Salivary cortisol and cognitive development in infants from low-income communities

Early stress exposure is proposed to have significant lasting effects on cognitive development. The glucocorticoid hormone cortisol, a product of the hypothalamic-pituitary-adrenal (HPA) axis, is a particular focus of research, however, the majority of past research has been based on studies of older children and adults. Evidence linking cortisol levels in infancy with cognitive development is lacking. In a large cohort sample of infants (N = 1,091) oversampled for psychosocial risk, we tested whether basal cortisol levels and cortisol reactivity to emotional stressors administered at 7 and 15 months of age were associated with cognitive development measured at 15 months. Cognitive development was measured using the Mental Development Index of the Bayley Scales of Infant Development. Multiple regression analyses indicated that basal cortisol levels at 15 months, and to a lesser extent at 7 months, were inversely associated with infant cognitive development after adjusting for psychosocial and obstetric risk. The findings provide some of the first evidence that HPA axis activity in infancy is associated with early cognitive development

Toward a neuroscience of interactive parent–infant dyad empathy

In accord with social neuroscience's progression to include interactive experimental paradigms, parents' brains have been activated by emotionally charged infant stimuli - especially of their own infant - including baby cry and picture. More recent research includes the use of brief video clips and opportunities for maternal response. Among brain systems important to parenting are those involved in empathy. This research may inform recent studies of decreased societal empathy, offer mechanisms and solutions

Psychobiological influences on maternal sensitivity in the context of adversity.

This study evaluated prospective longitudinal relations among an index of poverty-related cumulative risk, maternal salivary cortisol, child negative affect, and maternal sensitivity across the first two postpartum years. Participants included 1,180 biological mothers residing in rural and predominantly low-income communities in the US. Multilevel growth curve analyses indicated that an index of cumulative risk was positively associated with maternal cortisol across the postpartum (study visits occurring at approximately 7, 15, and 24 months postpartum) over and above effects for African American ethnicity, time of day of saliva collection, age, parity status, having given birth to another child, contraceptive use, tobacco smoking, body mass index, and breastfeeding. Consistent with a psychobiological theory of mothering, maternal salivary cortisol was negatively associated with maternal sensitivity observed during parent-child interactions across the first two postpartum years over and above effects for poverty-related cumulative risk, child negative affect, as well as a large number of covariates associated with cortisol and maternal sensitivity. Child negative affect expressed during parent-child interactions was negatively associated with observed maternal sensitivity at late (24 months) but not early time points of observation (7 months) and cumulative risk was negatively associated with maternal sensitivity across the postpartum and this effect strengthened over time. Results advance our understanding of the dynamic, transactional, and psychobiological influences on parental caregiving behaviors across the first two postpartum years

Parenting and Beyond: Common Neurocircuits Underlying Parental and Altruistic Caregiving

Interpersonal relationships constitute the foundation on which human society is based. The infant–caregiver bond is the earliest and most influential of these relationships. Driven by evolutionary pressure for survival, parents feel compelled to provide care to their biological offspring. However, compassion for non-kin is also ubiquitous in human societies, motivating individuals to suppress their own self-interests to promote the well-being of non-kin members of the society. We argue that the process of early kinship-selective parental care provides the foundation for non-exclusive altruism via the activation of a general Caregiving System that regulates compassion in any of its forms. We propose a tripartite structure of this system that includes (1) the perception of need in another, (2) a caring motivational or feeling state, and (3) the delivery of a helping response to the individual in need. Findings from human and animal research point to specific neurobiological mechanisms including activation of the insula and the secretion of oxytocin that support the adaptive functioning of this Caregiving System

Framework, principles and recommendations for utilising participatory methodologies in the co-creation and evaluation of public health interventions

