Iodine, through the thyroid hormones, is required for the development of the auditory cortex and cochlea (the sensory organ for hearing). Deafness is a well-documented feature of endemic cretinism resulting from severe iodine deficiency. However, the range of effects of suboptimal iodine intake during auditory development on the hearing ability of children is less clear. We therefore aimed to systematically review the evidence for the association between iodine exposure (i.e. intake/status/supplementation) during development (i.e. pregnancy and/or childhood) and hearing outcomes in children. We searched PubMed and Embase and identified 330 studies, of which thirteen were included in this review. Only three of the thirteen studies were of low risk of bias or of good quality, this therefore limited our ability to draw firm conclusions. Nine of the studies (69 %) were in children (one RCT, two non-RCT interventions and six cross-sectional studies) and four (31 %) were in pregnant women (one RCT, one cohort study and two case reports). The RCT of iodine supplementation in mildly iodine-deficient pregnant women found no effect on offspring hearing thresholds. However, hearing was a secondary outcome of the trial and not all women were from an iodine-deficient area. Iodine supplementation of severely iodine-deficient children (in both non-RCT interventions) resulted in improved hearing thresholds. Five of six cross-sectional studies (83 %) found that higher iodine status in children was associated with better hearing. The current evidence base for the association between iodine status and hearing outcomes is limited and further good-quality research on this topic is needed.

Type of feeding during early life influences growth trajectory and metabolic risk at later ages. Modifications in infant formula composition have led to evaluate their effects on growth and energetic efficiency (EE) compared with breast-feeding. Main goal was to analyse type of feeding potential effects during first months of life, plus its EE, on growth patterns in healthy formula fed (standard infant formula (SF) vs. experimental infant formula enriched with bioactive nutrients (EF)) and breastfed (BF) infants participating in the COGNIS RCT (http://www.ClinicalTrials.gov, Identifier: NCT02094547) up to 18 months of age. Infants follow-up to 18 months of age (n 141) fed with a SF (n 48), EF(n 56), or BF (n 37), were assessed for growth parameters using WHO standards. Growth velocity (GV) and catch-up were calculated to identify growth patterns. EE of breast milk/infant formula was also estimated. Infants’ growth at 6 months showed higher length and lower head circumference gains in SF and EF infants than BF infants. Both weight-for-length and weight-for-age catch-up growth showed significant differences in formula fed groups compared with the BF. No significant differences in GV or catch-up were found at 6–12 and 12–18 months. Regarding EE, infant formula groups showed significantly lower weight and length gains/g of milk protein, and higher weight and length gains/g of milk lipids, than the BF infants. GV during first 6 months, which may be influenced by feeding, seems to be the main predictor of subsequent growth trajectory. Breast-feeding may have positive effects on growth programming due to its nutrients’ EE.

Healthy dietary patterns may protect against age-related cognitive decline, but results of studies have been inconsistent and few have had extensive longitudinal follow-up with comprehensive cognitive testing. The aim of the present study was to determine associations of dietary patterns with trajectories of global- and domain-specific cognitive change over a 12-year period. Data from 863 community-dwelling, dementia-free participants from the Lothian Birth Cohort 1936 study of ageing completed a FFQ at baseline (aged 70 years) and underwent cognitive testing at baseline, and at the ages of 73, 76, 79 and 82 years. Composite cognitive scores were constructed for four cognitive domains (visuospatial ability, processing speed, memory and verbal ability) and global cognitive function. A Mediterranean-style pattern and a traditional pattern were derived using principal component analysis of self-reported dietary intakes. In fully adjusted latent growth curve models, higher baseline adherence to the Mediterranean-style dietary pattern (β = 0·056, P = 0·009) and lower baseline adherence to the traditional dietary pattern (β  =  −0·087, P < 0·001) were cross-sectionally associated with better verbal ability. A slightly steeper decline in verbal ability over 12 years was observed in those with higher Mediterranean-style diet scores at baseline (β = −0·003, P = 0·008). All other associations were non-significant. Our findings in this well-characterised Scottish cohort indicate that adherence to a healthy Mediterranean-style diet is associated cross-sectionally with better verbal (crystallised) ability, with the converse being true for the traditional diet. A healthier baseline diet did not predict a reduced risk of global- or domain-specific cognitive decline.

