In eastern North America, Indigenous peoples domesticated several crops that are now extinct. We present experimental data that alters our understanding of the domestication of one of these—goosefoot (Chenopodium berlandieri). Ancient domesticated goosefoot has been recognized on the basis of seed morphology, especially a decrease in the thickness of the seed coat (testa). Nondomesticated goosefoot also sometimes produces seeds that look similar or even identical to domesticated ones, but researchers believed that such seeds were rare (1%–3%). We conducted a common garden experiment and a series of carbonization experiments to better understand the determinants of seed polymorphism in archaeobotanical assemblages. We found that goosefoot produces much higher percentages of thin-testa seeds (mean 50% in our experiment, 15%–34% in free-living parent populations) than previously reported. We also found that cultivated plants produce more thin-testa seeds than their free-living parents, demonstrating that this trait is plastic in response to a garden environment. The carbonization experiments suggest that thin-testa seeds preserve under a larger window of conditions than thick-testa seeds, contrary to our expectations. These results suggest that (1) carbonized, phenotypically mixed assemblages should be interpreted cautiously, and (2) developmental plasticity and genetic assimilation played a role in the domestication of goosefoot.

Two extant frameworks – the harshness-unpredictability model and the threat-deprivation model – attempt to explain which dimensions of adversity have distinct influences on development. These models address, respectively, why, based on a history of natural selection, development operates the way it does across a range of environmental contexts, and how the neural mechanisms that underlie plasticity and learning in response to environmental experiences influence brain development. Building on these frameworks, we advance an integrated model of dimensions of environmental experience, focusing on threat-based forms of harshness, deprivation-based forms of harshness, and environmental unpredictability. This integrated model makes clear that the why and the how of development are inextricable and, together, essential to understanding which dimensions of the environment matter. Core integrative concepts include the directedness of learning, multiple levels of developmental adaptation to the environment, and tradeoffs between adaptive and maladaptive developmental responses to adversity. The integrated model proposes that proximal and distal cues to threat-based and deprivation-based forms of harshness, as well as unpredictability in those cues, calibrate development to both immediate rearing environments and broader ecological contexts, current and future. We highlight actionable directions for research needed to investigate the integrated model and advance understanding of dimensions of environmental experience.

Alloparental caregiving is key to humans’ highly flexible reproductive strategies. Across species and across societies, alloparental care is more common in harsh and/or unpredictable environments (HUEs). Currently, however, it is unclear whether HUEs predict intra-population variation in alloparental care, or whether early life HUEs might predict later alloparental care use in adulthood, consistent with adaptive developmental plasticity. We test whether harshness measures (socioeconomic status (SES), environmental hygiene, crowding) and unpredictability measures (parental unemployment, paternal absence, household moves) predicted how much alloparental assistance families in Cebu, Philippines received, in a multigenerational study with data collected across four decades. Though worse environmental hygiene predicted more concurrent alloparental care in 1994, we found little evidence that HUEs predict within-population variation in alloparental care in this large-scale, industrialized society. Indeed, less-crowded conditions and higher SES predicted more alloparental care, not less, in the 1980s and in 2014 respectively, while paternal absence in middle childhood predicted less reliance on alloparental care in adulthood. In this cultural context, our results generally do not provide support for the translation of interspecific or intersocietal patterns linking HUEs and alloparental care to intra-population variation in alloparental care, nor for the idea that a reproductive strategy emphasizing alloparental care use may be preceded by early life HUEs.

Predictive adaptive responses (PARs) are a form of developmental plasticity in which the developmental response to an environmental cue experienced early in life is delayed and yet, at the same time, the induced phenotype anticipates (i.e., is completely developed before) exposure to the eventual environmental state predicted by the cue, in which the phenotype is adaptive. We model this sequence of events to discover, under various assumptions concerning the cost of development, what lengths of delay, developmental time, and anticipation are optimal. We find that in many scenarios modeled, development of the induced phenotype should be completed at the exact same time that the environmental exposure relevant to the induced phenotype begins: that is, in contrast to our observed cases of PARs, there should be no anticipation. Moreover, unless slow development is costly, development should commence immediately after the cue: there should be no delay. Thus, PARs, which normally have non-zero delays and/or anticipation, are highly unusual. Importantly, the exceptions to these predictions of zero delays and anticipation occurred when developmental time was fixed and delaying development was increasingly costly. We suggest, therefore, that PARs will only evolve under three kinds of circumstances: (i) there are strong timing constraints on the cue and the environmental status, (ii) delaying development is costly, and development time is either fixed or slow development is costly, or (iii) when the period between the cue and the eventual environmental change is variable and the cost of not completing development before the change is high. These predictions are empirically testable.

