The causes of obesity are complex and multifactorial. We propose that one unconsidered but likely important factor is the energetic demand of brain development, which could constrain energy available ...for body growth and other functions, including fat deposition. Humans are leanest during early childhood and regain body fat in later childhood. Children reaching this adiposity rebound (AR) early are at risk for adult obesity. In aggregate data, the developing brain consumes a lifetime peak of 66% of resting energy expenditure in the years preceding the AR, and brain energy use is inversely related to body weight gain from infancy until puberty. Building on this finding, we hypothesize that individual variation in childhood brain energy expenditure will help explain variation in the timing of the AR and subsequent obesity risk. The idea that brain energetics constrain fat deposition is consistent with evidence that genes that elevate BMI are expressed in the brain and mediate a trade-off between the size of brain structures and BMI. Variability in energy expended on brain development and function could also help explain widely documented inverse relationships between the BMI and cognitive abilities. We estimate that variability in brain energetics could explain the weight differential separating children at the 50th and 70th BMI-for-age centiles immediately before the AR. Our model proposes a role for brain energetics as a driver of variation within a population’s BMI distribution and suggests that educational interventions that boost global brain energy use during childhood could help reduce the burden of obesity.
In species in which males care for young, testosterone (T) is often high during mating periods but then declines to allow for caregiving of resulting offspring. This model may apply to human males, ...but past human studies of T and fatherhood have been cross-sectional, making it unclear whether fatherhood suppresses T or if men with lower T are more likely to become fathers. Here, we use a large representative study in the Philippines (n = 624) to show that among single nonfathers at baseline (2005) (21.5 ± 0.3 y), men with high waking T were more likely to become partnered fathers by the time of follow-up 4.5 y later (P < 0.05). Men who became partnered fathers then experienced large declines in waking (median: –26%) and evening (median: –34%) T, which were significantly greater than declines in single nonfathers (P < 0.001). Consistent with the hypothesis that child interaction suppresses T, fathers reporting 3 h or more of daily childcare had lower T at follow-up compared with fathers not involved in care (P < 0.05). Using longitudinal data, these findings show that T and reproductive strategy have bidirectional relationships in human males, with high T predicting subsequent mating success but then declining rapidly after men become fathers. Our findings suggest that T mediates tradeoffs between mating and parenting in humans, as seen in other species in which fathers care for young. They also highlight one likely explanation for previously observed health disparities between partnered fathers and single men.
Early life experiences have a significant influence on adult health and aging processes in humans. Despite widespread interest in the evolutionary roots of this phenomenon, very little research on ...this topic has been conducted in humans’ closest living relatives, the great apes. The longitudinal data sets that are now available on wild and captive great ape populations hold great promise to clarify the nature, evolutionary function, and mechanisms underlying these connections in species which share key human life history characteristics. Here, we explain features of great ape life history and socioecologies that make them of particular interest for this topic, as well as those that may limit their utility as comparative models; outline the ways in which available data are complementary to and extend the kinds of data that are available for humans; and review what is currently known about the connections among early life experiences, social behavior, and adult physiology and biological fitness in our closest living relatives. We conclude by highlighting key next steps for this emerging area of research.
Significance The metabolic costs of brain development are thought to explain the evolution of humans’ exceptionally slow and protracted childhood growth; however, the costs of the human brain during ...development are unknown. We used existing PET and MRI data to calculate brain glucose use from birth to adulthood. We find that the brain’s metabolic requirements peak in childhood, when it uses glucose at a rate equivalent to 66% of the body’s resting metabolism and 43% of the body’s daily energy requirement, and that brain glucose demand relates inversely to body growth from infancy to puberty. Our findings support the hypothesis that the unusually high costs of human brain development require a compensatory slowing of childhood body growth.
Human health tends to mirror gradients in social standing related to class, ethnicity and race. Past research in the social sciences suggests that environmental experiences related to social status ...contribute to these disparities, but the underlying biological mechanisms are only partially understood. Here, we review research related to three domains of environmental exposure that point to epigenetic contributions to health disparities: nutrition, psychosocial stress, and environmental toxicant exposure. Each exposure has effects that may persist across the life course and in some instances may be transmitted to offspring via epigenetic inheritance. Since epigenetic markings provide a "memory" of past experiences, minimizing future disparities in health will be partially contingent upon our ability to address inequality in the current environment. We suggest that future research in environmental epigenetics focus on establishing the reversibility of stress-induced epigenetic modifications, and also on identifying positive epigenetic effects of environmental enrichment.
