Research Article: Birth Weight, Season of Birth and Postnatal Growth Do Not Predict Levels of Systemic Inflammation in Gambian Adults

Date Published: July 10, 2013

Publisher: Blackwell Publishing Ltd

Author(s): Anna A Richards, Anthony J Fulford, Andrew M Prentice, Sophie E Moore.

http://doi.org/10.1002/ajhb.22413

Abstract

Studies testing whether systemic inflammation might lie on the causal pathway between aberrant fetal and post-natal growth patterns and later cardiovascular disease have been inconclusive, possibly due to the use of single markers of unknown predictive value. We used repeated measures of a comprehensive set of inflammatory markers to investigate the relationship between early life measures and systemic inflammation in an African population.

Individuals born in three rural villages in The Gambia, and for whom early life measurements were recorded, were traced (n = 320). Fasting levels of eight inflammatory markers (C-reactive protein, serum amyloid A, orosomucoid, fibrinogen, α 1-antichymotrypsin, sialic acid, interleukin-6 and neopterin) were measured, and potential confounding factors recorded. The association between early life measurements and systemic inflammation was assessed using regression analysis.

Levels of most markers were unrelated to early growth patterns. In analyses adjusted for age and sex, more rapid growth between birth and 3 months of age was associated with higher levels of fibrinogen, orosomucoid, and sialic acid. These relationships persisted after further adjustment for body mass index but after full adjustment only the association with fibrinogen remained.

This study provides little evidence that size at birth or growth in early infancy determine levels of inflammatory markers in young Gambian adults. Am. J. Hum. Biol. 25:457–464, 2013. © 2013 Wiley Periodicals, Inc.

Partial Text

A total of 209 (65.3%) participants had a CRP and 266 (83.1%) an IL-6 measurement below the minimum assay detection level (<1.1 and <0.8 pg/ml, respectively). CRP and IL-6 were therefore analyzed as binary variables (CRP <1.1 vs. ≥ 1.1 mg/l; IL-6 <0.8 vs. ≥ 0.8 pg/ml). Orosomucoid, ACT, sialic acid and neopterin were loge transformed to normality. A loge transformation of serum amyloid A failed to produce a normal distribution and it was necessary to add 100 to each serum amyloid A value and then take the loge transformation to obtain a normal distribution. Table 1 describes the characteristics of the study population by gender. Forty-one participants (12.8%) were born low birth weight with a higher prevalence in female compared with male participants (17.5 vs. 8.4%.; P = 0.02). Gestational age ranged from 32.0 to 41.6 weeks with 30 participants (11.2%) born premature (<37 weeks gestation). The majority of participants had a BMI within the normal range although the percentage overweight, or centrally obese, was considerably higher in females compared to males (P < 0.001 for both). As expected in young Gambian adults there was a low prevalence of hypertension (<3%), IFG (<1%) and type 2 diabetes (<1%). Less than 1% of the study population had asymptomatic malaria. There was a clear sex-difference in tobacco use with no females, compared with 30% of males reporting ever using tobacco regularly. Few women (3.3%) used hormonal contraceptives. The current study aimed to test the hypothesis that systemic inflammation is young adulthood is predicted by early life exposures. Using a comprehensive set of markers in a cohort of 320 young Gambian adults, we have found little evidence for an effect of a number of early life parameters on later inflammatory status. This is the first published study to investigate this association in an indigenous African population. The inclusion of a range of early life measures, in particular early postnatal growth, and a large and varied number of markers to assess systemic inflammation considerably widens the evidence base in this field. The main hypothesis of this study was that early life programming of systemic inflammation was a mechanism to explain the association between poor early life growth and increased risk of adult CVD; this study provided little evidence to support this hypothesis among young, lean Gambians.   Source: http://doi.org/10.1002/ajhb.22413

 

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