- Title
- Early-life nutrition and child behavioural and cognitive outcomes
- Creator
- Taylor, Rachael
- Relation
- University of Newcastle Research Higher Degree Thesis
- Resource Type
- thesis
- Date
- 2018
- Description
- Research Doctorate - Doctor of Philosophy (PhD)
- Description
- The ‘Developmental Origins of Health and Disease’ hypothesis recognises that the nutritional environment during prenatal and postnatal life can impact on human brain development which may result in cognitive deficits and behavioural disorders throughout the lifespan. Evidence from human and animal studies suggest that both folate and iodine deficiencies during pregnancy can significantly impair brain development and cognitive function in the offspring. However, based on human studies the impact of other nutrients on brain development and cognitive function is inconclusive. Epidemiological evidence indicates that the duration and exclusivity of breastfeeding is associated with child cognitive ability in later life. It is speculated that this association could be partly explained by epigenetics, given that DNA methylation is a mechanism which is influenced by nutrition. DNA methylation occurs via one-carbon metabolism which is regulated by methyl donors and cofactors derived from nutrients (methionine, choline, betaine, folate and vitamins B2, B6 and B12) in food. Therefore, the primary purpose of this thesis was to investigate whether early-life nutrition is an important mediator of child cognitive and behavioural outcomes via DNA methylation. Four research studies were undertaken to achieve this aim which are summarised below. A systematic review and meta-analysis of randomised controlled trials (RCTs) were conducted to evaluate whether any causative relationships exists between maternal dietary patterns and nutrients and/or specific domains of offspring cognition and behaviour. This review found that nutritional interventions during the prenatal and postnatal period did not significantly impact on child cognitive or behavioural outcomes. However, the review also identified that many of the included trials were likely to be underpowered, since child cognitive outcomes were secondary outcomes and sample sizes were small. Most studies analysed the impact of nutritional interventions exclusively during pregnancy, therefore further investigation is warranted during the postnatal period. This review also demonstrated the need for high-quality RCTs that examine the impact of food-based intervention, rather than solely nutrient supplementation trials, on child cognitive and behavioural outcomes. The Women And Their Children’s Health (WATCH) study, a prospective longitudinal cohort, previously identified that breastfed infants had lower plasma B12 and folate, and higher homocysteine levels compared to formula fed infants at six months of age. These nutrients are involved in the regulation of one-carbon metabolism, required for DNA methylation. Therefore, the remaining studies of this thesis analysed data using a subset of children from the Australian WATCH cohort to investigate whether DNA methylation is a mechanism that underpins the association between nutrition and cognition. An analysis using a subset of data from this cohort was conducted and no association was found between the intake of one-carbon metabolism nutrients (methionine, folate, choline, vitamins B2, B6 and B12) during the first three years of life and the percentage of global DNA methylation at age four years, before or after adjustment for, child gender and pregnancy nutrient supplement use. Most of the buccal DNA samples were 0-3% methylated and global methylation levels were significantly higher in males compared to females. An investigation of the relationship between global DNA methylation and child cognitive and behavioural outcomes were then performed. The study analysis did not find any associations between cognition or behaviour scores with global DNA methylation, after adjustments for age at completion of the behavioural and cognitive assessment. However, the sample size of this cross-sectional study was small and therefore only powered to detect large changes in DNA methylation levels. The impact of a single nutrient on DNA methylation may be too subtle to detect, therefore the final study of this thesis analysed how dietary patterns more broadly impacted on the intake of one-carbon metabolism nutrients required for DNA methylation. Most children consumed inadequate daily serves of grains (1.9 vs 4.0 servings), vegetables (1.4 vs 2.5 servings) and meat and alternatives (0.7 vs 1.0 servings) and excessive daily serves of discretionary, energy-dense, nutrient poor foods (2.3 vs 0-1 servings). Dairy and alternatives (18-44%), discretionary foods (6-33%) and meat and alternatives (6-31%) were the main sources of most one-carbon metabolism nutrients. For most children, intakes of one-carbon metabolism nutrients exceeded the nutrient reference values (NRVs), except for the intake of choline, for which the mean intake was 9% lower than the adequate intake (AI). In conclusion, further evidence from high quality RCTs is required to determine whether causative relationships exist between dietary intake and cognitive outcomes. The research presented in this thesis was unable to confirm whether DNA methylation is a potential mechanism that partly explains the relationship between dietary intake and cognitive outcomes. Therefore, replicating these studies in a larger and more heterogeneous sample warrants further investigation. Finally, the impact of dietary patterns on the epigenome should be further analysed, especially in paediatric populations.
- Subject
- nutrition; cognition; behaviour; epigenetics; DNA methylation; pregnancy; postnatal; thesis by publication
- Identifier
- http://hdl.handle.net/1959.13/1395030
- Identifier
- uon:33803
- Rights
- Copyright 2018 Rachael Taylor
- Language
- eng
- Full Text
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| Thumbnail | File | Description | Size | Format | |||
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| View Details Download | ATTACHMENT01 | Thesis | 8 MB | Adobe Acrobat PDF | View Details Download | ||
| View Details Download | ATTACHMENT02 | Abstract | 468 KB | Adobe Acrobat PDF | View Details Download |