The Effect of Longer-Term and Exclusive Breastfeeding Promotion on Visual Outcome in Adolescence.

Purpose: Breastfeeding may influence early visual development. We examined whether an intervention to promote increased duration and exclusivity of breastfeeding improves visual outcomes at 16 years of age. Methods: Follow-up of a cluster-randomized trial in 31 Belarusian maternity hospitals/polyclinics randomized to receive a breastfeeding promotion intervention, or usual care, where 46% vs. 3% were exclusively breastfed at 3 months respectively. Low vision in either eye was defined as unaided logMAR vision of ≥0.3 or worse (equivalent to Snellen 20/40) and was used as the primary outcome. Open-field autorefraction in a subset (n = 963) suggested that 84% of those with low vision were myopic. Primary analysis was based on modified intention-to-treat, accounting for clustering within hospitals/clinics. Observational analyses also examined the effect of breastfeeding duration and exclusivity, as well as other sociodemographic and environmental determinants of low vision. Results: A total of 13,392 of 17,046 (79%) participants were followed up at 16 years. Low vision prevalence was 19.6% (95% confidence interval [CI]: 17.5, 22.0%) in the experimental group versus 21.6% (19.5, 23.8%) in the control group. Cluster-adjusted odds ratio (OR) of low vision associated with the intervention was 0.92 (95% CI: 0.73, 1.16); 0.88 (95% CI: 0.74, 1.05) after adjustment for parental and early life factors. In observational analyses, breastfeeding duration and exclusivity had no significant effect on low vision. However, maternal age at birth (OR: 1.13, 95% CI: 1.07, 1.14/5-year increase) and urban versus rural residence were associated with increased risk of low vision. Lower parental education, number of older siblings was associated with a lower risk of low vision; boys had lower risk compared with girls (0.64, 95% CI: 0.59,0.70). Conclusions: Exclusive breastfeeding promotion had no significant effect on visual outcomes in this study, but other environmental factors showed strong associations. (ClinicalTrials.gov number, NCT01561612.

Breastfeeding during infancy and neurocognitive function in adolescence: 16-year follow-up of the PROBIT cluster-randomized trial

10.1371/journal.pmed.1002554PLoS Medicine154e100255

Analysis of maternal prenatal weight and offspring cognition and behavior:Results from the Promotion of Breastfeeding Intervention Trial (PROBIT) cohort

IMPORTANCE: Prenatal experiences can influence fetal brain development. OBJECTIVE: To examine associations of maternal prenatal body mass index (BMI) with cognition and behavior of offspring born full-term. DESIGN, SETTING, AND PARTICIPANTS: This cohort study examined follow-up data from a breastfeeding promotion intervention at 31 hospitals and affiliated polyclinics in the Republic of Belarus. Participants included 11 276 children who were evaluated from birth (1996-1997) to adolescence (2017-2019), with maternal BMI information available in prenatal medical records. EXPOSURES: Maternal BMI, calculated as weight in kilograms divided by height in meters squared, after 35 weeks gestation; secondary analyses examined maternal BMI at other time points and paternal BMI. MAIN OUTCOMES AND MEASURES: Trained pediatricians assessed child cognition with the Wechsler Abbreviated Scales of Intelligence (WASI) at 6.5 years and the computerized self-administered NeuroTrax battery at 16 years, both with an approximate mean (SD) of 100 (15). Parents and teachers rated behaviors at 6.5 years using the Strengths and Difficulties Questionnaire (SDQ, range 0-40). Mixed-effects linear regression analyses corrected for clustering, adjusted for the randomized intervention group and baseline parental sociodemographic characteristics, and were considered mediation by child BMI. RESULTS: Among 11 276 participants, 9355 women (83%) were aged 20 to 34 years, 10 128 (89.8%) were married, and 11 050 (98.0%) did not smoke during pregnancy. Each 5-unit increase in of maternal late-pregnancy BMI (mean [SD], 27.2 [3.8]) was associated with lower offspring WASI performance intelligence quotient (IQ) (−0.52 points; 95% CI, −0.87 to −0.17 points) at 6.5 years and lower scores on 5 of 7 NeuroTrax subscales and the global cognitive score at 16 years (−0.67 points; 95% CI, −1.06 to −0.29 points). Results were similar after adjustment for sociodemographic characteristics, pregnancy complications, and paternal BMI and were not mediated by child weight. Higher late pregnancy maternal BMI was also associated with more behavioral problems reported on the SDQ by teachers but not associated with parent-reported behaviors (externalizing behaviors: 0.13 points; 95% CI, 0.02 to 0.24 points; and total difficulties: 0.14 points, 95% CI, −0.02 to 0.30 points). Results were similar for maternal BMI measured in the first trimester or postpartum. In contrast, higher 6.5-year paternal BMI was associated with slightly better child cognition (WASI verbal IQ: 0.42 points; 95% CI, 0.02 to 0.82 points; NeuroTrax executive function score: 0.68 points; 95% CI, 0.24 to 1.12 points) and fewer teacher-reported behavioral problems (total difficulties: −0.29 points; 95% CI, −0.46 to −0.11 points). CONCLUSIONS AND RELEVANCE: This cohort study supports findings from animal experiments and human observational studies in settings with higher maternal BMI and obesity rates. Higher maternal prenatal BMI may be associated with poorer offspring brain development, although residual confounding cannot be excluded

