2018
DOI: 10.1016/j.clnu.2017.09.007
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Circulating fatty acids in relation to alcohol consumption: Cross-sectional results from a cohort of 60-year-old men and women

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Cited by 15 publications
(9 citation statements)
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“…Our results show an association between higher alcohol intake and higher 16:0, 16:1 and estimated SCD activity. This is in line with previous studies showing that alcohol consumption is positively associated with 16:0 in plasma PL [32] and in erythrocyte membranes [25,33,34]. As a potential mechanism, alcohol consumption may increase the activity of acetyl-CoA carboxylase, a key lipogenic enzyme, and thereby the synthesis of 16:0 [33].…”
Section: Discussionsupporting
confidence: 92%
“…Our results show an association between higher alcohol intake and higher 16:0, 16:1 and estimated SCD activity. This is in line with previous studies showing that alcohol consumption is positively associated with 16:0 in plasma PL [32] and in erythrocyte membranes [25,33,34]. As a potential mechanism, alcohol consumption may increase the activity of acetyl-CoA carboxylase, a key lipogenic enzyme, and thereby the synthesis of 16:0 [33].…”
Section: Discussionsupporting
confidence: 92%
“…At least six cross-sectional studies observed significant inverse associations between circulating odd-chain SFAs, particularly C17:0, and lipid profiles, markers of inflammation, or glucose metabolism, although these correlations seem to be observed mostly in overweight and obese participants 36,[66][67][68][69][70] . Two cross-sectional studies also suggested potential influences of other nutrients such as alcohol or different dietary patterns on the relationship between circulating odd-chain SFAs and lipid profiles 69,71 . Stronger evidence from well-controlled intervention studies investigating the specific role of odd-chain SFAs is still very limited.…”
Section: Associations With Markers Of Cardiometabolic Healthmentioning
confidence: 99%
“…Previously, in a cohort of Dutch postmyocardial infarction patients, weak correlations of dietary with circulating LA and lower circulating LA with higher alcohol intakes at similar intakes of LA [45] were reported, which were also observed in the present study. High alcohol intake is an established cause of liver fat accumulation [46] and higher alcohol intake has been associated with lower circulating LA in several crosssectional studies [47][48][49]. It is, therefore, possible that the inverse association between circulating LA and GGT in this study may reflect alcohol influence.…”
Section: Discussionmentioning
confidence: 69%