“Poor brain development” in the global South? Challenging the science of early childhood interventions

Global Early Childhood Development (ECD)—an applied field with the aim to improve the “brain structure and function” of future generations in the global South—has moved to the center of international development. Global ECD rests heavily on evidence claims about widespread cognitive, social, and emotional deficits in the global South and the benefits of changing parenting practices in order to optimize early childhood development. We challenge these claims on the grounds that the leading ECD literature excludes research from anthropology, cultural psychology, and related fields that could provide crucial insights about childrearing and children's development in the targeted communities. We encourage anthropologists and other scholars with ethnographic expertise on childhood to critically engage with global ECD. To facilitate such an endeavor, this article sketches the history, scientific claims, and interventions of global ECD, points out the critical potential of ethnographic research, and suggests strategies to make ethnography more relevant

“Poor brain development” in the global South? Challenging the science of early childhood interventions

Global Early Childhood Development (ECD)—an applied field with the aim to improve the “brain structure and function” of future generations in the global South—has moved to the center of international development. Global ECD rests heavily on evidence claims about widespread cognitive, social, and emotional deficits in the global South and the benefits of changing parenting practices in order to optimize early childhood development. We challenge these claims on the grounds that the leading ECD literature excludes research from anthropology, cultural psychology, and related fields that could provide crucial insights about childrearing and children's development in the targeted communities. We encourage anthropologists and other scholars with ethnographic expertise on childhood to critically engage with global ECD. To facilitate such an endeavor, this article sketches the history, scientific claims, and interventions of global ECD, points out the critical potential of ethnographic research, and suggests strategies to make ethnography more relevant

Different is not deficient: respecting diversity in early childhood development

CORRESPONDENCE to: Black, M. M., & Richter, L. M. (2022). "Different is not deficient: respecting diversity in early childhood development." The Lancet Child & Adolescent Health, 6(12), e26. ; https://doi.org/10.1016/S2352-4642(22)00276-0An estimated 250 million children under 5 years in low-income and middle-income countries (LMICs) are considered to be at risk of not achieving their full developmental potential because of inadequate care. 1 This assessment was crucial for establishing the Nurturing Care Framework, a roadmap for improving early childhood development globally. Although the number is still based on proxy measures (stunting and poverty rates), newer research draws directly on indicators of nurturing care, provided by UNICEF's Multiple Indicator Cluster Surveys. On the basis of these data, in The Lancet Child & Adolescent Health Dana McCoy and colleagues 2 claimed that the problem is even bigger: they calculated that 74·6% of children in LMICs aged 3–4 years do not even receive minimally adequate nurturing care. This figure increases to 92·1% for sub-Saharan Africa and to 99·5% in Chad.

Respecting diversity in early childhood development – A response to Seiden et al. and Black and Richter

A RESPONSE to: Seiden, J., Pisani, L., Cuartas, J., Waldman, M., & McCoy, D. C. (2022). "Different is not deficient: respecting diversity in early childhood development–Authors' reply." The Lancet Child & Adolescent Health, 6(12), e27 ; https://doi.org/10.1016/S2352-4642(22)00307-8This contribution is a continuation of a debate in The Lancet Child & Adolescent Health about the scientific and ethical challenges associated with globalizing early childhood interventions. It consists of an original article, a critical response, and two replies

Feeding, Bonding, and the Formation of Social Relationships. Ethnographic Challenges to Attachment Theory and Early Childhood Interventions

This Element explores multi-faceted linkages between feeding and relationship formation based on ethnographic case studies in Morocco, Madagascar, Sri Lanka, Taiwan, and Costa Rica. Research demonstrates that there are many culturally valued ways of feeding children, contradicting the idea of a single universally optimal feeding standard. It demonstrates further that in many parts of the world, feeding plays a central role in bonding and relationship formation, something largely overlooked in current developmental theories. Analysis shows that feeding contributes to relationship formation through what we call proximal, transactional, and distal dimensions. This Element argues that feeding practices can lead to qualitatively distinct forms of relationships. It has important theoretical and practical implications, calling for the expansion of attachment theory to include feeding and body-centered caregiving and significant changes to global interventions currently based on 'responsive feeding.' This title is also available as Open Access on Cambridge Core

Function of the central domain of streptokinase in substrate plasminogen docking and processing revealed by site-directed mutagenesis

The possible role of the central β -domain (residues 151-287) of streptokinase (SK) was probed by site-specifically altering two charged residues at a time to alanines in a region (residues 230-290) previously identified by Peptide Walking to play a key role in plasminogen (PG) activation. These mutants were then screened for altered ability to activate equimolar "partner" human PG, or altered interaction with substrate PG resulting in an overall compromised capability for substrate PG processing. Of the eight initial alanine-linker mutants of SK, one mutant, viz. SKKK256, 257aa (SK-D1), showed a roughly 20-fold reduction in PG activator activity in comparison to wild-type SK expressed in Escherichia coli (nSK). Five other mutants were as active as nSK, with two [SKRE248.249AA and SKEK281.282AA, referred to as SK(C) and SK(H), respectively] showing specific activities approximately one-half and two-thirds, respectively, that of nSK. Unlike SK(C) and SK(H), however, SK(D1) showed an extended initial delay in the kinetics of PG activation. These features were drastically accentuated when the charges on the two Lys residues at positions 256 and 257 of nSK were reversed, to obtain SKKK256.257EE [SK(D2)]. This mutant showed a PG activator activity approximately 10-fold less than that of SK(D1). Remarkably, inclusion of small amounts of human plasmin (PN) in the PG activation reactions of SK(D2) resulted in a dramatic, PN dose-dependent rejuvenation of its PG activation capability, indicating that it required pre-existing PN to form a functional activator since it could not effect active site exposure in partner PG on its own, a conclusion further confirmed by its inability to show a "burst" of p-nitrophenol release in the presence of equimolar human PG and p-nitrophenyl guanidino benzoate. The steady-state kinetic parameters for HPG activation of its 1:1 complex with human PN revealed that although it could form a highly functional activator once "supplied" with a mature active site, the Km for PG was increased nearly eightfold in comparison to that of nSK-PN. SK mutants carrying simultaneous two- and three-site charge-cluster alterations, viz., SKRE248.249AA;EK281.282AA [SK(CH)], SKEK272.273AA;EK281.282AA [SK(FH)], and SKRE248.249AA;EK272.273AA;EK281.282AA [SK(CFH)], showed additive/synergistic influence of multiple charge-cluster mutations on HPG activation when compared to the respective "single-site" mutants, with the "triple-site" mutant [SK(CFH)] showing absolutely no detectable HPG activation ability. Nevertheless, like the other constructs, the double- and triple-charge cluster mutants retained a native like affinity for complexation with partner PG. Their overall structure also, as judged by far-ultraviolet circular dichroism, was closely similar to that of nSK. These results provide the first experimental evidence for a direct assistance by the SK β-domain in the docking and processing of substrate PG by the activator complex, a facet not readily evident probably because of the flexibility of this domain in the recent X-ray crystal structure of the SK-plasmin light chain complex

Correction to: Age Patterns in Risk Taking Across the World

n/