Low-grade inflammation might mediate associations between size at birth, early life growth, excessive weight gain, and subsequent risk of cardiovascular disease in adult life. Our aim was to investigate relationships between fetal growth, weight over the life course, and low-grade inflammation measured by serum high sensitivity C-reactive protein (CRP) levels at 31 years.
General population-based northern Finland 1966 Birth Cohort study of 5840 participants attending a clinical examination at 31 years, including measurement of CRP. Weight and height were assessed at birth, 12 months, and 14 and 31 years of age. CRP levels at 31 years were 16% [95% confidence interval (CI) 8, 23] higher per 1 kg lower birth weight, 21% (95% CI 2, 37) higher per 10 cm lower birth length, and 24% (95% CI 10, 36) higher per 1 kg/m3 lower ponderal index, after adjustment for potential confounders. Participants with highest tertile body mass index (BMI) at 31 years and lowest tertile birth weight had the highest average CRP levels. Per unit increase in BMI from 14 to 31 years was associated with 16% (95% CI 14, 17) higher CRP levels; the association was larger for those in the top BMI tertile at age 14 years.
Systemic low-grade inflammation may lie on the causal pathway that relates impaired fetal growth and weight gain from childhood to adulthood to adverse adult cardiovascular health. Lifestyle changes from early life might be an important step in reducing cardiovascular risk in adults.
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"from birth into adulthood. Due to the fact that reasonably high temporal resolution is required over long periods of time, only a few studies have been able to link early life course body size explicitly to inflammation in adulthood (Nazmi et al., 2009; Tzoulaki et al., 2008). "
[Show abstract][Hide abstract] ABSTRACT: This paper examines how body size changes over the early life course to predict high sensitivity C-reactive protein in a U.S. based sample. Using three waves of the National Longitudinal Study of Adolescent Health (Add Health), we test the chronic disease epidemiological models of fetal origins, sensitive periods, and chains of risk from birth into adulthood. Few studies link birth weight and changes in obesity status over adolescence and early adulthood to adult obesity and inflammation. Consistent with fetal origins and sensitive periods hypotheses, body size and obesity status at each developmental period, along with increasing body size between periods, are highly correlated with adult CRP. However, the predictive power of earlier life course periods is mediated by body size and body size change at later periods in a pattern consistent with the chains of risk model. Adult increases in obesity had effect sizes of nearly 0.3 sd, and effect sizes from overweight to the largest obesity categories were between 0.3 and 1 sd. There was also evidence that risk can be offset by weight loss, which suggests that interventions can reduce inflammation and cardiovascular risk, that females are more sensitive to body size changes, and that body size trajectories over the early life course account for African American- and Hispanic-white disparities in adult inflammation.
Full-text · Article · Nov 2015 · Social Science [?] Medicine
"Although previous study in children has failed to find significant association between birth weight and hs-CRP , our epidemiologic study is consistent with the MIDSPAN family study and Northern Finland 1966 birth cohort study in adults [14,15]. However, this inverse relationship was not observed in black subjects in our analysis. "
[Show abstract][Hide abstract] ABSTRACT: Both low birth weight, an indicator of intrauterine growth restriction, and low grade systemic inflammation depicted by high sensitivity C-reactive protein (hs-CRP) have emerged as independent predictors of cardiovascular (CV) disease and type 2 diabetes. However, information linking low birth weight and hs-CRP in a biracial (black/white) population is scant. We assessed a cohort of 776 black and white subjects (28% black, 43% male) aged 24-43 years (mean 36.1 years) enrolled in the Bogalusa Heart Study with regard to birth weight and gestational age data were retrieved from Louisiana State Public Health Office.
Black subjects had significantly lower birth weight than white subjects (3.145 kg vs 3.441 kg, p < 0.0001) and higher hs-CRP level (3.29 mg/L vs 2.57 mg/L, p = 0.011). After adjusting for sex, age, body mass index (BMI), smoking status and race (for total sample), the hs-CRP level decreased across quartiles of increasing birth weight in white subjects (p = 0.001) and the combined sample (p = 0.002). Adjusting for sex, age, BMI, smoking status and race for the total sample in a multivariate regression model, low birth weight was retained as an independent predictor variable for higher hs-CRP levels in white subjects (p = 0.004) and the total sample (p = 0.007). Conversely, the area under the receiver operative curve (c statistic) analysis adjusted for race, sex, age, smoking status and BMI yielded a value of 0.777 with regard to the discriminating value of hs-CRP for predicting low birth weight.
The deleterious effect of low birth weight on systemic inflammation depicted by the hs-CRP levels in asymptomatic younger adults may potentially link fetal growth retardation, CV disease and diabetes, with important health implications.
Full-text · Article · Mar 2011 · BMC Research Notes
"Over an eight year follow-up, adults born small for gestational age gained more BMI than those born appropriate for gestational age, despite their lower likelihood of becoming obese, resulting in greater fat mass with more abdominal fat . Small body size at birth and excessive weight gain during adolescence and young adulthood may predispose to low-grade inflammation in adulthood , which in turn also may increase the risk of developing CHD. "
[Show abstract][Hide abstract] ABSTRACT: Low birth weight and high childhood body mass index (BMI) is each associated with an increased risk of coronary heart disease (CHD) in adult life. We studied individual and combined associations of birth weight and childhood BMI with the risk of CHD in adulthood.
Birth weight and BMI at age seven years were available in 216,771 Danish and Finnish individuals born 1924-1976. Linkage to national registers for hospitalization and causes of death identified 8,805 CHD events during up to 33 years of follow-up (median = 24 years) after age 25 years. Analyses were conducted with Cox regression based on restricted cubic splines. Using median birth weight of 3.4 kg as reference, a non-linear relation between birth weight and CHD was found. It was not significantly different between cohorts, or between men and women, nor was the association altered by childhood BMI. For birth weights below 3.4 kg, the risk of CHD increased linearly and reached 1.28 (95% confidence limits: 1.13 to 1.44) at 2 kg. Above 3.4 kg the association weakened, and from about 4 kg there was virtually no association. BMI at age seven years was strongly positively associated with the risk of CHD and the relation was not altered by birth weight. The excess risk in individuals with a birth weight of 2.5 kg and a BMI of 17.7 kg/m(2) at age seven years was 44% (95% CI: 30% to 59%) compared with individuals with median values of birth weight (3.4 kg) and BMI (15.3 kg/m(2)).
Birth weight and BMI at age seven years appeared independently associated with the risk of CHD in adulthood. From a public health perspective we suggest that particular attention should be paid to children with a birth weight below the average in combination with excess relative weight in childhood.