Maternal protein restriction and physical activity can affect the interaction mother–placenta–fetus. This study quantified the gene expression of brain-derived neurotrophic factor (BDNF), neurothrophin 4, tyrosine kinase receptor B (TrkB/NTRK2), insulin-like growth factor (IGF-1), and insulin-like growth factor receptor (IGF-1r) in the different areas of mother’s brain (hypothalamus, hippocampus, and cortex), placenta, and fetus’ brain of rats. Female Wistar rats (n = 20) were housed in cages containing a running wheel for 4 weeks before gestation. According to the distance spontaneously traveled daily, rats were classified as inactive or active. During gestation, on continued access to the running wheel, active and inactive groups were randomized to receive normoprotein diet (18% protein) or a low-protein (LP) diet (8% protein). At day 20 of gestation, gene expression of neurotrophic factors was analyzed by quantitative polymerase chain reaction in different brain areas and the placenta. Dams submitted to a LP diet during gestation showed upregulation of IGF-1r and BDNF messenger RNA in the hypothalamus, IGF-1r and NTRK2 in the hippocampus, and BDNF, NTRK2, IGF-1 and IGF-1r in the cortex. In the placenta, there was a downregulation of IGF-1. In the brain of pups from mothers on LP diet, IGF-1r and NTRK2 were downregulated. Voluntary physical activity attenuated the effects of LP diet on IGF-1r in the hypothalamus, IGF-1r and NTRK2 in the hippocampus, IGF-1 in the placenta, and NTRK2 in the fetus’ brain. In conclusion, both maternal protein restriction and spontaneous physical activity influence the gene expression of BDNF, NTRK2, IGF-1, and IGF-1r, with spontaneous physical activity being able to normalize in part the defects caused by protein restriction during pregnancy.

Most human variation is structured around symbolically marked cultural (‘ethnic’) groups that require common codes of communication. Consequently, many have hypothesised that using others’ linguistic competences as markers of their descent is part of an evolved human psychology. However, there is also evidence that the use of language as ethnic markers is not universally applied, but context specific. We explore the tension between these views by studying responses to bilingualism among 121 adults living in Mayan communities undergoing rapid socioeconomic changes involving increased contact with Spanish-speaking towns. We show that, although competences in Mayan were strongly tied to perceiving others as having a Mayan ethnic identity, ethnolinguistic category membership was not seen as stable through life, vertically transmitted, nor regarded as incompatible with competences in Spanish. Moreover, we find variation in how people reasoned about ethnolinguistic identities depending on their own linguistic repertoires. Our work suggests that, while there may be an evolved predisposition to use language as a signal of group identity, our developmental plasticity allows us to respond adaptively to social information around us, leading to psychological and behavioural variation within and across populations. How people reason about others based on their linguistic profiles will affect the payoffs of acquiring different languages and ultimately the long-term sustainability of linguistic diversity.

This study evaluated the effects of a post-weaning high-fat (HF) diet on somatic growth, food consumption, metabolic parameters, phagocytic rate and nitric oxide (NO) production of peritoneal macrophages in young rats submitted to a maternal low-protein (LP) diet. Male Wistar rats (aged 60 d) were divided in two groups (n 22/each) according to their maternal diet during gestation and lactation: control (C, dams fed 17 % casein) and LP (dams fed 8 % casein). At weaning, half of the groups were fed HF diet and two more groups were formed (HF and low protein–high fat (LP-HF)). Somatic growth, food and energy intake, fat depots, serum glucose, cholesterol and leptin concentrations were evaluated. Phagocytic rate and NO production were analysed in peritoneal macrophages under stimulation of zymosan and lipopolysaccharide (LPS)+interferon γ (IFN-γ), respectively. The maternal LP diet altered the somatic parameters of growth and development of pups. LP and LP-HF pups showed a higher body weight gain and food intake than C pups. HF and LP-HF pups showed increased retroperitoneal and epididymal fat depots, serum level of TAG and total cholesterol compared with C and LP pups. After LPS+IFN-γ stimulation, LP and LP-HF pups showed reduced NO production when compared with their pairs. Increased phagocytic activity and NO production were seen in LP but not LP-HF peritoneal macrophages. However, peritoneal macrophages of LP pups were hyporesponsive to LPS+IFN-γ induced NO release, even after a post-weaning HF diet. Our data demonstrated that there was an immunomodulation related to dietary fatty acids after the maternal LP diet-induced metabolic programming.

