Dietary trans fatty acid intake is associated with increased fetal loss
Received 19 April 2007; received in revised form 14 June 2007; accepted 14 June 2007. published online 29 November 2007.
Objective
To examine whether dietary trans fatty acids (TFAs) were associated with fetal loss (no. of pregnancies − no. of live births). The basis of our inquiry derives from the facts that the PPAR-gamma receptor plays a pivotal role in placental function and that TFAs down-regulate PPAR-gamma gene mRNA expression.
Design
Retrospective study comparing dietary data on TFAs and total calories from Block 98 quantitative food frequency questionnaire on 104 women with insulin data and reporting one or more pregnancies.
Setting
Twenty-five- to 30-year follow-up as young adults (age 39.5 ± 4.5 years) of schoolgirls in the Princeton School cardiovascular risk study.
Patient(s)
Former participants in school-based research program at ages 6–18 years (1973–78), screened as part of follow-up study (1998–2003).
Main Outcome Measure(s)
Fetal loss.
Result(s)
By stepwise logistic regression, with fetal loss (≥1 vs. 0) as the dependent variable and total calories, percent calories from TFAs (linear and squared terms), diabetes (yes/no), serum insulin, age, race, body mass index, leisure and work physical activity, and education as explanatory variables, percent calories from TFAs was positively, curvilinearly, independently associated with fetal loss. For each 1-unit increase in the squared term of percent calories from TFAs, the odds of having fetal loss versus no fetal loss increased 1.106 times (odds ratio = 1.106; 95% confidence interval 1.026–1.192).
Conclusion(s)
Since PPAR-gamma plays a pivotal role in placental biology and is down-regulated by TFAs, TFAs may be a reversible risk factor for fetal loss.
aChildren's Hospital Medical Center, Cincinnati, Ohio
bJewish Hospital Cholesterol Center, Cincinnati, Ohio
Reprint requests: C. J. Glueck, M.D., ABC Building, Cholesterol Center, 3200 Burnet Avenue, Cincinnati OH, 45229 (FAX: 513-585-7950).
Supported in part by National Institutes of Health, National Heart, Lung and Blood Institute grant no. HL62394 and the Lipoprotein Research Fund and by the Medical Research Fund, Jewish Hospital of Cincinnati.
ABSTRACT