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Randomized Controlled Trial
. 2015 Jun;16(4):271-9.
doi: 10.1111/pedi.12170. Epub 2014 Jul 12.

Effect of Docosahexaenoic Acid Supplementation on Inflammatory Cytokine Levels in Infants at High Genetic Risk for Type 1 Diabetes

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Randomized Controlled Trial

Effect of Docosahexaenoic Acid Supplementation on Inflammatory Cytokine Levels in Infants at High Genetic Risk for Type 1 Diabetes

H Peter Chase et al. Pediatr Diabetes. .
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Abstract

Objective: Type 1 diabetes (T1D) results from the inflammatory destruction of pancreatic β-cells. In this study, we investigated the effect of docosahexaenoic acid (DHA) supplementation on stimulated inflammatory cytokine production in white blood cells (WBC) from infants with a high genetic risk for T1D.

Research design and methods: This was a multicenter, two-arm, randomized, double-blind pilot trial of DHA supplementation, beginning either in the last trimester of pregnancy (41 infants) or in the first 5 months after birth (57 infants). Levels of DHA in infant and maternal red blood cell (RBC) membranes and in breast milk were analyzed by gas chromatography/mass spectrometry. Inflammatory cytokines were assayed from whole blood culture supernatants using the Luminex multiplex assay after stimulation with high dose lipopolysaccharide (LPS), 1 µg/mL.

Results: The levels of RBC DHA were increased by 61-100% in treated compared to control infants at ages 6-36 months. There were no statistically significant reductions in production of the inflammatory cytokines, IL-1β, TNFα, or IL-12p40 at any of the six timepoints measured. The inflammatory marker, high-sensitivity C-reactive protein (hsCRP), was significantly lower in breast-fed DHA-treated infants compared to all formula-fed infants at the age of 12 months. Three infants (two received DHA) were removed from the study as a result of developing ≥two persistently positive biochemical islet autoantibodies.

Conclusions: This pilot trial showed that supplementation of infant diets with DHA is safe and fulfilled the pre-study goal of increasing infant RBC DHA levels by at least 20%. Inflammatory cytokine production was not consistently reduced.

Keywords: breast milk DHA; cytokines; docosahexaenoic acid (DHA); red blood cell DHA; type 1 diabetes.

Conflict of interest statement

No conflicts of interest were reported by any co-investigators.

Figures

Figure 1
Figure 1
Flow Chart of Study Design.
Figure 2
Figure 2. Breast milk DHA levels
Figure 2a: Breast milk DHA levels in Group A mothers (who entered the trial in the last trimester of pregnancy). Insufficient mothers were still nursing at 12 months so a value is not provided. Values were significantly different (P<0.01) at 0 and 3 months (when adequate samples were available for analysis). Figure 2b: Breast milk DHA levels in Group B mothers, with infants entering the trial anytime between birth and the fifth post-natal month. Zero-time reflects the enrollment time, with all infants then studied at age 6 months. Values were significantly different (P<0.01) at 6, and 9 months. Inadequate control samples were available at 12 months for statistical analysis.
Figure 2
Figure 2. Breast milk DHA levels
Figure 2a: Breast milk DHA levels in Group A mothers (who entered the trial in the last trimester of pregnancy). Insufficient mothers were still nursing at 12 months so a value is not provided. Values were significantly different (P<0.01) at 0 and 3 months (when adequate samples were available for analysis). Figure 2b: Breast milk DHA levels in Group B mothers, with infants entering the trial anytime between birth and the fifth post-natal month. Zero-time reflects the enrollment time, with all infants then studied at age 6 months. Values were significantly different (P<0.01) at 6, and 9 months. Inadequate control samples were available at 12 months for statistical analysis.
Figure 3
Figure 3. RBC membrane DHA levels
Infant RBC membrane DHA levels (mg/dL) were higher for all treatment infants compared to all control infants (P<0.001 for all comparisons except at age 30 months [P<0.01]). Data in Table 4, Appendix.

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