Flow diagram of clusters and participants of PROBIT recruitment follow-up phases at 12 mo, 6.5 y, 11.5 y, and 16 y.

<p>^a: During the 11.5-y follow-up, 6 deaths were reported in the intervention arm. Data-checking during the 16-y follow-up found one of these children had been incorrectly reported as deceased and data were amended. ^b: Of the 13,557 seen at the 16-y follow-up, 12,072 were seen at both 11.5-y and 16-y follow-ups, 274 were not seen at either 6.5-y or 11.5-y follow-ups, 449 were seen at 6.5 y but not seen at 11.5 y, and 762 were seen at 11.5 y but not seen at 6.5 y. Of the 3,489 children randomized but not followed up at 16 y, 267 attended the excluded site, 116 died after randomization, 2,674 were lost to follow-up, and 432 were unable or unwilling to come for their clinic visit.</p

Intraclass correlation and ITT analysis of mean differences (95% CI) of neurocognitive scores at age 16 years in treatment (<i>N</i> = 6,967) versus control (<i>N</i> = 6,460) groups.

<p>Intraclass correlation and ITT analysis of mean differences (95% CI) of neurocognitive scores at age 16 years in treatment (<i>N</i> = 6,967) versus control (<i>N</i> = 6,460) groups.</p

IV estimates of breastfeeding effects (95% CI) on neurocognitive scores at age 16 years by breastfeeding exclusivity and duration, (<i>N</i> = 12,912).

<p>IV estimates of breastfeeding effects (95% CI) on neurocognitive scores at age 16 years by breastfeeding exclusivity and duration, (<i>N</i> = 12,912).</p

Baseline and follow-up characteristics of 13,427 participants with the cognitive scores at 16-year follow-up by intervention group (<i>N</i>, percentage).

<p>Baseline and follow-up characteristics of 13,427 participants with the cognitive scores at 16-year follow-up by intervention group (<i>N</i>, percentage).</p

Observational analysis of multivariable associations of exclusive breastfeeding (≥3 versus <3 months) and nonbreastfeeding factors (mean differences and 95% CI) with global cognitive score at age 16 years (without multiple imputation).

<p>Observational analysis of multivariable associations of exclusive breastfeeding (≥3 versus <3 months) and nonbreastfeeding factors (mean differences and 95% CI) with global cognitive score at age 16 years (without multiple imputation).</p