Hurtado 2015.

Methods	RCT: NCT01947426 (NUGELA)
Participants	110 women randomised Inclusion criteria: healthy term infants with no presence of diseases that may affect the normal development of pregnancy or lactation, singleton gestation, normal course of pregnancy, BMI of 18 to 30 kg/m² at the start of pregnancy, weight gain of 8 kg to 12 kg since pregnancy onset, no intake of DHA supplements during pregnancy, term birth, spontaneous vaginal birth, appropriate weight for GA, Apgar index ≥ 7 at 1st and fifth minute of life, normal monitoring results, and breast‐feeding of the neonate Exclusion criteria: see above Setting: 2 hospitals, Hospital Materno‐Infantil (Granada, Spain) and Hospital Universitario Materno‐Infantil (Las Palmas de Gran Canaria, Spain), between June 2009 and August 2010
Interventions	SUPPLEMENTATION + FOOD: DHA + EPA versus placebo (in the form of a dairy product) Group 1: Fish oil enriched dairy drink (400 mL enriched with omega‐3 (total 392 mg – 72 mg EPA and 320 mg DHA/day; fish oil from tuna)): total number randomised = 56 Group 2: dairy drink with no fish oil: 400 mL: total number randomised = 54 Timing of supplementation: from 28 weeks GA to 4th month of lactation Both groups of women received dietary advice DHA + EPA dose/day: low: 320 mg DHA + 72 mg EPA
Outcomes	Women/birth: fatty acid profiles were determined in the mother’s (at enrolment, at birth, and at 2.5 and 4 months) and newborn (at birth, and at 2.5 months) placenta and breast milk (colostrum and at 1, 2, and 4 months); maternal diet (enrolment, 1 month after enrolment and first month of lactation); GWG; GA; placenta DMT1, FPN1, TfR1 and Hamp1 mRNA and protein expression; hepcidin expression; oxidative damage biomarkers (enrolment, birth, 2.5 and 4 months postpartum); inflammatory markers (birth and 2.5 months); cytokines Babies/infants/children: hepcidin expression; oxidative damage biomarkers (birth; 2.5 months); Apgar at 1 and 5 minutes; birthweight; birth length; head circumference at birth; pattern reversal visual evoked potentials (VEPs) (at 2.5 and 7.5 months) and Bayley test (at 12 months) – BSID II MDI; PDI
Notes	Funding: Excellence grant (mP‐BS‐9) from the Campus de Excelencia Internacional GREIB (Granada Research of Excellence Initiative on BioHealth) Declarations of interest: “F.L.‐V is an employee of Lactalis Puleva”. No other conflicts declared.
Risk of bias
Bias	Authors' judgement	Support for judgement
Random sequence generation (selection bias)	Low risk	Quote: "unpredictable sequence computer‐generated"
Allocation concealment (selection bias)	Unclear risk	Quote: "randomly assigned"
Blinding of participants and personnel (performance bias) All outcomes	Low risk	Identical white packaging used; trial investigators and participants were unaware of the treatment allocation.
Blinding of outcome assessment (detection bias) All outcomes	Low risk	Not reported, but probably done.
Incomplete outcome data (attrition bias) All outcomes	High risk	34/110 (31%) lost to follow‐up by the end of the intervention. In the omega‐3 group 18/56: 1 lactose intolerant 4 did not attend 1 gestational diabetes 3 no reason given 1 DHA supplemented 4 did not like the milkshakes 4 did not breastfeed In the control group 16/54: 1 lactose intolerant 2 did not attend 3 no reason given 4 DHA supplemented 1 congenital heart disease 1 moved 4 did not breastfeed Likely to have been post randomisation exclusions (e.g. preterm) but none were mentioned. At 12 months: 24/56 (43%) in the DHA group and 25/54 (46%) in the placebo group were lost to follow‐up.
Selective reporting (reporting bias)	Unclear risk	Inadequate information to assess confidently.
Other bias	Low risk	Similar baseline characteristics