Several studies have investigated the potential health benefits, including those associated with neurological function, of the n-3 fatty acid DHA. This has arisen in part because of the association between higher intakes of fish, which is a major dietary source of DHA, and reduced disease risk. In addition to DHA, fish also provides choline and vitamin D. The objective of the present study was to assess whether women in the first half of pregnancy with low fish intake also had low blood concentrations of vitamin D, choline and DHA. A total of 222 pregnant women at 16 weeks of gestation were examined for dietary intake, erythrocyte (phosphatidylethanolamine PE) DHA, plasma free choline and 25-hydroxyvitamin D (25(OH)D). Women who consumed ≤ 75 g fish/week (n 56) compared to ≥ 150 g fish/week (n 116) had lower dietary intake of DHA, total choline and vitamin D (P< 0·001), and lower erythrocyte PE DHA (5·25 (sd 1·27), 6·83 (sd 1·62) g/100 g total fatty acid, respectively, P< 0·01), plasma free choline (6·59 (sd 1·65), 7·40 (sd 2·05) μmol/l, respectively, P= 0·023) and 25(OH)D (50·3 (sd 20·0), 62·5 (sd 29·8) nmol/l, respectively, P< 0·01). DHA intake was positively related to the intake of vitamin D from foods (ρ 0·47, P< 0·001) and total choline (ρ 0·32, P< 0·001). Dietary intakes and biomarkers of DHA, choline and vitamin D status were assessed to be linked. This raises the possibility that unidentified concurrent nutrient inadequacies might have an impact on the results of studies addressing the benefits of supplemental DHA.

The aim of the present study was to validate a food photograph album (FPA) as a tool to visually estimate food amounts, and to compare this estimation with that attained through the use of measuring cups (MC) and food models (FM). We tested 163 foods over fifteen sessions (thirty subjects/session; 10–12 foods presented in two portion sizes, 20–24 plates/session). In each session, subjects estimated food amounts with the assistance of FPA, MC and FM. We compared (by portion and method) the mean estimated weight and the mean real weight. We also compared the percentage error estimation for each portion, and the mean food percentage error estimation between methods. In addition, we determined the percentage error estimation of each method. We included 463 adolescents from three public high schools (mean age 17·1 (sd 1·2) years, 61·8 % females). All foods were assessed using FPA, 53·4 % of foods were assessed using MC, and FM was used for 18·4 % of foods. The mean estimated weight with all methods was statistically different compared with the mean real weight for almost all foods. However, a lower percentage error estimation was observed using FPA (2·3 v. 56·9 % for MC and 325 % for FM, P< 0·001). Also, when analysing error rate ranges between methods, there were more observations (P< 0·001) with estimation errors higher than 40 % with the MC (56·1 %), than with the FPA (27·5 %) and FM (44·9 %). In conclusion, although differences between estimated and real weight were statistically significant for almost all foods, comparisons between methods showed FPA to be the most accurate tool for estimating food amounts.

The Inuit population is often described as being protected against CVD due to their traditional dietary patterns and their unique genetic background. The objective of the present study was to examine gene–diet interaction effects on plasma lipid levels in the Inuit population. Data from the Qanuippitaa Nunavik Health Survey (n 553) were analysed via regression models which included the following: genotypes for thirty-five known polymorphisms (SNP) from twenty genes related to lipid metabolism; dietary fat intake including total fat (TotFat) and saturated fat (SatFat) estimated from a FFQ; plasma lipid levels, namely total cholesterol (TC), LDL-cholesterol (LDL-C), HDL-cholesterol (HDL-C) and TAG. The results demonstrate that allele frequencies were different in the Inuit population compared with the Caucasian population. Further, seven SNP (APOA1 − 75G/A (rs670), APOB XbAI (rs693), AGT M235T (rs699), LIPC 480C/T (rs1800588), APOA1 84T/C (rs5070), PPARG2 − 618C/G (rs10865710) and APOE 219G/T (rs405509)) in interaction with TotFat and SatFat were significantly associated with one or two plasma lipid parameters. Another four SNP (APOC3 3238C>G (rs5128), CETP I405V (rs5882), CYP1A1 A4889G (rs1048943) and ABCA1 Arg219Lys (rs2230806)) in interaction with either TotFat or SatFat intake were significantly associated with one plasma lipid variable. Further, an additive effect of these SNP in interaction with TotFat or SatFat intake was significantly associated with higher TC, LDL-C or TAG levels, as well as with lower HDL-C levels. In conclusion, the present study supports the notion that gene–diet interactions play an important role in modifying plasma lipid levels in the Inuit population.

Adequate intake of n-3 fatty acids plays an important role in human health. The analysis of various blood lipids is used as a measure of fatty acid status in humans. Cheek cell phospholipids (PL) have also been proposed as biological markers, but are rarely used in clinical studies due to limitations in sample quality and quantity. An improved method for the analysis of cheek cell glycerophospholipid fatty acids is applied in a 29 d supplementation trial with 510 mg DHA daily. The DHA increases in cheek cell, plasma and erythrocyte glycerophospholipids are compared. High correlations are shown for glycerophospholipid DHA between cheek cells and plasma (r 0·88) and erythrocytes (r 0·76) before study commencement. After the daily supplementation of DHA, the half-maximal glycerophospholipid DHA level is reached after about 4 d in plasma, 6 d in erythrocytes and 10 d in cheek cells. The mean DHA increase (mol%) relative to baseline was most prominent in plasma (186 %), followed by cheek cells (180 %) and erythrocytes (130 %). Considering a lag phase of about 5 d, cheek cells reflect short-term changes in dietary fat uptake. Based on the data of the present study, they can be used alternatively to plasma and erythrocyte PL as non-invasive n-3 fatty acid status markers.