Errors inherent in self-reported measures of energy intake (EI) are substantial and well documented, but correlates of misreporting remain unclear. Therefore, potential predictors of misreporting were examined. In Study One, fifty-nine individuals (BMI = 26·1 (sd 3·8) kg/m2, age = 42·7 (sd 13·6) years, females = 29) completed a 14-d stay in a residential feeding behaviour suite where eating behaviour was continuously monitored. In Study Two, 182 individuals (BMI = 25·7 (sd 3·9) kg/m2, age = 42·4 (sd 12·2) years, females = 96) completed two consecutive days in a residential feeding suite and five consecutive days at home. Misreporting was directly quantified by comparing covertly measured laboratory weighed intakes (LWI) with self-reported EI (weighed dietary record (WDR), 24-h recall, 7-d diet history, FFQ). Personal (age, sex and %body fat) and psychological traits (personality, social desirability, body image, intelligence quotient and eating behaviour) were used as predictors of misreporting. In Study One, those with lower psychoticism (P = 0·009), openness to experience (P = 0·006) and higher agreeableness (P = 0·038) reduced EI on days participants knew EI was being measured to a greater extent than on covert days. Isolated associations existed between personality traits (psychoticism and openness to experience), eating behaviour (emotional eating) and differences between the LWI and self-reported EI, but these were inconsistent between dietary assessment techniques and typically became non-significant after accounting for multiplicity of comparisons. In Study Two, sex was associated with differences between LWI and the WDR (P = 0·009), 24-h recall (P = 0·002) and diet history (P = 0·050) in the laboratory, but not home environment. Personal and psychological correlates of misreporting identified displayed no clear pattern across studies or dietary assessment techniques and had little utility in predicting misreporting.

Data on average iodine requirements for the Chinese population are limited following implementation of long-term universal salt iodisation. We explored the minimum iodine requirements of young adults in China using a balance experiment and the ‘iodine overflow’ hypothesis proposed by our team. Sixty healthy young adults were enrolled to consume a sequential experimental diet containing low, medium and high levels of iodine (about 20, 40 and 60 μg/d, respectively). Each dose was consumed for 4 d, and daily iodine intake, excretion and retention were assessed. All participants were in negative iodine balance throughout the study. Iodine intake, excretion and retention differed among the three iodine levels (P < 0·01 for all groups). The zero-iodine balance derived from a random effect model indicated a mean iodine intake of 102 μg/d, but poor correlation coefficients between observed and predicted iodine excretion (r 0·538 for μg/d data) and retention (r 0·304 for μg/d data). As iodine intake increased from medium to high, all of the increased iodine was excreted (‘overflow’) through urine and faeces by males, and 89·5 % was excreted by females. Although the high iodine level (63·4 μg/d) might be adequate in males, the corresponding level of 61·6 μg/d in females did not meet optimal requirements. Our findings indicate that a daily iodine intake of approximately half the current recommended nutrient intake (120 μg/d) may satisfy the minimum iodine requirements of young male adults in China, while a similar level is insufficient for females based on the ‘iodine overflow’ hypothesis.

Fish-oil supplements are marketed as enhancing intelligence and cognitive performance. However, empirical data concerning the utility of these products in healthy term infants are mixed, particularly with respect to lasting effects into childhood. We evaluated whether fish-oil supplementation during infancy leads to better neurocognitive/behavioural development at 6 years. We conducted a double-blind randomised controlled trial of supplementation with n-3 long-chain PUFA in 420 healthy term infants. Infants received either fish oil (containing at least 250 mg DHA and at least 60 mg EPA) or placebo (olive oil) daily from birth to 6 months of age. Neurodevelopmental follow-up was conducted at a mean age of 6 years (sd 7 months), whereby 335 children were assessed for language, executive functioning, global intelligence quotient and behaviour. No significant differences were observed between the groups for the main neurocognitive outcomes. However in parent-report questionnaire, fish-oil supplementation was associated with negative externalising (P = 0·035, d = 0·24) and oppositional/defiant behaviour (P = 0·006, d = 0·31), particularly in boys (P = 0·01, d = 0·45; P = 0·004, d = 0·40). Our results provide evidence that fish-oil supplementation to predominantly breast-fed infants confers no significant cognitive or behavioural benefit to children at 6 years.

