Previous research has reported that children who have a high birth weight or a low birth weight followed by high infant growth are at a higher risk of developing cardiovascular diseases in adulthood.
Variation in growth during infancy as well as fetal life is associated with adverse body fat distribution along with the risk of cardiovascular diseases from school age.
Several postmortem pathologic studies reported the development of atherosclerosis in children, fetuses, and adolescents as a result of altered early life growth. The adverse fetal environment has also been associated with carotid distensibility and carotid intima-media thickness (cIMT) in adolescence.
A recent systematic review showed that small size for gestational age (SGA) was associated with increased cIMT in individuals of 18 years or younger. However, a positive association between higher birth weight with cIMT has also been reported. Therefore, understanding critical periods during infancy or the fetal period that is associated with atherosclerosis and arterial health is important for the development of novel prevention strategies.
A new study published in JAMA Network Open examined the association of weight growth patterns during infancy and fetal periods with carotid distensibility and cIMT in children who were 10 years of age.
About the study
The study included pregnant women who had a delivery date between 1st April 2002 and 31st January 2006. Ultrasonography examinations were done to measure fetal head circumference, femur length, and abdominal circumference in the second and third trimesters. The birth weight, gestational age at birth, and sex were collected from midwives.
Gestational age was defined as preterm if it was less than 37 weeks, term if it was 37 to 42 weeks, and post-term if it was greater than 42 weeks. Birth weight was defined as low if it was less than 2500g, normal if it was 2500 to 4500g and high if it was greater than 4500g. Additionally, infants were measured at 6 months, 12 months, and 24 months after birth. An increase of more than 0.67 standard deviation (SD) was considered a growth acceleration while a decrease of more than 0.67 SD was considered a growth deceleration.
The cIMT and carotid distensibility was measured at the median age of 9.7 years. Data on race, maternal age, parity, prepregnancy weight, smoking, educational level, gestational hypertensive disorders, and folic acid supplementation were collected. Prepregnancy body mass index was calculated and maternal height was also measured. The child’s height and weight were also measured at 9.7 years.
The results reported that the mothers without birth outcome measurements had a lower educational level, smoked more often during pregnancy, were of non-European descent, and also used folic acid supplements during pregnancy. Children who did not participate in the study were reported to have lower third-trimester fetal weight and were most often born preterm as compared to those who participated in the study.
The results also reported that an increase in 500 g of birth weight was associated with increased cIMT as well as a lower carotid distensibility. Children with a birth weight of more than 4500 g were found to have the lowest carotid distensibility. Additionally, gestational age-adjusted birth weight was found to be associated with a lower carotid distensibility and increased cIMT while the small size for gestational age was associated with a higher carotid distensibility and decreased cIMT. Moreover, gestational age was not found to be associated with carotid measurements during childhood.
Furthermore, a higher third-trimester fetal weight, weight at birth, and weight at 6, 12, and 24 months were found to be associated with increased cIMT while the higher weight at 6, 12, and 24 months was found to be associated with lower carotid distensibility. Children with a normal fetal growth followed by accelerated infant growth were found to have the lowest carotid distensibility and highest cIMT.
Therefore, the current study demonstrated that higher infant and fetal weight growth was associated with impaired arterial health markers in children who were 10 years of age. Further studies are required to determine the causal pathways and how they are associated with the development of atherosclerosis in adulthood.
The study has certain limitations. First, all the children who participated in the study did not have data on childhood carotid measurements. Second, the study might not be free from observer bias and residual confounding.