Infant growth trajectories and lipid levels in adolescence
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Von Holle, Ann. Infant Growth Trajectories and Lipid Levels In Adolescence. 2018. https://doi.org/10.17615/je0a-fd56APA
Von Holle, A. (2018). Infant growth trajectories and lipid levels in adolescence. https://doi.org/10.17615/je0a-fd56Chicago
Von Holle, Ann. 2018. Infant Growth Trajectories and Lipid Levels In Adolescence. https://doi.org/10.17615/je0a-fd56- Last Modified
- March 21, 2019
- Creator
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Von Holle, Ann
- Affiliation: Gillings School of Global Public Health, Department of Epidemiology
- Abstract
- Developmental Origins of Health and Disease theory posits that elements of early life affect susceptibility to chronic disease during adulthood. Postnatal growth is one such element of early life that has been hypothesized as influencing chronic disease such as Atherosclerotic Cardiovascular Disease (ASCVD), which is responsible for one out of every three deaths in the United States. Researchers in the field of developmental origins hypothesize that postnatal growth is an environmental factor that permanently programs lipid metabolism, a known and well-established risk factor for ASCVD. We investigated the association between early postnatal anthropometric change and adverse lipid levels in adolescence in a contemporary Chilean birth cohort. Primary aims included: a) characterize predictors of infant growth, b) investigate the association between early infant growth trajectories and lipid levels, and c) evaluate the capacity of postnatal growth trajectories to modify the association between functional genetic variants and lipid levels in adolescence. Results from this research demonstrated distinct patterns of growth in which faster anthropometric growth groups were associated with a more favorable lipid profile. In the first manuscript, lower socioeconomic position was associated with a lower length velocity SITAR parameter (-0.22, 95\% CI=-0.31,-0.13). In the second manuscript, the length velocity SITAR parameter was positively associated with HDL-C levels in adolescence (11.5, SE=4.0) indicating higher HDL-C levels with faster length growth. Second, latent growth mixture models supported the strongest associations between higher LDL-C and slower WFL growth although no associations were statistically significant after adjustment for multiple comparisons. Lastly, the third manuscript provided little evidence supporting a concept that growth is an effect modifier when assessing genetic associations with lipids. Taken together, these results identify faster growth in early infancy as a protective factor. Mechanisms by which this occurs remain an open question, and postnatal growth remains a possible environmental cue for lipid metabolism programming. In turn, this information can support the search for optimal postnatal growth and with it, the potential for modification of chronic disease risk factor development later in life.
- Date of publication
- May 2018
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- Rights statement
- In Copyright
- Advisor
- Gahagan, Sheila
- Howard, Annie Green
- North, Kari
- Heiss, Gerardo
- Graff, Mariaelisa
- Degree
- Doctor of Philosophy
- Degree granting institution
- University of North Carolina at Chapel Hill Graduate School
- Graduation year
- 2018
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