Telomeres are repeating DNA sequences at the ends of chromosomes that protect and buffer genes from nucleotide loss as cells divide. Telomere length (TL) shortens with age in most proliferating ...tissues, limiting cell division and thereby contributing to senescence. However, TL increases with age in sperm, and, correspondingly, offspring of older fathers inherit longer telomeres. Using data and samples from a longitudinal study from the Philippines, we first replicate the finding that paternal age at birth is associated with longer TL in offspring (n = 2,023, P = 1.84 × 10 ⁻⁶). We then show that this association of paternal age with offspring TL is cumulative across multiple generations: in this sample, grandchildren of older paternal grandfathers at the birth of fathers have longer telomeres (n = 234, P = 0.038), independent of, and additive to, the association of their father’s age at birth with TL. The lengthening of telomeres predicted by each year that the father’s or grandfather’s reproduction are delayed is equal to the yearly shortening of TL seen in middle-age to elderly women in this sample, pointing to potentially important impacts on health and the pace of senescent decline in tissues and systems that are cell-replication dependent. This finding suggests a mechanism by which humans could extend late-life function as average age at reproduction is delayed within a lineage.
The human gut microbiome and health inequities Amato, Katherine R; Arrieta, Marie-Claire; Azad, Meghan B ...
Proceedings of the National Academy of Sciences - PNAS,
06/2021, Letnik:
118, Številka:
25
Journal Article
Recenzirano
Odprti dostop
Individuals who are minoritized as a result of race, sexual identity, gender, or socioeconomic status experience a higher prevalence of many diseases. Understanding the biological processes that ...cause and maintain these socially driven health inequities is essential for addressing them. The gut microbiome is strongly shaped by host environments and affects host metabolic, immune, and neuroendocrine functions, making it an important pathway by which differences in experiences caused by social, political, and economic forces could contribute to health inequities. Nevertheless, few studies have directly integrated the gut microbiome into investigations of health inequities. Here, we argue that accounting for host-gut microbe interactions will improve understanding and management of health inequities, and that health policy must begin to consider the microbiome as an important pathway linking environments to population health.
Prolonged myelination in human neocortical evolution Miller, Daniel J; Duka, Tetyana; Stimpson, Cheryl D ...
Proceedings of the National Academy of Sciences - PNAS,
10/2012, Letnik:
109, Številka:
41
Journal Article
Recenzirano
Odprti dostop
Nerve myelination facilitates saltatory action potential conduction and exhibits spatiotemporal variation during development associated with the acquisition of behavioral and cognitive maturity. ...Although human cognitive development is unique, it is not known whether the ontogenetic progression of myelination in the human neocortex is evolutionarily exceptional. In this study, we quantified myelinated axon fiber length density and the expression of myelin-related proteins throughout postnatal life in the somatosensory (areas 3b/3a/1/2), motor (area 4), frontopolar (prefrontal area 10), and visual (areas 17/18) neocortex of chimpanzees (N = 20) and humans (N = 33). Our examination revealed that neocortical myelination is developmentally protracted in humans compared with chimpanzees. In chimpanzees, the density of myelinated axons increased steadily until adult-like levels were achieved at approximately the time of sexual maturity. In contrast, humans displayed slower myelination during childhood, characterized by a delayed period of maturation that extended beyond late adolescence. This comparative research contributes evidence crucial to understanding the evolution of human cognition and behavior, which arises from the unfolding of nervous system development within the context of an enriched cultural environment. Perturbations of normal developmental processes and the decreased expression of myelin-related molecules have been related to psychiatric disorders such as schizophrenia. Thus, these species differences suggest that the human-specific shift in the timing of cortical maturation during adolescence may have implications for vulnerability to certain psychiatric disorders.
Despite growing research emphasis on understanding the health effects of ethnic discrimination, little work has focused on how such exposures may influence a woman's biology and health during ...pregnancy. Understanding such effects is important given evidence that maternal stress experience in pregnancy can have long term effects on offspring health. Here we present data evaluating the relationship between perceived discrimination, self-rated health, and the stress hormone cortisol measured in late pregnancy among a diverse sample of women living in Auckland, New Zealand (N = 55). We also evaluated possible intergenerational impacts of maternal discrimination on stress reactivity in a subset of offspring (N = 19). Pregnant women were recruited from two antenatal care clinics in Auckland. Women were met in their homes between 34 and 36 weeks gestation, during which time a prenatal stress questionnaire was administered and saliva samples (morning and evening from two days) were obtained. Offspring cortisol reactivity was assessed at the standard six week postnatal vaccination visit. We found that 34% of women reported having experienced ethnic discrimination, with minority and immigrant women being more likely to report being angry or upset in response to discrimination experience compared with NZ-born women of European descent. Women reporting discrimination experience had worse self-rated health, higher evening cortisol and gave birth to infants with higher cortisol reactivity, all independent of ethnicity and material deprivation. These findings suggest that discrimination experience can have biological impacts in pregnancy and across generations, potentially contributing to the ethnic gradient in health.
•Ethnic discrimination associated with higher evening cortisol in late pregnancy.•Ethic discrimination associated with poorer self-rated health in late pregnancy.•Ethnic discrimination associated with cortisol reactivity in offspring.•Maternal discrimination experience affects maternal and offspring biology.
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