Arachidonic acid (ARA) and DHA, supplied primarily from the mother, are required for early development of the central nervous system. Thus, variations in maternal ARA or DHA status may modify neurocognitive development. We investigated the relationship between maternal ARA and DHA status in early (11·7 weeks) or late (34·5 weeks) pregnancy on neurocognitive function at the age of 4 years or 6–7 years in 724 mother–child pairs from the Southampton Women’s Survey cohort. Plasma phosphatidylcholine fatty acid composition was measured in early and late pregnancy. ARA concentration in early pregnancy predicted 13 % of the variation in ARA concentration in late pregnancy (β=0·36, P<0·001). DHA concentration in early pregnancy predicted 21 % of the variation in DHA concentration in late pregnancy (β=0·46, P<0·001). Children’s cognitive function at the age of 4 years was assessed by the Wechsler Preschool and Primary Scale of Intelligence and at the age of 6–7 years by the Wechsler Abbreviated Scale of Intelligence. Executive function at the age of 6–7 years was assessed using elements of the Cambridge Neuropsychological Test Automated Battery. Neither DHA nor ARA concentrations in early or late pregnancy were associated significantly with neurocognitive function in children at the age of 4 years or the age of 6–7 years. These findings suggest that ARA and DHA status during pregnancy in the range found in this cohort are unlikely to have major influences on neurocognitive function in healthy children.

Objectives: Cognitive reserve (CR), defined as individual differences in the ability to cope with brain damage, seem to be associated to the several psychopathological features in psychiatric patients, such as the functional outcome. This study aims to identify different profiles of CR by combining intelligence quotient (IQ) and premorbid functioning, two measures independently associated to CR in previous works, as well as to explore CR effect on both Theory of Mind (ToM) baseline performance and improvement after socio-cognitive trainings. Methods: Sixty patients with chronic schizophrenia underwent a socio-cognitive rehabilitation. All patients were assessed for psychopathology, neurocognition, and ToM at baseline and post-treatment. CR profiles were explored with K-means cluster analysis, while differences between clusters in both baseline assessments and post-treatment ToM improvement, were analyzed by means of analysis of variance and repeated measures analysis of covariance. Results: The analysis revealed three CR profiles, respectively, characterized by low early premorbid functioning and mild intellectual impairment, average/high early premorbid functioning trend with moderate intellectual impairment and good early premorbid functioning associated to IQ within normal limits. Analyses showed a significant effect of CR on both baseline ToM performance and treatment outcome: patients with higher CR reached significantly better ToM scores. Conclusions: These results underline the clinical relevance of defining CR profiles of patients to customize trainings: subjects with a lower CR may benefit from more intensive programs. A deeper knowledge about CR may considerably increase our understanding of individual differences and thus potentiate treatment outcome. (JINS, 2018, 24, 563–571)

DHA is an important component of neural lipids accumulating in neural tissue during development. Inadequate DHA in gestation may compromise infant development, but it is unknown whether there are lasting effects. We sought to determine whether the observed effects of fetal DHA inadequacy on infant development persist into early childhood. This follow-up study assessed children (5–6 years) whose mothers received 400 mg/d DHA or a placebo during pregnancy. Child neurodevelopment was assessed with several age-appropriate tests including the Kaufman Assessment Battery for Children. A risk-reduction model was used whereby the odds that a child from the maternal placebo group would fail to achieve a test score in the top quartile was calculated. The association of maternal DHA intake and status in gestation with child test scores, as well as with child DHA intake and status, was also determined. No differences were detected in children (n 98) from the maternal placebo and DHA groups achieving a high neurodevelopment test score (P>0·05). However, maternal DHA status was positively related to child performance on some tests including language and short-term memory. Furthermore, child DHA intake and status were related to the mother’s intake and status in gestation. The neurodevelopment effects of fetal DHA inadequacy may have been lost or masked by other variables in the children. Although we provide evidence that maternal DHA status is related to child cognitive performance, the association of maternal and child DHA intake and status limits the interpretation of whether DHA before or after birth is important.

A link between infection, inflammation, neurodevelopment and adult illnesses has been proposed. The objective of this study was to examine the association between infection burden during childhood – a critical period of development for the immune and nervous systems – and subsequent systemic inflammatory markers and general intelligence. In the Avon Longitudinal Study of Parents and Children, a prospective birth cohort in England, we examined the association of exposure to infections during childhood, assessed at seven follow-ups between age 1·5 and 7·5 years, with subsequent: (1) serum interleukin 6 and C-reactive protein (CRP) levels at age 9; (2) intelligence quotient (IQ) at age 8. We also examined the relationship between inflammatory markers and IQ. Very high infection burden (90+ percentile) was associated with higher CRP levels, but this relationship was explained by body mass index (adjusted odds ratio (OR) 1·19; 95% confidence interval (CI) 0·95–1·50), maternal occupation (adjusted OR 1·23; 95% CI 0·98–1·55) and atopic disorders (adjusted OR 1·24; 95% CI 0·98–1·55). Higher CRP levels were associated with lower IQ; adjusted β = −0·79 (95% CI −1·31 to −0·27); P = 0·003. There was no strong evidence for an association between infection and IQ. The findings indicate that childhood infections do not have an independent, lasting effect on circulating inflammatory marker levels subsequently in childhood; however, elevated inflammatory markers may be harmful for intellectual development/function.

