A prospective study of prepregnancy dietary fat intake and risk of gestational diabetes1,2,3

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Background: Fatty acids play a vital role in glucose homeostasis; however, studies on habitual dietary fat intakes and gestational diabetes mellitus (GDM) risk are limited and provide conflicting findings.

Objective: We determined whether the total amount and the type and source of prepregnancy dietary fats are related to risk of GDM.

Design: A prospective study was conducted in 13,475 women who reported a singleton pregnancy between 1991 and 2001 in the Nurses’ Health Study II. In these women, 860 incident GDM cases were reported. The adjusted RR of GDM was estimated for quintiles of total fat, specific fat, and the source of fat intakes by pooled logistic regression.

Results: Higher animal fat and cholesterol intakes were significantly associated with increased GDM risk. Across increasing quintiles of animal fat, RRs (95% CIs) for GDM were 1.00 (reference), 1.55 (1.20, 1.98), 1.43 (1.09, 1.88), 1.40 (1.04, 1.89), and 1.88 (1.36, 2.60) (P-trend = 0.05). Corresponding RRs (95% CIs) for dietary cholesterol were 1.00 (reference), 1.08 (0.84, 1.32), 1.02 (0.78, 1.29), 1.20 (0.93, 1.55), and 1.45 (1.11, 1.89) (P-trend = 0.04). The substitution of 5% of energy from animal fat for an equal percentage of energy from carbohydrates was associated with significantly increased risk of GDM [RR (95% CI): 1.13 (1.08, 1.18); P < 0.0001]. No significant associations were observed between dietary polyunsaturated fat, monounsaturated fat, or trans fat intakes and GDM risk.

Conclusion: Higher prepregnancy intakes of animal fat and cholesterol were associated with elevated GDM risk.

Abbreviations used:

ABCA1
ATP-binding cassette transporter, subfamily A member 1
FFQ
food-frequency questionnaire
GDM
gestational diabetes mellitus

Cited by (0)

1

From the Epidemiology Branch, Division of Epidemiology, Statistics and Prevention Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD (KB, EY, and CZ); the Departments of Epidemiology and Nutrition, Harvard School of Public Health, Boston, MA (DKT and FBH); and the Channing Laboratory, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA (FBH).

2

Supported by research grants CA50385 and DK58845 from the NIH and the Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH (KB, CZ, and EY).

3

Address correspondence to C Zhang (e-mail: [email protected]) or K Bowers (e-mail: [email protected]) at Epidemiology Branch, Division of Epidemiology, Statistics, and Preventive Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, 6100 Executive Boulevard, Room 7B03, Rockville, MD 20852.