Adequacy of Maternal Iron Status Protects against Behavioral, Neuroanatomical, and Growth Deficits in Fetal Alcohol Spectrum Disorders

Fetal alcohol spectrum disorders (FASD) are the leading non-genetic cause of neurodevelopmental disability in children. Although alcohol is clearly teratogenic, environmental factors such as gravidity and socioeconomic status significantly modify individual FASD risk despite equivalent alcohol intake. An explanation for this variability could inform FASD prevention. Here we show that the most common nutritional deficiency of pregnancy, iron deficiency without anemia (ID), is a potent and synergistic modifier of FASD risk. Using an established rat model of third trimester-equivalent binge drinking, we show that ID significantly interacts with alcohol to impair postnatal somatic growth, associative learning, and white matter formation, as compared with either insult separately. For the associative learning and myelination deficits, the ID-alcohol interaction was synergistic and the deficits persisted even after the offsprings’ iron status had normalized. Importantly, the observed deficits in the ID-alcohol animals comprise key diagnostic criteria of FASD. Other neurobehaviors were normal, showing the ID-alcohol interaction was selective and did not reflect a generalized malnutrition. Importantly ID worsened FASD outcome even though the mothers lacked overt anemia; thus diagnostics that emphasize hematological markers will not identify pregnancies at-risk. This is the first direct demonstration that, as suggested by clinical studies, maternal iron status has a unique influence upon FASD outcome. While alcohol is unquestionably teratogenic, this ID-alcohol interaction likely represents a significant portion of FASD diagnoses because ID is more common in alcohol-abusing pregnancies than generally appreciated. Iron status may also underlie the associations between FASD and parity or socioeconomic status. We propose that increased attention to normalizing maternal iron status will substantially improve FASD outcome, even if maternal alcohol abuse continues. These findings offer novel insights into how alcohol damages the developing brain

Firearm Safety, Gun Violence and Chicago Families: Voices of Child Health in Chicago Report

Chicago has seen continuing firearm violence, with over 2,000 shooting victims so far in 2021. The epidemic of firearm violence impacts children across the state, as it remains the number one cause of death in children and youth across Illinois. In some of our previous reports, Chicago parents identified gun violence as their top social concern for kids in the city, and in recent years, they reported it was the main social problem getting worse the fastest for Chicago youth. In this month's Voices of Child Health in Chicago Report, we focus on the importance of firearm safety and parents' concerns about gun violence in the city. We asked 1,505 Chicago parents from all 77 community areas in the city about their experiences with firearm safety as well as other gun violence prevention and concern-related questions.

Adverse childhood experiences, child behavioral health needs, and family characteristics associated with the presence of a firearm in the home: a survey of parents in Chicago

Abstract Background Firearm violence is the leading cause of pediatric mortality in the USA. The presence of a firearm in the home poses an immense risk to children with increased rates of suicide and unintentional injury by firearm. Recent literature has not explored child ACEs and child behavioral health needs with the presence of a firearm in the home. The objective of this study was to explore an association between these factors, parent health, family experience with firearm violence, and demographics, and the presence of a firearm in the home. Results Overall, 382 of 1,436 (weighted to 22.0%) responding parents reported the presence of a firearm in the home. In an adjusted model, the odds ratio of firearm presence increased incrementally with a child’s increasing exposure to ACEs. Compared to a child in the household exposed to no ACEs, a child in the household exposed to two or more ACEs was associated with a 5.16 times higher odds of firearm presence in the home (95% confidence interval (CI) 2.92–9.10). Similarly, a child in the household who had used behavioral health services was associated with a 2.10 times higher odds of firearm presence in the home (95% CI 1.35–3.26), compared to a child in the household who had not. Presence of firearm in the home was also associated with higher household income, younger parent age (under 35 years), and male parent gender. Conclusions Chicago parents have higher odds of reporting the presence of a firearm in the home when living in a household with a child exposed to ACEs and with behavioral health needs. These findings could inform future public health interventions and targeted safe storage messaging to prevent pediatric firearm injury in the home

Rat dams fed an ID diet have moderate ID without anemia.

<p>Hematocrit (<b>A</b>), hemoglobin (<b>B</b>), red-cell distribution width (<b>C</b>), and liver iron (<b>D</b>) in rat dams on P5 and/or P22 fed IS or ID diets. Dashed lines indicate the normal reference range for non-pregnant adult rats <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0047499#pone.0047499-Car1" target="_blank">[19]</a>. N = 6–8 rats per group at each time point. <b>*</b>, significantly different from IS rats at the same time point as determined by linear mixed modeling.</p

Maternal ID increases alcohol-induced cerebellar apoptosis at P10.