The suppression of prolactin production with bromocriptine (BRO) in the last 3 d of lactation reduces milk yield (early weaning) and increases the transfer of leptin through the milk, causing hyperleptinaemia in pups. In adulthood, several changes occur in the offspring as a result of metabolic programming, including overweight, higher visceral fat mass, hypothyroidism, hyperglycaemia, insulin resistance, hyperleptinaemia and central leptin resistance. In the present study, we investigated whether overweight rats programmed by early weaning with maternal BRO treatment have hypothalamic alterations in adulthood. We analysed the expression of neuropeptide Y (NPY), cocaine- and amphetamine-regulated transcript (CART), pro-opiomelanocortin (POMC) and α-melanocyte-stimulating hormone (α-MSH) by immunohistochemistry in the following hypothalamic nuclei: medial and lateral arcuate nucleus (ARC); paraventricular nucleus (PVN); lateral hypothalamus (LH). Additionally, we sought to determine whether these programmed rats exhibited hypothalamic inflammation as indicated by astrogliosis. NPY immunostaining showed a denser NPY-positive fibre network in the ARC and PVN (+82 % in both nuclei) of BRO offspring. Regarding the anorexigenic neuropeptides, no difference was found for CART, POMC and α-MSH. The number of astrocytes was higher in all the nuclei of BRO rats. The fibre density of glial fibrillary acidic protein was also increased in both medial and lateral ARC (6·06-fold increase and 9·13-fold increase, respectively), PVN (5·75-fold increase) and LH (2·68-fold increase) of BRO rats. We suggest that early weaning has a long-term effect on the expression of NPY as a consequence of developmental plasticity, and the presence of astrogliosis indicates hypothalamic inflammation that is closely related to overweight and hyperleptinaemia observed in our model.

Stress experienced early in life exerts a powerful, lasting influence on development. Converging empirical findings show that stressful experiences become deeply embedded in the child’s neurobiology, with an astonishing range of long-term effects on cognition, emotion, and behavior. In contrast with the prevailing view that such effects are the maladaptive outcomes of ‘toxic’ stress, adaptive models regard them as manifestations of evolved developmental plasticity. In this paper, I offer a brief introduction to adaptive models of early stress and human behavioral development, with emphasis on recent theoretical contributions and emerging concepts in the field. I begin by contrasting dysregulation models of early stress with their adaptive counterparts; I then introduce life history theory as a unifying framework, and review recent work on predictive adaptive responses (PARs) in human life history development. In particular, I discuss the distinction between forecasting the future state of the environment (external prediction) and forecasting the future state of the organism (internal prediction). Next, I present the adaptive calibration model, an integrative model of individual differences in stress responsivity based on life history concepts. I conclude by examining how maternal–fetal conflict may shape the physiology of prenatal stress and its adaptive and maladaptive effects on postnatal development. In total, I aim to show how theoretical work from evolutionary biology is reshaping the way we think about the role of stress in human development, and provide researchers with an up-to-date conceptual map of this fascinating and rapidly evolving field.

Maternal undernutrition increases the risk of adult arterial hypertension. The present study investigated the short- and long-term effects of a maternal low-protein diet on respiratory rhythm, O2/CO2 chemosensitivity and arterial blood pressure (ABP) of the offspring. Male Wistar rats were divided into two groups according to their mothers' diets during gestation and lactation: control (NP, 17 % of casein) and low-protein (LP, 8 % of casein) groups. Direct measurements of ABP, respiratory frequency (RF), tidal volume (VT) and ventilation (VE), as well as hypercapnia (7 % CO2) and hypoxia (7 % O2) evoked respiratory responses were recorded from the awake male offspring at the 30th and 90th days of life. Blood samples were collected for the analyses of protein, creatinine and urea concentrations. The LP offspring had impaired body weight and length throughout the experiment. At 30 d of age, the LP rats showed a reduction in the concentrations of total serum protein (approximately 24 %). ABP in the LP rats was similar to that in the NP rats at 30 d of age, but it was 20 % higher at 90 d of age. With respect to ventilatory parameters, the LP rats showed enhanced RF (approximately 34 %) and VE (approximately 34 %) at 30 d of age, which was associated with increased ventilatory responses to hypercapnia (approximately 21 % in VE) and hypoxia (approximately 82 % in VE). At 90 d of age, the VE values and CO2/O2 chemosensitivity of the LP rats were restored to the control range, but the RF values remained elevated. The present data show that a perinatal LP diet alters respiratory rhythm and O2/CO2 chemosensitivity at early ages, which may be a predisposing factor for increased ABP at adulthood.

