In models adjusted for BMI, age, race, and sex, we found that total daily fat intake, total MUFA intake, total PUFA intake, MUFA 18:1 (octadecenoic), PUFA 18:2 (octadecadienoic), and PUFA 18:3 (octadecatrienoic) monotonically decreased across hs-CRP quarters (all P < 0.001), whereas dietary total SFA, SFA 4:0 (Butanoic), SFA 6:0 (Hexanoic), SFA 8:0 (octanoic), SFA 10:0 (decanoic), and SFA 14:0 (tetradecanoic) increased across hs-CRP quarters (all P < 0.001). In models adjusted for age, race, sex, BMI, and energy, we found that total PUFA intake, PUFA 18:2 (octadecadienoic), and PUFA 18:3 (octadecatrienoic) monotonically decreased across hs-CRP quarters (all P < 0.001), whereas total SFA intake, SFA 4:0 (butanoic), SFA 6:0 (hexanoic), SFA 8:0 (octanoic), SFA 10:0 (decanoic), SFA 14:0 (tetradecanoic), and SFA 18:0 (Octadecanoic) increased across hs-CRP quarters (all P < 0.001, Supplemental Table 1, http://links.lww.com/MD/B547).
This study investigated the association between dietary fatty acid intake and serum hs-CRP concentrations in a representative sample of US adults. The main findings were the association of increasing serum hs-CRP levels with increasing cholesterol intake and decreasing PUFA intake, suggesting a relationship between fatty acid intake and subclinical inflammation in this population.
Consistent with our findings, there are reports in the literature to suggest that inflammatory markers such as hs-CRP increase quickly after consumption of an excess amount of dietary lipids, while nutritional cholesterol itself is closely linked to inflammation markers through particular transcriptional regulators and may contribute to increasing the inflammatory component of atherogenesis.[23–25] We also recently reported an inverse relationship between cholesterol intake and hs-CRP in adult Iranians without a history of CVD. Murakami et al stated no significant association between SFA intake and raised hs-CRP, and they ascribed their results to the low baseline degree of raised hs-CRP level in their population (Japanese women). In this regard, a study in an elderly subjects could not detect a significant association between concentration of saturated myristic, palmitic or stearic acids, measured in serum cholesteryl esters, and hs-CRP level. In line with these previous results, an augmented SFA intake was not significantly related with changes in hs-CRP in an Italian subjects. They stated that, in dysmetabolic subjects, the role of dietary factors including PUFA is associated with enhanced postprandial inflammatory factors and lipids profile.[29,30] Moreover, it has been proposed that the Mediterranean diet has a converse correlation with inflammatory factors such as hs-CRP level.[20,31]
Studies have reported that n-3 FAs work both directly by substituting arachidonic acid as an eicosanoid substrate and stopping arachidonic acid metabolism, and indirectly by changing the expression of inflammatory genes via influences on transcription factor activation.[6,32] Additionally, it has been suggested that both n-3 PUFAs and n-6 PUFAs halt the activities of δ-6 desaturase, δ-5 desaturase, and cyclooxygenase, all of which have a role in fatty acid control that affects pro- and anti-inflammatory mediators. Therefore, high intake of both n-3 PUFAs and n-6 PUFAs could lessen inflammation.[5,33] Additional proposed mechanism is that PUFAs can change the action of transcription factors, such as peroxisome proliferator-activated receptors (PPARs) and nuclear factor κB. PPARs via stopping signaling molecules can impact the initiation of nuclear factor κB, and hence obstructs the construction production of pro-inflammatory cytokines.[5,34]
Some inconsistent findings have been reported in different type of studies, with some suggesting no significant differences in subjects with a MUFA-rich diet.[35–37] In line with our study, recently Muke et al, in a prospective study of 4707 individuals, found that higher intakes of PUFAs (mainly n-6 PUFAs) were correlated with lower levels of hs-CRP, which might reflect reduced chronic systemic inflammation. Julia et al hypothesized that the inverse relation found between total n-3 PUFAs and hs-CRP was mostly driven by long-chain n-3 PUFAs.
The present study has some limitations. Its cross-sectional nature does not allow inferences about causality. Also, the use of a single 24-hour dietary recall may not fully capture the usual dietary behaviors. However, this concern is mitigated by the large sample size, increasing the probability of inclusion of diverse dietary behaviors. Moreover, we did not control for chronic diseases that might elevate hs-CRP.
As fatty acid intake has been a topic of interest in relation to CVD risk, understanding the effects of SFA, MUFA, and PUFA on subclinical inflammation could yield useful clinical insights and therapeutic potential. Our findings provide further evidence on the association between fatty acid intake and subclinical inflammation as reflected in hs-CRP levels. This raises the possibility that hs-CRP concentrations could be improved by changes in dietary fatty acid intake. However, these need to be formally tested in well-designed trials to comprehensively understand the impact of dietary fatty acids on subclinical inflammation.
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