficulty, there is little evidence that pelvic constraints have altered the timing of birth.

Consideration of the outcomes of developmental plasticity acting over the intermediate timescale is now important.20 Developmental plasticity evolved because it is adaptive, promoting Darwinian fitness by enhancement of survival and reproductive success.21 Plasticity uses environmental cues (which in mammals are transduced and buffered by the mother) to optimise the life-course strategy for maximum fitness, both making the best of present conditions and being well prepared for the future environment.22 Hormones and nutrients that cross the placenta can be affected by the mother's body composition, metabolism, and long-term lifestyle and by her immediate diet and stress levels. [...] environmental cues affecting development provide historical information that offspring use to predict the future.23 However, this anticipatory strategy has limitations, especially for long-lived species such as human beings, with the result that challenges during development can induce responses that have short-term benefits for the mother or the fetus but then longer term costs in terms of reduced fitness.24,25 When environmental conditions change strikingly between conception and adulthood, as has happened in most current human populations, the potential for a substantial mismatch is especially great, and this difference contributes to disease risk.

The 'challenge hypothesis' posits that testosterone facilitates reproductive effort (investment in male-male competition and mate-seeking) at the expense of parenting effort (investment in offspring and mates). Multiple studies, primarily in North America, have shown that men in committed relationships, fathers, or both maintain lower levels of testosterone than unpaired men. Data from non-western populations, however, show inconsistent results. We hypothesized that much of this cross-cultural variation can be attributed to differential investment in mating versus parenting effort, even among married fathers. Here, we directly test this idea by comparing two neighbouring Tanzanian groups that exhibit divergent styles of paternal involvement: Hadza foragers and Datoga pastoralists. We predicted that high levels of paternal care by Hadza fathers would be associated with decreased testosterone in comparison with non-fathers, and that no such difference between fathers and non-fathers would be evident in Datoga men, who provide minimal direct paternal care. Twenty-seven Hadza men and 80 Datoga men between the ages of 17 and 60 provided morning and afternoon saliva samples from which testosterone was assayed. Measurements in both populations confirmed these predictions, adding further support to the hypothesis that paternal care is associated with decreased testosterone production in men.

A large body of research has demonstrated that variation in competitive behavior across species and individuals is linked to variation in physiology. In particular, rapid changes in testosterone and cortisol during competition differ according to an individual's or species' psychological and behavioral responses to competition. This suggests that among pairs of species in which there are behavioral differences in competition, there should also be differences in the endocrine shifts surrounding competition. We tested this hypothesis by presenting humans' closest living relatives, chimpanzees (Pan troglodytes) and bonobos (Pan paniscus), with a dyadic food competition and measuring their salivary testosterone and cortisol levels. Given that chimpanzees and bonobos differ markedly in their food-sharing behavior, we predicted that they would differ in their rapid endocrine shifts. We found that in both species, males showed an anticipatory decrease (relative to baseline) in steroids when placed with a partner in a situation in which the two individuals shared food, and an anticipatory increase when placed with a partner in a situation in which the dominant individual obtained more food. The species differed, however, in terms of which hormone was affected; in bonobo males the shifts occurred in cortisol, whereas in chimpanzee males the shifts occurred in testosterone. Thus, in anticipation of an identical competition, bonobo and chimpanzee males showed differential endocrine shifts, perhaps due to differences in perception of the situation, that is, viewing the event either as a stressor or a dominance contest. In turn, common selection pressures in human evolution may have acted on the psychology and the endocrinology of our competitive behavior.

New applications of evolutionary biology in medicine are being discovered at an accelerating rate, but few physicians have sufficient educational background to use them fully. This article summarizes suggestions from several groups that have considered how evolutionary biology can be useful in medicine, what physicians should learn about it, and when and how they should learn it. Our general conclusion is that evolutionary biology is a crucial basic science for medicine. In addition to looking at established evolutionary methods and topics, such as population genetics and pathogen evolution, we highlight questions about why natural selection leaves bodies vulnerable to disease. Knowledge about evolution provides physicians with an integrative framework that links otherwise disparate bits of knowledge. It replaces the prevalent view of bodies as machines with a biological view of bodies shaped by evolutionary processes. Like other basic sciences, evolutionary biology needs to be taught both before and during medical school. Most introductory biology courses are insufficient to establish competency in evolutionary biology. Premedical students need evolution courses, possibly ones that emphasize medically relevant aspects. In medical school, evolutionary biology should be taught as one of the basic medical sciences. This will require a course that reviews basic principles and specific medical applications, followed by an integrated presentation of evolutionary aspects that apply to each disease and organ system. Evolutionary biology is not just another topic vying for inclusion in the curriculum; it is an essential foundation for a biological understanding of health and disease.

