TY - JOUR
T1 - Weight at birth and infancy in relation to adult leukocyte count: A population-based study of 5619 men and women followed from the fetal period to adulthood
AU - Canoy, Dexter
AU - Pouta, Anneli
AU - Ruokonen, Aimo
AU - Hartikainen, Anna Liisa
AU - Saikku, Pekka
AU - Järvelin, Marjo Riitta
PY - 2009/6
Y1 - 2009/6
N2 - Context: Impaired fetal growth is associated with increased risk for coronary heart disease and diabetes in adulthood, but the underlying mechanism is unclear. Objective: The objective of the study was to examine the relation between early growth (weight at birth and first year) and adult total leukocyte count, the primary cell effectors of inflammation. Design: This was a birth cohort study (Northern Finland Birth Cohort 1966) with participants prospectively and longitudinally followed up from birth to age 31 yr. Setting: This was a general population-based cohort in Finland. Participants: A total of 5619 offspring of expectant mothers who attended a clinical examination and blood draw at 31-yr follow-up (4486 with complete data on weight at 1 yr) participated in the study. Main Exposure Variables: Weight at birth and at 1 year. Main Outcome Measure: Absolute leukocyte count was measured. Results: Total leukocyte count was lower at higher birth weight categories with or without adjustments for adult systolic blood pressure, total cholesterol, fasting insulin, body mass index, cigarette smoking, sex, gestational age, and other life course factors. The covariate-adjusted regression coefficient for log-transformed total leukocyte count(×109 cells/liter) per 1 SD (525 g) increase in birth weight was -0.012(95% confidence interval -0.021 to -0.004). The association persisted, even when limiting our analyses among healthy and nonsmoking individuals, and the inversely linear relation was steepest among those with lower weight attained at 1 yr (P for interaction = 0.027). Conclusion: Poorer growth in early life was associated with systemic low-grade inflammation in adulthood. This relation suggests a plausible inflammatory mechanism linking early growth impairment with risk of coronary heart disease and diabetes later in life. Copyright © 2009 by The Endocrine Society.
AB - Context: Impaired fetal growth is associated with increased risk for coronary heart disease and diabetes in adulthood, but the underlying mechanism is unclear. Objective: The objective of the study was to examine the relation between early growth (weight at birth and first year) and adult total leukocyte count, the primary cell effectors of inflammation. Design: This was a birth cohort study (Northern Finland Birth Cohort 1966) with participants prospectively and longitudinally followed up from birth to age 31 yr. Setting: This was a general population-based cohort in Finland. Participants: A total of 5619 offspring of expectant mothers who attended a clinical examination and blood draw at 31-yr follow-up (4486 with complete data on weight at 1 yr) participated in the study. Main Exposure Variables: Weight at birth and at 1 year. Main Outcome Measure: Absolute leukocyte count was measured. Results: Total leukocyte count was lower at higher birth weight categories with or without adjustments for adult systolic blood pressure, total cholesterol, fasting insulin, body mass index, cigarette smoking, sex, gestational age, and other life course factors. The covariate-adjusted regression coefficient for log-transformed total leukocyte count(×109 cells/liter) per 1 SD (525 g) increase in birth weight was -0.012(95% confidence interval -0.021 to -0.004). The association persisted, even when limiting our analyses among healthy and nonsmoking individuals, and the inversely linear relation was steepest among those with lower weight attained at 1 yr (P for interaction = 0.027). Conclusion: Poorer growth in early life was associated with systemic low-grade inflammation in adulthood. This relation suggests a plausible inflammatory mechanism linking early growth impairment with risk of coronary heart disease and diabetes later in life. Copyright © 2009 by The Endocrine Society.
U2 - 10.1210/jc.2008-2545
DO - 10.1210/jc.2008-2545
M3 - Article
C2 - 19276227
SN - 1945-7197
VL - 94
SP - 1916
EP - 1922
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
IS - 6
ER -