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Nutritional and Oxidative Stress Risk Factors for Fetal Alcohol Spectrum Disorder
Nutritional and Oxidative Stress Risk Factors for Fetal Alcohol Spectrum Disorder
상세정보
- 자료유형
- 학위논문 서양
- 최종처리일시
- 20260202105146
- ISBN
- 9798297647893
- DDC
- 641
- 저자명
- Chima, Harpreet.
- 서명/저자
- Nutritional and Oxidative Stress Risk Factors for Fetal Alcohol Spectrum Disorder
- 발행사항
- [Sl] : University of California, Davis, 2025
- 발행사항
- Ann Arbor : ProQuest Dissertations & Theses, 2025
- 형태사항
- 233 p
- 주기사항
- Source: Dissertations Abstracts International, Volume: 87-04, Section: B.
- 주기사항
- Advisor: Keen, Carl L.
- 학위논문주기
- Thesis (Ph.D.)--University of California, Davis, 2025.
- 초록/해제
- 요약Fetal alcohol spectrum disorder is a leading preventable cause of neurodevelopmental disability. Prenatal alcohol exposure causes these disorders, but maternal nutritional status and oxidative stress responses can modify fetal vulnerability. Animal studies demonstrate that alcohol induces oxidative stress and disrupts maternal micronutrient homeostasis. Human studies linking these physiological disruptions to infant outcomes are lacking.We analyzed alcohol consumption patterns in pregnant Ukrainian women using growth mixture modeling to identify longitudinal alcohol trajectories. Women who maintained very high drinking levels throughout pregnancy showed elevated oxidative stress markers, lower plasma zinc and copper, and activation of the acute phase response. These biochemical changes correlated with impaired infant growth and neurodevelopment.The highest alcohol exposure group showed elevated inflammatory markers and compromised micronutrient status. This combination predicted poorer infant outcomes, with effects varying by infant sex. Multivitamin/multimineral supplementation during pregnancy partially improved maternal biochemical markers but did not prevent adverse developmental outcomes.Our findings provide the first human evidence suggesting that alcohol exposure, acute phase response, and conditional nutrient deficiency may interact to magnify teratogenicity beyond alcohol's direct effects alone. Maternal biochemical status mediates the relationship between prenatal alcohol exposure and developmental outcomes. Preventing FASD may require comprehensive interventions that address both alcohol cessation and maternal physiological support.
- 일반주제명
- Nutrition
- 일반주제명
- Neurosciences
- 일반주제명
- Biology
- 일반주제명
- Biochemistry
- 일반주제명
- Clinical psychology
- 키워드
- Oxidative stress
- 기타저자
- University of California, Davis Nutritional Biology
- 기본자료저록
- Dissertations Abstracts International. 87-04B.
- 전자적 위치 및 접속
- 로그인 후 원문을 볼 수 있습니다.
MARC
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■020 ▼a9798297647893
■035 ▼a(MiAaPQ)AAI32241239
■040 ▼aMiAaPQ▼cMiAaPQ
■0820 ▼a641
■1001 ▼aChima, Harpreet.
■24510▼aNutritional and Oxidative Stress Risk Factors for Fetal Alcohol Spectrum Disorder
■260 ▼a[Sl]▼bUniversity of California, Davis▼c2025
■260 1▼aAnn Arbor▼bProQuest Dissertations & Theses▼c2025
■300 ▼a233 p
■500 ▼aSource: Dissertations Abstracts International, Volume: 87-04, Section: B.
■500 ▼aAdvisor: Keen, Carl L.
■5021 ▼aThesis (Ph.D.)--University of California, Davis, 2025.
■520 ▼aFetal alcohol spectrum disorder is a leading preventable cause of neurodevelopmental disability. Prenatal alcohol exposure causes these disorders, but maternal nutritional status and oxidative stress responses can modify fetal vulnerability. Animal studies demonstrate that alcohol induces oxidative stress and disrupts maternal micronutrient homeostasis. Human studies linking these physiological disruptions to infant outcomes are lacking.We analyzed alcohol consumption patterns in pregnant Ukrainian women using growth mixture modeling to identify longitudinal alcohol trajectories. Women who maintained very high drinking levels throughout pregnancy showed elevated oxidative stress markers, lower plasma zinc and copper, and activation of the acute phase response. These biochemical changes correlated with impaired infant growth and neurodevelopment.The highest alcohol exposure group showed elevated inflammatory markers and compromised micronutrient status. This combination predicted poorer infant outcomes, with effects varying by infant sex. Multivitamin/multimineral supplementation during pregnancy partially improved maternal biochemical markers but did not prevent adverse developmental outcomes.Our findings provide the first human evidence suggesting that alcohol exposure, acute phase response, and conditional nutrient deficiency may interact to magnify teratogenicity beyond alcohol's direct effects alone. Maternal biochemical status mediates the relationship between prenatal alcohol exposure and developmental outcomes. Preventing FASD may require comprehensive interventions that address both alcohol cessation and maternal physiological support.
■590 ▼aSchool code: 0029.
■650 4▼aNutrition
■650 4▼aNeurosciences
■650 4▼aBiology
■650 4▼aBiochemistry
■650 4▼aClinical psychology
■653 ▼aFetal alcohol spectrum disorder
■653 ▼aOxidative stress
■653 ▼aNeurodevelopmental disability
■653 ▼aMaternal biochemical status
■690 ▼a0570
■690 ▼a0487
■690 ▼a0317
■690 ▼a0306
■690 ▼a0622
■71020▼aUniversity of California, Davis▼bNutritional Biology.
■7730 ▼tDissertations Abstracts International▼g87-04B.
■790 ▼a0029
■791 ▼aPh.D.
■792 ▼a2025
■793 ▼aEnglish
■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T17359616▼nKERIS▼z이 자료의 원문은 한국교육학술정보원에서 제공합니다.