Seafood intake in pregnancy has been positively associated with childhood cognitive outcomes which could potentially relate to the high vitamin D content of oily fish. However, whether higher maternal vitamin D status (serum 25-hydroxyvitamin D (25(OH)D)) in pregnancy is associated with a reduced risk of offspring suboptimal neurodevelopmental outcomes is unclear. A total of 7065 mother–child pairs were studied from the Avon Longitudinal Study of Parents and Children cohort who had data for both serum total 25(OH)D concentration in pregnancy and at least one measure of offspring neurodevelopment (pre-school development at 6–42 months; ‘Strengths and Difficulties Questionnaire’ scores at 7 years; intelligence quotient (IQ) at 8 years; reading ability at 9 years). After adjustment for confounders, children of vitamin D-deficient mothers (<50·0 nmol/l) were more likely to have scores in the lowest quartile for gross-motor development at 30 months (OR 1·20; 95 % CI 1·03, 1·40), fine-motor development at 30 months (OR 1·23; 95 % CI 1·05, 1·44) and social development at 42 months (OR 1·20; 95 % CI 1·01, 1·41) than vitamin D-sufficient mothers (≥50·0 nmol/l). No associations were found with neurodevelopmental outcomes, including IQ, measured at older ages. However, our results suggest that deficient maternal vitamin D status in pregnancy may have adverse effects on some measures of motor and social development in children under 4 years. Prevention of vitamin D deficiency may be important for preventing suboptimal development in the first 4 years of life.

Early-life nutrition is critical for optimal brain development; however, few studies have evaluated the impact of diet as a whole in early childhood on neurological development with inconsistent results. The present analysis is a cross-sectional study nested within an ongoing prospective birth cohort, the Rhea study, and aims to examine the association of dietary patterns with cognitive and psychomotor development in 804 preschool (mean age 4·2 years) children. Parents completed a validated FFQ, and dietary patterns were identified using principal component analysis. Child cognitive and psychomotor development was assessed by the McCarthy Scales of Children’s Abilities (MSCA). Multivariable linear regression models were used to investigate the associations of dietary patterns with the MSCA scales. After adjustment for a large number of confounding factors, the ‘Snacky’ pattern (potatoes and other starchy roots, salty snacks, sugar products and eggs) was negatively associated with the scales of verbal ability (β=−1·31; 95 % CI −2·47, −0·16), general cognitive ability (β=−1·13; 95 % CI −2·25, −0·02) and cognitive functions of the posterior cortex (β=−1·20; 95 % CI −2·34, −0·07). Further adjustment for maternal intelligence, folic acid supplementation and alcohol use during pregnancy attenuated the observed associations, but effect estimates remained at the same direction. The ‘Western’ and the ‘Mediterranean’ patterns were not associated with child neurodevelopmental scales. The present findings suggest that poorer food choices at preschool age characterised by foods high in fat, salt and sugar are associated with reduced scores in verbal and cognitive ability.

Lutein and zeaxanthin are xanthophyll carotenoids present in highly pigmented vegetables and fruits. Lutein is selectively accumulated in the brain relative to other carotenoids. Recent evidence has linked lutein to cognition in older adults, but little is known about lutein in young children, despite structural brain development. We determined lutein intake using FFQ, one 24 h recall and three 24 h recalls, plasma lutein concentrations and their association with cognition in 160 children 5·6–5·9 years of age, at low risk for neurodevelopmental delay. Plasma lutein was skewed, with a median of 0·23 (2·5th to 95th percentile range 0·11–0·53) µmol/l. Plasma lutein showed a higher correlation with lutein intake estimated as the average of three 24 h recalls (r 0·479; P = 0·001), rather than one 24 h recall (r 0·242; P = 0·003) or FFQ (r 0·316; P = 0·001). The median lutein intake was 697 (2·5th to 95th percentile range 178–5287) µg/d based on three 24 h recalls. Lutein intake was inversely associated with SFA intake, but dietary fat or SFA intakes were not associated with plasma lutein. No associations were found between plasma lutein or lutein intake and any measure of cognition. While subtle independent effects of lutein on child cognition are possible, separating these effects from covariates making an impact on both child diet and cognition may be difficult.