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Malnutrition among women of reproductive age is a significant public health concern in low- and middle-income countries. Of particular concern are undernutrition from underweight and iron deficiency, along with overweight and obesity, all of which have negative health consequences for mothers and children. Accumulating evidence suggests that risk for poor nutritional outcomes may be mitigated by social support, yet how social support is measured varies tremendously and its effects likely vary by age, kinship and reproductive status. We examine the effects of different measures of social support on weight and iron nutrition among 677 randomly sampled women from rural Bangladesh. While we find that total support network size mitigates risk for underweight, other results point to a potential tradeoff in the effects of kin proximity, with nearby adult children associated with both lower risk for underweight and obesity and higher risk for iron deficiency and anaemia. Social support from kin may then enhance energy balance but not diet quality. Results also suggest that a woman's network of caregivers might reflect their greater need for help, as those who received more help with childcare and housework had worse iron nutrition. IKE Ferroptosis modulator Overall, although some findings support the hypothesis that social support can be protective, others emphasize that social relationships often have neutral or negative effects, illustrating the kinds of tradeoffs expected from an evolutionary perspective. The complexities of these effects deserve attention in future work, particularly within public health, where what is defined as 'social support' is often assumed to be positive. This article is part of the theme issue 'Multidisciplinary perspectives on social support and maternal-child health'.Non-maternal carers (allomothers) are hypothesized to lighten the mother's workload, allowing for the specialized human life history including relatively short interbirth intervals and multiple dependent offspring. Here, using in-depth observational data on childcare provided to 78 Agta children (a foraging population in the northern Philippines; aged 0-6 years), we explore whether allomaternal childcare substitutes and decreases maternal childcare. We found that allomother caregiving was associated with reduced maternal childcare, but the substitutive effect varied depending on the source and type of care. Children-only playgroups consistently predicted a decrease in maternal childcare. While grandmothers were rarely available, their presence was negatively associated with maternal presence and childcare, and grandmothers performed similar childcare activities to mothers. These results underscore the importance of allomothering in reducing maternal childcare in the Agta. Our findings suggest that flexibility in childcare sources, including children-only playgroups, may have been the key to human life-history evolution. Overall, our results reinforce the necessity of a broad conceptualization of social support in human childcare. This article is part of the theme issue 'Multidisciplinary perspectives on social support and maternal-child health'.In humans, support from partners and alloparents is crucial for successful child-rearing and optimal child development. However, the complex relationships among childcare support, children's outcomes and parental characteristics have not been fully examined. We investigate how three sources of partner and alloparental support-partner's childcare participation, support from children's grandparents and support from non-kin-can be associated with child social development. We hypothesize that the associations between childcare support from partners/alloparents and child social development are partly mediated by parental psychological condition and parenting style. To test this, we conducted path analyses on online survey data collected in 2016 from parents of 3- to 5-year-old children in Japan. We found no evidence that childcare support had direct positive effects on child social development. Rather, the benefit of childcare support was mediated by its effects on parental psychological condition and parenting style, which in turn improved children's outcomes. At the same time, we found some evidence that greater availability of childcare support was directly associated with more behavioural difficulties in children. Our findings reveal the complex pathways between childcare support, parental characteristics and children's outcomes in Japan, showing potential mechanisms behind parental and alloparental effects in industrialized populations. This article is part of the theme issue 'Multidisciplinary perspectives on social support and maternal-child health'.
Genome-wide association studies have identified a significant risk gene,
, for schizophrenia. In this study, we comprehensively investigated a large set of
single-nucleotide polymorphisms (SNPs) to identify the replicable risk alleles for schizophrenia and explore their biological functions.
One Jewish (1044 cases vs 2052 controls), one European (1350 cases vs 1378 controls) and one exploratory African American samples (98 cases vs 20 controls) were analyzed to identify replicable single-nucleotide polymorphism-schizophrenia associations. The regulatory effects of risk alleles on
messenger RNA expression were examined. The most robust risk tagSNP (rs1006737) was meta-analyzed on 17 studies (74,122 cases vs 109,062 controls), and associated with the gray matter volumes of seven subcortical structures in 38,258 Europeans, and the surface areas and thickness of 34 cortical regions in 33,992 Europeans and 2944 non-Europeans.
Forty-seven replicable risk single-nucleotide polymorphisms, including a 20of transverse temporal and superior temporal sulcus cortexes (0.005 ⩽
⩽ 0.043).
We identified an independent, replicable, functional, and significant risk variant block at
for schizophrenia, which could be tagged by the most robust risk marker rs1006737, suggesting an important role of
in the pathogenesis of schizophrenia.
We identified an independent, replicable, functional, and significant risk variant block at CACNA1C for schizophrenia, which could be tagged by the most robust risk marker rs1006737, suggesting an important role of CACNA1C in the pathogenesis of schizophrenia.
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