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The association between birth weight and long-term within-individual variability of blood pressure (BP) was examined in a longitudinal cohort of 1,454 adults (939 whites and 515 blacks; adulthood age = 19-50 years) enrolled in the Bogalusa Heart Study in Bogalusa, Louisiana, in 1973-2010. BP variability was depicted as standard deviation, coefficient of variation, and deviation from age-predicted values using 6-15 serial BP measurements from childhood to adulthood over an average of 25.7 years. Birth weight was significantly and negatively associated with adulthood BP levels, long-term BP levels, and rate of change. Importantly, low birth weight was significantly associated with increased BP variability in terms of standard deviation, coefficient of variation, and deviation. As evaluated using the regression coefficients, a 1-kg lower birth weight was associated with increases in systolic BP variability measures (-0.38 mm Hg, P = 0.04 for standard deviation; -0.004 mm Hg, P = 0.01 for coefficient of variation; and -0.16 mm Hg, P = 0.04 for deviation) after adjustment for race, age, sex, mean BP levels, and gestational age; similar trends in the associations were noted for diastolic BP variability measures. In conclusion, these findings suggest that birth weight affects not only BP levels but also the magnitude of within-individual BP fluctuations over time through fetal programming in BP regulation mechanisms.

Blood pressure (BP) is a highly variable physiologic trait with short-term and long-term fluctuations within the same individual at different time points. The burden of BP on the cardiovascular (CV) system has been studied in terms of multiple cross-sectional BP measurements at rest, response of BP to stresses, and long-term longitudinal variability of BP. Observations from childhood are available extending into early middle age in the biracial (black-white) population of Bogalusa, Louisiana. Left ventricular mass index was used to illustrate damaging effects on the CV system by both resting BP levels and fluctuations. Long-term BP variability reflecting intermittent and repeated variability was shown to have a greater effect in blacks. The childhood BP response to several stressors was found to be greater in blacks. These observations suggest that, although at rest a greater vagal effect occurs in blacks, they show a greater response when reacting to a stimulus. This, along with aspects such as carbohydrate-insulin metabolism or other biochemical/physiological differences, may account for the greater acceleration of CV atherosclerosis in blacks. The racial contrasts suggest, in part, that effects of lipoproteins may be greater in whites, whereas the effects of excess BP levels and variability of BP and Na(+)-K(+) intake and diet as well as other environmental effects result in more CV damage in blacks. The strong association of hemodynamic measures with anatomic, metabolic, and environmental factors emphasizes the need to begin prevention of risk factors at an early age. Taken together, understanding racial (black-white) contrasts to stress contribute to both prevention and treatment of hypertension, especially for black males., (Copyright © 2011 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)

Not all obese adults have cardiometabolic abnormalities. It is unknown whether this is true in children and, if true, whether children who have metabolically healthy overweight/obesity (MHO) will also have favorable cardiometabolic profiles in adulthood. These aspects were examined in 1,098 individuals who participated as both children (aged 5–17 years) and adults (aged 24–43 years) in the Bogalusa Heart Study between 1997 and 2002 in Bogalusa, Louisiana. MHO was defined as being in the top body mass index quartile, while low density lipoprotein cholesterol, triglycerides, mean arterial pressure, and glucose were in the bottom 3 quartiles, and high density lipoprotein cholesterol was in the top 3 quartiles. Forty-six children (4.2%) had MHO, and they were more likely to retain MHO status in adulthood compared with children in other categories (P < 0.0001). Despite markedly increased obesity in childhood and in adulthood, these same MHO children and adults showed a cardiometabolic profile generally comparable to that of nonoverweight/obese children (P > 0.05 in most cases). Moreover, there was no difference in carotid intima-media thickness in adulthood between MHO children and nonoverweight/obese children. Further, carotid intima-media thickness in adulthood was lower in MHO children than in metabolically abnormal, overweight/obese children (P = 0.003). In conclusion, the MHO phenotype starts in childhood and continues into adulthood. [ABSTRACT FROM PUBLISHER]