Background: Due to the chronic disease burden on society, there is a need for preventive public health interventions to stimulate society towards a healthier lifestyle. To deal with the complex variability between individual lifestyles and settings, collaborating with end-users to develop interventions tailored to their unique circumstances has been suggested as a potential way to improve effectiveness and adherence. Co-creation of public health interventions using participatory methodologies has shown promise but lacks a framework to make this process systematic. The aim of this paper was to identify and set key principles and recommendations for systematically applying participatory methodologies to co-create and evaluate public health interventions. Methods: These principles and recommendations were derived using an iterative reflection process, combining key learning from published literature in addition to critical reflection on three case studies conducted by research groups in three European institutions, all of whom have expertise in co-creating public health interventions using different participatory methodologies. Results: Key principles and recommendations for using participatory methodologies in public health intervention co-creation are presented for the stages of: Planning (framing the aim of the study and identifying the appropriate sampling strategy); Conducting (defining the procedure, in addition to manifesting ownership); Evaluating (the process and the effectiveness) and Reporting (providing guidelines to report the findings). Three scaling models are proposed to demonstrate how to scale locally developed interventions to a population level. Conclusions: These recommendations aim to facilitate public health intervention co-creation and evaluation utilising participatory methodologies by ensuring the process is systematic and reproducible

Exenatide Sensitizes Insulin-Mediated Whole-Body Glucose Disposal and Promotes Uptake of Exogenous Glucose by the Liver

OBJECTIVE— Recent progress suggests that exenatide, a mimetic of glucagon-like peptide-1 (GLP-1), might lower glycemia independent of increased β-cell response or reduced gastrointestinal motility. We aimed to investigate whether exenatide stimulates glucose turnover directly in insulin-responsive tissues dependent or independent of insulinemia

The need for a complex systems model of evidence for public health

Despite major investment in both research and policy, many pressing contemporary public health challenges remain. To date, the evidence underpinning responses to these challenges has largely been generated by tools and methods that were developed to answer questions about the effectiveness of clinical interventions, and as such are grounded in linear models of cause and effect. Identification, implementation, and evaluation of effective responses to major public health challenges require a wider set of approaches1,2 and a focus on complex systems.This work was funded by a grant from The Health Foundation (London, UK) that supported HR, KG, and NS. HR was also supported by the UK National Institute for Health Research (NIHR) Collaboration for Leadership in Applied Health Research and Care (CLAHRC) North Thames at Bart's Health NHS Trust. LM is supported by the UK Medical Research Council ( MC_UU_12017/14 ) and the Chief Scientist Office ( SPHSU14 ). MW is funded in part by the UK NIHR as Director of its Public Health Research Programme

Ectopic Expression of E2F1 Stimulates β-Cell Proliferation and Function

OBJECTIVE-Generating functional beta-cells by inducing their proliferation may provide new perspectives for cell therapy in diabetes. Transcription factor E2F1 controls G(1)- to S-phase transition during the cycling of many cell types and is required for pancreatic beta-cell growth and function. However, the consequences of overexpression of E2F1 in beta-cells are unknown. RESEARCH DESIGN AND METHODS-The effects of E2F1 overexpression on beta-cell proliferation and function were analyzed in isolated rat beta-cells and in transgenic mice. RESULTS-Adenovirus AdE2F1-mediated overexpression of E2F1 increased the proliferation of isolated primary rat beta-cells 20-fold but also enhanced beta-cell death. Coinfection with adenovirus Ad Akt expressing a constitutively active form of Akt (protein kinase B) suppressed beta-cell death to control levels. At 48 h after infection, the total beta-cell number and insulin content were, respectively, 46 and 79% higher in AdE2F1+AdAkt-infected cultures compared with untreated. Conditional overexpression of E2F1 in mice resulted in a twofold increase of beta-cell proliferation and a 70% increase of pancreatic insulin content, but did not increase beta-cell mass. Glucose-challenged insulin release was increased, and the mice showed protection against toxin-induced diabetes. CONCLUSIONS-Overexpression of E2F1, either in vitro or in vivo, can stimulate beta-cell proliferation activity. In vivo E2F1 expression significantly increases the insulin content and function of adult beta-cells, making it a strategic target for therapeutic manipulation of beta-cell function. Diabetes 59:1435-1444, 201

Endurance Exercise as a Countermeasure for Aging

OBJECTIVE— We determined whether reduced insulin sensitivity, mitochondrial dysfunction, and other age-related dysfunctions are inevitable consequences of aging or secondary to physical inactivity