<p>(<b>A</b>) There were no significant main effects of Iron status or Alcohol dose on proliferation, quantified using phosphorylated histone-H3 immunoreactivity. (<b>B</b>) Apoptosis, assessed using cleaved-caspase-3 immunoreactivity, was decreased in the P10 cerebellum. Both ID (<i>P</i> = 004) and alcohol (<i>P</i> = 0.001) increased apoptosis and their effects were additive. N≥5 rats per treatment group. <b>*</b>, significantly different from IS pups within the same alcohol dose; <b>†</b>, significantly different from 0 g/kg alcohol within the same Iron status.</p

ID-alcohol exposure impairs myelination.

<p><b>A–L,</b> Immunostain for myelin basic protein (MBP) of P35 cerebellum following the indicated treatments. <b>B, E, H, K</b> are the corresponding enlargements of Lobule I, and <b>C, F, I, L</b> are enlargements of Lobule VIa. There were fewer myelin tracts within the granule cell layer (arrows) in ID-alcohol cerebellum (<b>K, L</b> ) compared with controls (<b>B, C</b>) or alcohol-only (<b>H, I</b> ) or ID (<b>E, F</b>), and confirmed by quantifying the MBP⁺ area within the granule cell layer for lobule I (<b>M</b>) and lobule VIa (<b>N</b>). N = 6–8 rats per group. <b>*</b> Significantly different from IS pups at same alcohol dose, <b>†</b> significantly different from 0 g/kg alcohol within same iron status.</p

Maternal ID modulates cued and contextual fear conditioning in alcohol-exposed pups.

<p>Percent freezing to cue (<b>A</b>) and context (<b>B</b>) in male and female pups. N = 7–11 rats per treatment group per sex. There was a main effect of Alcohol within ID males on cued (F_(2,16) =6.1, <i>P</i> = 0.011) and within ID males (F_(2,6) =7.4, <i>P</i> = 0.024) and females (F_(2,14) =6.9, <i>P</i> = 0.008) on contextual fear conditioning. <b>†</b>, significantly different from 0 g/kg alcohol within the same Iron status.</p

Maternal ID and alcohol interact to adversely affect somatic growth in males but not females.

<p>Body weight on P1–10 in male (A, C, E) and female (B, D, F) pups treated with 0 (A, B), 3.5 (C, D), or 5 g/kg alcohol (E, F). N≥22 rats per treatment group per sex. ID-only reduced growth in both males and females. Alcohol-only did not affect growth in either sex, but interacted with ID to reduce growth in males and not females. Markers of significance were omitted for clarity purposes.</p

Maternal IDAA profoundly exacerbates alcohol-induced deficits in offspring’s delay ECC performance.

<p>Percent acquisition and amplitude of conditioned responses (CR) in IS and ID P35 offspring receiving 0 (<b>A, B</b>), 3.5 (<b>C, D</b>), or 5 (<b>E, F</b>) g/kg alcohol per day during the brain growth spurt. N = 9–16 rats per treatment group. There were significant main effects of Iron status, Alcohol dose, and an Iron status×Alcohol dose interaction. The interactive effect of Iron status and Alcohol was observed in ID rats that received 5 g/kg alcohol (<b>E, F</b>), where they were more impaired in acquiring CRs compared to IS rats that received 5 g/kg alcohol. Markers of significance omitted for clarity purposes.</p

Data from: Estimating the reproducibility of psychological science

This record contains the underlying research data for the publication "Estimating the reproducibility of psychological science" and the full-text is available from: https://ink.library.smu.edu.sg/lkcsb_research/5257Reproducibility is a defining feature of science, but the extent to which it characterizes current research is unknown. We conducted replications of 100 experimental and correlational studies published in three psychology journals using high-powered designs and original materials when available. Replication effects were half the magnitude of original effects, representing a substantial decline. Ninety-seven percent of original studies had statistically significant results. Thirty-six percent of replications had statistically significant results; 47% of original effect sizes were in the 95% confidence interval of the replication effect size; 39% of effects were subjectively rated to have replicated the original result; and if no bias in original results is assumed, combining original and replication results left 68% with statistically significant effects. Correlational tests suggest that replication success was better predicted by the strength of original evidence than by characteristics of the original and replication teams