The alleles that are detrimental to health, especially in older age, are thought to persist in populations because they also confer some benefits for individuals (through antagonistic pleiotropy). The ApoE4 allele at the ApoE locus, encoding apolipoprotein E (ApoE), significantly increases risk of poor health, and yet it is present in many populations at relatively high frequencies. Why has it not been replaced by natural selection with the health-beneficial ApoE3 allele? ApoE is a major supplier of cholesterol precursor for the production of ovarian oestrogen and progesterone, thus ApoE has been suggested as the potential candidate gene that may cause variation in reproductive performance. Our results support this hypothesis showing that in 117 regularly menstruating women those with genotypes with at least one ApoE4 allele had significantly higher levels of mean luteal progesterone (144.21 pmol l−1) than women with genotypes without ApoE4 (120.49 pmol l−1), which indicates higher potential fertility. The hormonal profiles were based on daily data for entire menstrual cycles. We suggest that the finding of higher progesterone in women with ApoE4 allele could provide first strong evidence for an evolutionary mechanism of maintaining the ancestral and health-worsening ApoE4 allele in human populations.

Physical characteristics, such as breast size and waist-to-hip ratio (WHR), function as important features used by human males to assess female attractiveness. Males supposedly pay attention to these features because they serve as cues to fecundity and health. Here, we document that women with higher breast-to-underbreast ratio (large breasts) and women with relatively low WHR (narrow waists) have higher fecundity as assessed by precise measurements of daily levels of 17-β-oestradiol (E2) and progesterone. Furthermore, women who are characterized by both narrow waists and large breasts have 26% higher mean E2 and 37% higher mean mid-cycle E2 levels than women from three groups with other combinations of body-shape variables, i.e. low WHR with small breasts and high WHR with either large or small breasts. Such gains in hormone levels among the preferred mates may lead to a substantial rise in the probability of conception, thus providing a significant fitness benefit.

Poor fetal environments are thought to produce adaptive changes in human developmental trajectories according to the Predictive Adaptive Response hypothesis. Although many studies have demonstrated correlations between indicators of fetal environment and negative adult health outcomes, the adaptive significance of these outcomes is unclear. Our study explicitly tests the adaptive nature of fetal programming in humans. We show that differences in nutritional status at birth are associated with adaptive differences in the sensitivity of adult ovarian function to energetic stress. Women who were born as relatively fat babies do not exhibit ovarian suppression in response to moderate levels of physical activity at adulthood, in contrast to women who were born as skinnier babies. The levels of estradiol in women born in the highest tertile of ponderal index (an indicator of neonatal nutritional status) were 37% and 46% higher, respectively, than levels of estradiol in women born in the low and middle ponderal index tertiles. These findings suggest that fetal programming of reproductive function results in developmentally plastic, but essentially adaptive, shifts in set points of ovarian response to energetic stress, such that women who were gestated under conditions of energetic constraint show greater sensitivity to energetic stress in adulthood. Our results have practical implications in terms of behavioral strategies for reducing the risk of breast cancer. We suggest that the amount of activity necessary to reduce levels of estrogen, which may in turn reduce cancer risk, can depend on a woman's nutritional status at birth.

Relative finger lengths, especially the second-to-fourth finger length ratio, have been proposed as useful markers for prenatal testosterone action. This claim partly depends on an association of relative finger lengths in adults with related sex differences in children and infants. This paper reports the results of a study using serial radiographs to test for both sex differences in the fingers of infants and children and for a relationship between sex differences in the children and infant finger and adult finger length ratios. This is the first study using long-term serial data to evaluate the validity of finger length ratios as markers. We found not only that sex differences in finger length ratios arise prior to puberty, but that sex differences in the fingers of children are highly correlated with adult finger length ratios. Our results strongly encourage the further use of finger length ratios as markers of perinatal testosterone action.