There is little record of birth weight of Irish Travellers, a minority group in Ireland. Travellers are known to have higher rate of adult chronic disease and to be exposed to life-long disadvantage. The aim of this study was to establish whether the birth weight and infant mortality rate patterns in Ireland's Travellers were consistent with the developmental plasticity hypothesis. A 1-year follow-up birth cohort study was conducted with linkage data from maternity hospital records of Traveller infants born on the island of Ireland over a 12-month period to self-identifying Traveller and general Irish population mothers from the Lifeways Cross-Generation Cohort Study. The main outcome measure was the rate of birth weight <3000 g in a cohort of Traveller children. There were 987 confirmed Traveller births, 500 of whose mothers consented to linkage to their records. A social gradient was observed in the distribution of birth weight in the general population and Traveller infants constituted the highest proportion of all social classes in the birth weight range of 3 kg or less (16.3%). There was a high rate of persistent smoking among Traveller mothers (53%). After adjustment for smoking and alcohol consumption in pregnancy, the birth weight differential persisted (OR 3.5, 95% CI 1.4–8.1). Infant mortality rate at 12.0/1000 births (95% CI 5.5–19.7) was almost four times that of the general population. This analysis confirms Travellers had a greater than expected incidence of low birth weight and high infant mortality with high rates of premature adult chronic diseases from all causes already demonstrated previously.

The effects of maternal moderate–low physical training on postnatal development, glucose homeostasis and leptin concentration in adult offspring subjected to a low-protein diet during the perinatal period were investigated. Male Wistar rats (aged 150 d old) were divided into four groups according to maternal group: untrained (NTp, n 8); trained (Tp, n 8); untrained with a low-protein diet (NT+LPp, n 8); trained with a low-protein diet (T+LPp, n 8). The trained mothers were subjected to a protocol of moderate physical training over a period of 4 weeks (treadmill, 5 d/week, 60 min/d, at 65 % VO2max) before mating. At pregnancy, the intensity and duration of exercise was progressively reduced (50–20 min/d, at 65–30 % VO2max). The low-protein diet groups received an 8 % casein diet, and their peers received a 17 % casein diet during gestation and lactation. The pups' birth weight and somatic growth were recorded weekly up to the 150th day. Fasting blood glucose, cholesterol, serum leptin concentration, glucose and insulin tolerance tests were evaluated. The Tp animals showed no changes in somatic and biochemical parameters, while the NT+LPp group showed a greater abdominal circumference, hyperglycaemia, hypercholesterolaemia, glucose intolerance and lower plasma leptin. In the T+LPp animals, all of those alterations were reversed except for plasma leptin concentration. In conclusion, the effects of a perinatal low-protein diet on growth and development, glucose homeostasis and serum leptin concentration in the offspring were attenuated in pups from trained mothers.

Developmental plasticity is the property of a given genotype to produce different phenotypes in response to the environmental conditions experienced during development. Chordates have two basic modes of development, direct and indirect. Direct development (mode of humans) was derived evolutionarily from indirect development (mode of many amphibians), the major difference being the presence of a larval stage with indirect development; larvae undergo metamorphosis to the juvenile adult. In amphibians, environmental conditions experienced during the larval stage can lead to extreme plasticity in behaviour, morphology and the timing of metamorphosis and can cause variation in adult phenotypic expression (carry-over effects, or developmental programming). Hormones of the neuroendocrine stress axis play pivotal roles in mediating environmental effects on animal development. Stress hormones, produced in response to a deteriorating larval habitat, accelerate amphibian metamorphosis; in mammals, stress hormones hasten the onset of parturition and play an important role in pre-term birth caused by intra-uterine stress. While stress hormones can promote survival in a deteriorating larval or intra-uterine habitat, costs may be incurred, such as reduced growth and size at metamorphosis or birth. Furthermore, exposure to elevated stress hormones during the tadpole or foetal stage can cause permanent neurological changes, leading to altered physiology and behaviour later in life. The actions of stress hormones in animal development are evolutionarily conserved, and therefore amphibians can serve as important model organisms for research on the mechanisms of developmental plasticity.

We investigated chromatic processing in the outer retina of the cichlid fish Aequidens pulcher. Intracellular recordings from cone-specific horizontal cells (CHCs) revealed that the two morphologically identified types (H1 and H2) also have different spectral responses. H1-L cells hyperpolarize to all wavelengths (“luminosity”). H2-Cb cells depolarize to long wavelengths and hyperpolarize to short wavelengths (“chromaticity”, biphasic). Furthermore, we verified by immunocytochemistry that H2-Cb cells of A. pulcher predominantly contact the middle-wavelength-sensitive (MWS) members of double cones. Developmental plasticity in the cone–CHC networks was induced by rearing fish under conditions of spectral deprivation and different levels of white light. H1-L spectral responses were unaffected by the rearing conditions. Different intensity levels of white light and deprivation of long wavelengths during rearing both induced changes in the spectral responses of H2-Cb. Deprivation of short and middle wavelengths had no effect. Our results indicate that spectral processing in the outer retina of fishes can be modulated in response to different visual experiences and suggest that developmental fine tuning of the color-vision system occurs at early levels of visual processing.