Abstract
BackgroundSaturated fatty acids (SFA) have been reported to promote inflammation. Nevertheless, evidence linking dietary SFA and low-grade inflammation in adolescents is scarce and inconsistent. The modulatory role of physical activity (PA) on fat metabolism and inflammation may provide a potential explanation. Thus, we assessed the association of dietary SFA with high-sensitivity C-reactive protein (hsCRP), a marker of low-grade inflammation, in 15-year-olds, and evaluated possible interactions between dietary SFA and different levels of PA.MethodsChildren participating in the 15-year follow-ups of the GINIplus and LISA German birth cohort studies were included (N = 824). SFA intake was estimated by means of a food frequency questionnaire and PA recorded by accelerometers. Average daily minutes of PA were classified into “sedentary”, “light” and “moderate-to-vigorous” (MVPA), using Freedson’s cut-offs. HsCRP concentrations were measured in serum and categorized into 3 sex-specific levels (below detection limit (I), above 75th percentile (III), in between (II)). Sex-stratified cross-sectional associations between SFA and hsCRP were assessed using multinomial logistic regression, adjusting for potential confounders. Interaction terms were included between SFA and the different PA levels; and if significant interactions were observed, analyses stratified by tertiles of the relevant PA levels were performed. Relative risk ratios (RRR) and 95% confidence intervals (95%CI) were presented for a 1% increase in SFA.ResultsAn inverse association was observed between SFA intake and hsCRP (II vs. I) in males (RRR = 0.85 [95%CI = 0.76;0.96], p = 0.008), whereas no significant association was observed in females. A significant interaction was observed with “sedentary” and “light” PA but not with MVPA in both sexes (p < 0.05). Stratified analyses indicated a significant inverse association between SFA and medium hsCRP levels in males in the highest light PA tertile (hsCRP II vs. I: 0.67 [0.517;0.858], p = 0.002).ConclusionOur findings do not support a detrimental role of dietary SFA in low-grade inflammation among adolescents. In males, higher dietary SFA was associated with lower hsCRP, although this should be interpreted in the context of possibly correlated nutrients. Children spending the most time in light PA drove the observed inverse association, suggesting a synergistic effect of SFA and lifestyle PA in the resultant inflammatory response.
Highlights
Saturated fatty acids (SFA) have been reported to promote inflammation
Children were excluded if they presented clear outliers in SFA intakes or in physical activity (PA) levels (2 subjects, 1 female with Moderate-to-vigorous physical activity (MVPA) = 257 min/day, 1 male with MVPA = 220 min/day), as identified by visual inspection of descriptive plots
Two aspects stand out among the analyses findings: 1) dietary SFA appears to have no association with high-sensitivity C-reactive protein (hsCRP) levels in adolescent females and to be inversely associated with hsCRP in males, albeit only for the middle hsCRP level with respect to the lowest, showing no clear exposure-response relationship; 2) a significant interaction between SFA intake and “light” PA likely plays a relevant role, given that the inverse association observed in males was only present among those spending the most time in “light” PA, as indicated by stratified analyses
Summary
Saturated fatty acids (SFA) have been reported to promote inflammation. evidence linking dietary SFA and low-grade inflammation in adolescents is scarce and inconsistent. The inflammatory marker high-sensitivity C-reactive protein (hsCRP) is used to predict the risk of atherosclerosis and CVD in adults [6] and has been observed in association with arterial alterations in children [7]. The underlying evidence for this recommendation has been questioned in a number of studies [20,21,22], fuelling an ongoing debate [23,24,25,26] Amidst this discussion, SFA have received much attention for their ability to promote inflammatory processes in vitro [27,28,29]. Processes following dietary intake, including digestion, absorption, uptake into tissues, and metabolism, all affect the ensuing fatty acid profile [38], and could partially explain the conflicting findings relative to dietary SFA
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